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Where do the four ADPs come from in the second stage of glycolysis?
In the first stage of glycolysis, the two molecules of ATP are broken down into 2 ADPs + 2 Pi through hydrolysis, then in the second stage of glycolysis they are phosphorilazed to obtain 2 ATPs. How can this process happen twice to yield 4 molecules of ATP if we only have 2 ADPs to begin with?
Note: I'm not asking why the process happens twice, since it's easy to see that the Fructose-1,6-biphosphate is being broken down into two Glyceraldehyde phosphate molecules. I'm asking how can the process of producing two ATPs happen twice if we only broke down two ATP molecules into ADP.

There are many other sources of ADP in the cell: various proteins that use ATP as an energy source hydrolyze it to form ADP + phosphate, thereby extracting energy. This ADP can then be re-phosphorylated by glycolysis to form ATP again. If glycolysis did not produce a net yield of ATP it would be pointless, so it really should be unbalanced in this sense.

This idea was my best guess, however most of the sources I checked out on glycolysis omitted this information. So, to be clear, what you're saying is that ADP doesn't have to come directly from the previous steps of glycolysis, but it usually comes from other sources in the cell?

Yes. The whole point of producing ATP is that it serves as a common source of energy for various energy-demanding reactions in the cell. And those reactions turn ATP back into ADP.

I think I understand your question, and stumbled upon it because i was wondering the same thing while studying for my Microbio test. I know its a year late, but someday someone else might need this info...so here it is.
To put it simply: there is a second pair of phosphates added to the two 3-carbon molecules cleaved from the preparatory stage before the 4 ATP are finally formed. These get added by an enzyme while reducing the NAD+ molecules.
In depth: The first pair of phosphates the cell uses to synthesize ATP come from the initial 2 ATP invested during the prep stage, but an additional 2 phosphates are added when the cell oxidizes the two Glyceraldehyde, 3 Phosphate (G3P) molecules to form NADH. In this step, two electrons are taken away from the G3Ps and an available inorganic phosphate is added to the "1" position, forming "1,3 Biphosphoglyceric Acid " (1,3BPG). Afterwards, the molecules each have 2 phosphates for a total of 4 phosphates available to get oxidized and used to synthesize 4 ATPs.
This step, (the addition of an inorganic phosphate as an intermediary step) is SO overlooked by regular textbooks that its not even funny. mine doesnt even list the enzyme; I had to look it up.
but yeah, that's the source of the additional phosphates available for forming the 4 ATP molecules of glycolysis, and possibly why you didnt see it from the diagram in your textbook (you're not alone!).
Hope that helps!
Sources, as of 4/18/17:

https://www.khanacademy.org/science/biology/cellular-respiration-and-fermentation/glycolysis/a/glycolysis
https://en.wikipedia.org/wiki/1,3-Bisphosphoglyceric_acid

It may help if I suggest two ways of looking at the situation.

The first way, which tries to reflect your line of thinking (as I understand it), looks at the situation as two reactions being needed to maintain ADP in the cell. The first reaction produces ATP:

Glycolysis: ADP + Pi → ATP

Whereas the second reaction regenerates ADP by using the ATP

Biosynthesis / Movement / Electrochemical work etc: ATP → ADP + Pi

If the second reaction doesn’t occur, the first one will stop too, but that is OK as the cell has no need to produce ATP if there is plenty.

A second (perhaps more sophisticated) way is to regard the situation as an equilibrium:

ADP + Pi ⇋ ATP

The position of this equilibrium (and hence the relative concentrations of ADP and ATP) will vary depending on the situation in the cell. The concentrations of ADP and ATP will effect glycolysis (and other aspects of metabolism) both by simple mass action, and also be something you may not have yet met, the regulation of certain key enzymes (allosteric regulation). (An equilibrium between ATP, ADP and AMP also exists.)
Finally, there are both open systems and (semi-) closed systems in biological chemistry. The conversion of foodstuffs into chemical energy and the structural components of a cell is obviously an open system — the substrates for glycolysis ultimately come from outside the organism. The interconversion of ATP and ADP (and NAD+/NADH) can be regarded as (semi-) closed, as the main part of the chemical moiety is being conserved. However one should not forget that, initially, when the organism is growing and cells are dividing, the adenosine backbone has to be synthesized, and it requires energy to do this and more energy to add phosphates (also from the diet) to the ribose.

i know that is simple because if you can just look at the first step there were 2ATP only and the energy in this molecule is used to phosphorylate the glucose molecule  to give fructose biphosphate and 2ADP and 2pi is left this to molecule may reorganize by the substrate level phosphoryalation to give 4ATP molecules as you know the enery is come from the chamical energy from the GP(glyceraldehyde 3 phosphate ) as initially we have 2ADP and 2Pi but finally we have 4ATP because  the energy is enough to reconstract  additional 2ADP and 2Pi which comes from other non glycolisis reactions


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Is this bacteria or fungi?
I've been growing bacteria on an agar plate and after putting the dishes in the incubator, this is what I saw. I'm new to bacteria identification, and is this just contamination by fungi or is this actually bacteria colonies? I suppose it is fungi, but what about the white, round white circles on top of the fungi(the top, left picture), is that bacteria colonies?

Well what did you put on the plate? Currently it's extremely hard to answer because we know very little about your experimental protocol.

@rg255 I put my thumb on the plate, to see the amount of bacteria on it to then compare the amount with after washing the hand using different methods. I suppose the plate may have been contaminated from the air because of insufficient sterile technique.

How about a side view? Do you see spores in the stalks?

It's probably mostly fungal contamination if you did not sterilize and left the container open. This video on how to isolate bacteria better may help: https://www.jove.com/video/3064/aseptic-laboratory-techniques-plating-methods
Good luck!

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How many cells does the hermaphrodite version of Caenorhabditis elegans have?
Wikipedia states:

The male C. elegans, for example, has 1031 cells

How many cells does the female version have?

Homework questions and trivial questions about basic biological concepts are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. https://www.google.com/#q=how+many+cells+in+female+c+elegans

959 Somatic Cells according to WormBase and The WormBook.

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How does the synaptic cleft exist?
I'm not asking why the synaptic cleft exists, i.e. what function it holds, rather how.
So I know that the neurotransmitter diffuses across it, it is 20-40 nm wide and contains basal lamina (in NMJs at least), but I cannot find any allusion as to what causes the gap; how the two membranes don't just touch, and how so consistent a distance is created across neurons.
Google has so far failed me on this one, though perhaps I am not searching well enough, any help would be greatly appreciated.

There are membrane proteins that act as structural components of the gap (i.e. the synapses aren't just floating there, they are anchored to each other via membrane proteins).
https://en.wikipedia.org/wiki/Neuroligin
https://en.wikipedia.org/wiki/Neurexin
The most common examples are neurexin (expressed on the pre-synaptic terminal) and neuroligin (expressed on the post-synaptic terminal). Not surprisingly, these proteins are involved in synapse formation in the developping brain, as well as the adult brain (in plastic processes where new synapses are formed). To a first approximation, as synapses are growing, their membrane proteins bind their partners and become anchored. This also leads to intracellular signalling and further maturation of the synapse. That's how synapses know where to attach.

Thank you very much this is a great answer and just what I was looking for :)


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Do any plants grow leaves beneath the ground?
We have a pretty common California weed in our yard. When we dig in the ground, we often find small ones there, with green leaves!  It's as if they form green leaves before they come to the surface. While that seems counterintuitive, there's no purpose in having green beneath the soil, it doesn't seem impossible.
We had our yard redone 6 months ago. It's possible that some mature plants were buried- but would they stay green for six months?  Or perhaps they expect to be close to the surface, so after creating a couple inches of roots, they form green leaves, even though they're buried deep enough that they're not at the surface yet.
Is this a known phenomenon?  How common is it for plants to be able to make green leaves before coming to the surface?
Thanks much...

Could it be the case that those plants have been brought underground by ants recently? Do you dig up any ant nests with the leaves?

It is a known phenomenon. A good example of the same can be observed in Philcoxia minensis.
This plant is predominantly found in sandy areas of Brazil and its underground leaves photosynthesize using sunlight energy through the relatively opaque sand particles.
These leaves also play the function of trapping and digesting nematodes underground supplementing nitrogen in the leached soils. This article [with pdf] explains this mechanism in detail.

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Data on Gene Position in Human Genome
I am trying to get some data on gene position in the human genome and I need some help
What I tried
I downloaded ftp://ftp.sanger.ac.uk/pub/gencode/Gencode_human/release_18/gencode.v18.annotation.gtf.gz
I am only interested in gene position, so I kept only the first columns.
awk -F "." '{print $1}' /Users/remi/Downloads/gencode.v18.annotation.gtf  >> HumanGenomePositions.txt

This operation will take a few minutes. The file contains information on exon position and transcript. I subsetted the table to get only the lines that concern genes
sed -i.bak '/gene/!d' HumanGenomePositions.txt

I am left with 57445 entries. 9872 are annotated by ENSEMBL and 47573 are annotated by HAVANA. Note that there is partial overlap between the two. According to Church et al. 2009, there are 19042 annotated genes in the human genome (reported from bionumbers). There is obviously something I am getting wrong!
Question
Can you help me to get data on gene positions in humans in a handy format (see below)?
start   end
15648   65487
129841  124984
...

I used the <homework> tag even though this is not a homework. The reason is that I think the question is introductory enough to be asked in an introductory course to bioinformatics.

Why did you pick GTF vs. GFF3? I only ask because I have way more experience using GFF3; also, in GFF3 column 2 tells you the type of sequence feature that is being annotated in a given row, so by using cut -f 2 | sort | uniq -c you can get a list of all the "known" features in that file, as well as a count of the number of them.  A potentially trivial explanation for the discrepancy you found is that Church at al., are only counting the protein coding genes, while your regex search will match tRNA genes, rRNA genes, miRNA genes, snoRNA genes, and pseudogenes, wouldn't it?

One extremely useful tool (in my hands) is the intermine family of data warehouses. I have primarily used modMine and FlyMine, but there is also a HumanMine. If you had a list of identifiers for those human protein coding genes you could upload that list into HumanMine and then use their query tool to generate a table of the genomic coordinates for those human genes.

I used GTF completely randomly. I don't know any of these format and I never heard of "interMine family of data warehouse" before either. Oh do you think we might have about 30,000 non-protein-coding genes? It seems huge to me but that would be a good explanation.

I recommend to filter using transcript_type value from description column. You need only proteine_coding genes. Now you have extra ~10K unprocessed pseudogenes, ~5K antisense genes, ~4K miRNA, ~7K lincRNA and more than thirty other categories of unprocessed pseudogenic stuff.
As far as I know current release for GRCh37 is 19th version, not 18.

Oh I missed this column. So is there really so many genes that do not code for proteins? I would have never guessed right. I'll just subset what I need based on this column. Thank you.

I took the 18th version completely randomly. I felt a little lost and just picked some random data to start doing things with it.

Side Question: Looking at ftp://ftp.sanger.ac.uk/pub/gencode/Gencode_human/ I can see 24 releases. Is the 19th really the newest one as you claim?

@Remi.b I suggested using the 19th release because I supposed that you use the 18th release and it is the GRCh37 assembly. As you do not have any specific needs, I think it is fine to use the latest stable release.

Gencode is 24th version afaik.


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Plant part adaptation vs animals
I have seen nurseries selling plants that grow to trees bearing different fruits. Eg: A single plant that produces fruits of peach, plum, apricot,etc. Here is one website that advertises such trees. So in conclusion any tree could be grafted to live in a trunk of a similar kind of tree. How come animal parts cannot be transplanted with other animals of the same kind. Why is it not possible to use any animal organs for humans using transplants.

Because humans have an immune system.

Can you elaborate?


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If human proteins are synthesized from only 20 different amino acids, then how can there be such variety of proteins in human cells?
I know that human proteins are synthesized using only 20 different amino acids. However, how can there be thousands of different proteins in human cells, if we only use 20 amino acids to make them?

because of length of proteins. for 100 amino acids long protein there are 20^100 combinations, roughly 10^130

There are only 26 letters in the English language, and more than 80% of words are under 10 letters. Yet there are over a million English words. Nonsense words don't count.
Now imagine the possibilities of a 20 letter alphabet, where the average "word" length is about 375 letters, and where words of up to 800 letters are possible. And that also does not include "nonsense words".
That should give you an idea of the possibilities, and why "thousands of different proteins in human cells" can exist.
How big is the “average” protein?

Heck, DNA and RNA use only five nucleobases (and individually only use four), and look at the possibilities there. And basically all modern computers use only two symbols to represent their state, yet we can encode pretty much anything we want with those two symbols (as long as we use enough repetitions).


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Fasting gastric pH versus normal gastric pH
I want to know if someone is fasting (no food or drink for a whole day) will they have a higher or lower pH than a person who is eating regularly? If so what is an estimate of both of those pH's in the stomach?

The stomach linings generally secrete gastric acid (HCl, KCl and NaCl) and the native pH of the stomach is around 2. The longer you fast, gastric acid levels keep increasing until it reaches around 1-1.5. The food that you eat increases the pH levels of your stomach because the acid reacts with the food while digestion. Depending upon the type of food you eat, the pH levels of your stomach vary, but it is generally around 4-5 (again it varies depending upon the type and amount of food there is in the stomach).

Do you know what goes wrong in heartburn? Clearly eating sometimes generates an excess of H+, which is treated by inhibiting proton pumps.

"The longer you fast, gastric acid levels keep increasing until it reaches around 1-1.5." do you have any references to back this up? I could find http://www.ncbi.nlm.nih.gov/pubmed/2395805 and    http://www.ncbi.nlm.nih.gov/pubmed/2070698 but those don't mention the levels changing when fasting for longer

@YviDe  (http://ncbi.nlm.nih.gov/pubmed/2395805 ) mentioned the median pH levels come back to nearly 1.7 within 2 hrs after meal. Another interesting article, mentioning stomach pH levels of modern humans to reach 1.5(with some other interesting facts). As I mentioned before, it is not that the pH will keep decreasing with longer fasting period. The initial secretion is high, when food reaches stomach, but based on existing acid levels, the secretion rate stabilizes down. Will post if I find any other relevant article.

@Jory here is an article on what happens in heartburn, but interestingly I found another article which mentions that heartburn is not always a resultant of acid reflux

@Grb okay, I thought with "the longer you fast" , you meant something more like 8 hours and over. The OP is asking about fasting a whole day after all.

@YviDe yes, the longer you fast, it can be thought of that the longer the stomach lining is exposed to high gastric acid levels, which becomes harmful afterwards (ulcer?). But, the increase in levels is fast and happens within few hours at the initial phase, I think.


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Hydrophobic proteins in the body?
I know that we can get hydrophobic amino acids, but are there any proteins in the body whose surface is hydrophobic? If so what is their typical function and where can they typically be found and if not why not?

Are there any proteins in the body whose surface is hydrophobic?

Sure. Although you are right in thinking that most proteins have hydrophilic surfaces, some are very hydrophobic. My favorite example is Elastin, it is the main component of the skin which grants it elasticity. In fact, the hydrophobic nature of elastin is what confers it its function. The idea, briefly said, is that a insoluble/hydrophobic structure will tend to minimize it's surface area with water, so if you stretch such a substance (i.e. increase the surface area), it will pull back to the minimum surface area state.
Reference: Li, Daggett. Molecular basis for the extensibility of elastin. Journal of Muscle Research & Cell Motility (2002).

Also many membrane proteins, as being hydrophobic is what allows them to sit in the membrane.


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Thermal ratchet model

Two models have been proposed to explain how ATP hydrolysis by mitochondrial hsp70 drives protein import.In the thermal ratchet model (Figure 12-28A), the emerging chain slides back and forth in the TIM23 translocation channel by thermal motion. Each time a sufficiently long portion of the chain is exposed in the matrix, an hsp70 molecule binds to it, preventing further backsliding and thereby making the movement directional. Thus, a hand-over-hand binding of multiple hsp70 proteins translocates the polypeptide chain into the matrix.

What does thermal motion mean here? I will be obliged if somebody could explain it.

It refers to the "random giggling" of molecules, which increases with increasing temperature (kinetic energy)

To repeat @Malijam comment, by thermal motion it is referring to the "random giggling" of molecules.
Temperature difference is nothing but a change in the frequency at which molecule move randomly. This movement has no specific direction. If a given molecule is prevented from moving into one specific direction (due to attachement to another molecule) but allowed to move into another, then the molecule will move directionally pushed by nothing but its thermal kinetic. This create a so called thermal ratchet.


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Pink Grasshoppers
The area I found this grasshopper was Canyon Country, California, USA In a desert/field area.
I have been reading up on grasshoppers because I recently came into possession of a pink grasshopper (It was identified below as the common meadow hopper Chorthippus parallelus). One of the pages that I've read covers the eating of toxic plants by grasshoppers and how they change to bright colors to warn that they are toxic after eating poisons. Is this true? Could that explain the coloring of this grasshopper, or is it due to a recessive gene, or even erythrism? I'm trying to breed it, so any and all info on how to treat this little guy, history of the coloring if its genes, and the color changing toxic effect would be much appreciated.
Here's a picture.

Could you add a specific species? It's more of a shot in the dark right now.

Can you add those links: the other sites and the resource that talks about the toxicity?

These two sites say that this is a common meadow grasshopper: Chorthippus parallelus. Have you already checked them? I can't find anything about toxic plants here, though.

Looks like an immature instar? You might be interested in this, too: http://biology.stackexchange.com/questions/20702/how-can-a-pink-grasshopper-exist

This is a page I found in the beginning of my research hinting on the eating of toxins and color change.  https://animalcorner.co.uk/animals/grasshopper/

Also, that ID describes the species that is native here in every aspect, I'll update the Description.

Chortippus parallelus is a common species in Europe that is according to my grasshopper id-guide extremely variable in color. It can be green, brown, yellow and even purple. I can verify that from field experience. Pink however is much more rare, and considered to be caused by Erythrism  See https://en.m.wikipedia.org/wiki/Erythrism for explanation and several references to pink grasshoppers/katydids.

If the wikipedia is right, and the pink coloration is a dominant trait, then OP should have an easy time breeding for it, assuming he can breed grasshoppers in captivity.


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How to improve A260/230 ratio?
I am extracting DNA from cicada exuviae using ethanol precipitation combined with either NaCl 6M or Ammonium acetate. After DNA extraction, my samples have quite low A260/230 ratio such as in the attached picture. I suspect this might be due to left-over salt in my samples, since I dont use kits or phenol/chloroform/isoamyl in DNA extraction protocol. I proceeded on with PCR using 16S primers but received no bands.
Could you advice what potential contaminants could appear in the samples that prohibit PCR? As well as what could I do to improve this ratio? Thank you so much!

Are the cultured cells you use in the beginning or tissues? How do you break your cells?

Actually, I used exokeleton, which contains left-over tissues of cicada when it molts.
For the lysis, I used 600 ul buffer including Tris 10 mM, pH 7.5, NaCl 400 mM, EDTA 100 mM, and SDS 0.6%, along with 30 ul Proteinase-K.


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Can HIV be transmitted via mosquitos?
It is known that HIV is usually transmitted by direct blood or body fluid contact between an infected individual and a healthy person (like blood transfusion or needle sharing):
Suppose a mosquito bites an individual suffering from AIDS and in the process sucks up some T cells infected with HIV along with RBCs. Then it bites another person not suffering from the disease, and transfers these infected T cells. Isn't there a high probability of the second individual contracting HIV?

Well.. that would probably be a much more important vector of transmission than sex or blood transfer, especially in the right parts of Africa. The number of infected there is rather big, so if mosquitoes were able to routinely transmit the virus, almost everyone would be infected by now. Of course, this is just a relatively weak conjencture, but it's a decent first guess.

@Luaan: And yet, not everyone in Africa has Malaria...

@eggyal That's not a bad argument. I suppose it's a combination of natural resistance, improved artificial defenses and perhaps the past mass deployments of insecticides. And of course, not all of Africa has massive mosquito trouble that's why I said "especially in the right parts of Africa". More importantly, malaria isn't necessarily terminal, and the people who survive are immune to further infection - and when it is terminal, it kills quite quickly. On the other hand, AIDS is a very prolonged infection. If you're dead, you're no longer part of the statistic :) http://tinyurl.com/yolhob

No, this is not possible. There are a few reasons for that, but most important are that the only thing a mosquito injects is its own saliva, while the blood is sucked into the stomach where it is digested.
To be able to infect other people HIV would need to be able to leave the gut intact and then also be able to replicate in the mosquitos which it cannot do, due to the missing of the CD4 antigen on the surface of the insect cells. These are needed as a surface receptor for the virus to bind and enter the cells. This is also true for other blood sucking insects like bed bugs or fleas.
Other pathogens can do this, examples would be Yellow fever or Malaria. In Yellow fever the virus first infects epithelial cells of the gut, then enters the blood system of the insect to finally end up in the salivary glands, where the virus is injected together with the saliva into the biten person. In Malaria the pathogen is also able to leave the gut region and mature in the salivary glands.
HIV can only be transmitted through blood (either through direct transmission, operations etc.), through semen (cum), pre-seminal fluid (pre-cum), rectal fluids, vaginal fluids, and breast milk. See reference 3.
References:

Why Mosquitoes cannot transmit AIDS
Can we get AIDS from mosquito bites?
HIV Transmission Risk:  A Summary of Evidence

Is there a zero probability that tiny droplets of blood remain on the proboscis of the mosquito long enough for said mosquito to inject its proboscis into the bloodstream of another person? In particular, in what physical aspects is the proboscis different than a needle or razor? I am not talking about blood sucked into the gut of the mosquito, I am talking about blood remaining on the proboscis.

@MarcusJuniusBrutus Very interesting question - I've asked it as a follow up question Why doesn't blood remain on a mosquito's proboscis in quantities that could spread blood-borne diseases?

What if you swatted the mosquito while it was attached? Leeches, for example, will vomit previously ingested blood into you if stressed.

@OrangeDog Good point, I have read something about this somewhere, I have to only find it back.

"Would it be posssible for a swatted mosquito that previously fed off a HIV carrier to infect your blood through the hole it made, or a nearby cut?" (copied from comment directed at Chris by @user2104648, posted as a now deleted answer)

@OrangeDog I don't find my reference back, so I only write this as a comment at the moment, but it was classified as highly unlikely but not impossible. First: HIV needs relatively high viral loads for a sure infection. Then mosquitoes usually only feed off one victim per time (given they are not disturbed), so they will not need another victim until this blood is digested. If they are disturbed the amount of blood is even smaller (we are talking about the range of 3µl and less) so an infection gets less likely. It would be really bad luck.

I am not a medical doctor but in my view this is within the realms of possibility. The probability has been estimated by Princeton at 1 in 10 million. This is per bite, assuming - I presume - that the mosquito that bit you was just feeding on an HIV-infected person of sufficiently high viral load. It is not against the laws of Physics that blood cells can remain for some time on the proboscis or other mouth-parts of a mosquito.
Whether this is probable is a matter of interpretation depending on your definition of 'probable'. But your question is about possibility, not probability. Personally, given that this is comparable, if not lower, to the probability of being struck by lightning I wouldn't give it a second thought.


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Why are plant cells rectangular and animal cells spherical shaped?
Is that because the plant cells have cell walls and animal cells don't, or is there a function performed by the different shapes? Perhaps round shapes assist the movement of cells?

Quite a few, perhaps even the majority, of animal cells are not round/spherical.  For extreme examples, consider neurons & astrocytes, muscle cells, etc.  Even blood cells aren't spherical, but disk-shaped.

@jamesqf - That is the basis for a good answer.

Animal cells
Generally all (animal) cells have different shapes because they do different things. Each cell type has a specific role which it has to play in order to assist the body in working efficiently and functionally. Thus their shape supports them to carry out these roles effectively.
Look at (animal cells):

Neurones
Photoreceptors
Immune Cells

Plant cells
They are often square shaped/rectangular because it is easier to build a "brick wall" (cell wall) out of rectangular bricks.  Any structure that minimises interstitial space will hence allow more "life", thus possibly making it stronger.
This is also due to:

Plant cells are not necessarily square, but they due tend to have distinct edges and be somewhat rectangular. This structure is caused by the cell wall which is very rigid and therefore forces the cell to have a defined shape.

However there is one exception I could think of, and those are pavement cells, they're neither round nor somewhat spherically shaped. Pavement cells are a cell type found in the outermost epidermal layer of plants.

Sources:

Beckett, B. S. Biology: A Modern Introduction. Oxford: Oxford UP, 1976. Print.
http://www.academia.edu/3786570/Plant_Cell
Rappaport, R. Cytokinesis in Animal Cells. Cambridge: Cambridge UP, 2005. Print.
http://biology.about.com/od/cellbiology/ss/plant-cell.htm
https://www.msu.edu/~whymerky/CellS&Funitplan.htm


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Is 5-HTP a SSRI?
Can 5-Hydroxytryptophan (oxitriptan) be categorized as selective serotonin reuptake inhibitor (SSRI)? Since they both act on the serotonin pathway and are used to treat depression and other mood disorders?
For example on this page, they're treated under the same category.
If they're not, how 5-HTP is different from SSRI?

That page you linked doesn't consider 5-HTP an SSRI: "Since 5 HTP (increase serotonin synthesis) and SSRIs (prolongs serotonin action) affects the serotonergic system in different ways,"

I know, it says: 5 HTP and SSRI in the title, but later on describes what are SSRIs, so like it's describing them both together. I'm sure some time ago I've seen some info that 5-HTP is same as SSRI, could be invalid, that's why I'm trying to double check that. Theoretically 5-HTP should work the same as SSRI, so I'm looking for some reliable sources how they're different.

No, it isn't considered an SSRI. SSRI stands for selective serotonin re-uptake inhibitor or serotonin-specific reuptake inhibitor, which designates the mechanism by which this category of drug (supposedly) works: on the serotonin transporters in the brain. It's a term only used for a limited range of drugs, like sertraline and citalopram.
5-HTP (Oxitriptan being a trade name) is a chemical precursor to serotonin. The way it affects the serotonergic system is by increasing the rate at which it is generated. The category to which it belongs is the "serotonin precursor" category, similarly to e.g. L-tryptophan (which is actually itself a precursor of 5-HTP).
If it is prescribed to treat depression, it might be called an anti-depressant, but SSRI is a term for a  mechanism of action moreso than an effect. Tetracyclic and tricyclic antidepressants, for example, also affect neurotransmitter uptake in the brain, but aren't called SSRIs.
Further reading: How Different Antidepressants Work

Thanks, so to which category 5-HTP/Oxitriptan goes then?

@kenorb I'm not sure what you mean. I can't find any reliable source that calls it an antidepressant right now. Until then, I'd just call it an amino acid...


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Yeast Strain with squalene synthase / farnesyltransferase (ERG9) gene deleted
I was interested in obtaining a yeast strain without the enzyme farnesyltransferase (Which catalyses conversion of FPP to Squalene). The Euroscraf database has thousands of yeast strains with individual genes deleted but when I search for "farnesyltransferase" I get a couple of hits that I am not being able to interpret.
Here's the link: http://www.euroscarf.de/search.php?search=farnesyltransferase&project=
What are all these different strains? In particular how does one interpret notation like which seems to be describing a particular strain:
BY4743; MATa/MATα; ura3Δ0/ura3Δ0; leu2Δ0/leu2Δ0; his3Δ1/his3Δ1; met15Δ0/MET15; LYS2/lys2Δ0; YKL019w/YKL019w::kanMX4

Seems like you should have searched for erg9 instead...

@MattDMo Ah! That explains it. Thanks! So what's the difference between these two strains that it throws up SC2489 and Y22884: http://www.euroscarf.de/search.php?search=ERG9&project= Are they both Squalene blocked strains? I still cannot interpret the "Genotype" goblydygook that the database entry has.......

Well, the genotype is simply describing what variants of certain genes the strain has - what mating type it is (MATa/MATα), what nutrients it requires in the medium and what it can synthesize for itself, and the type of mutation that occurred (or was engineered) to make the strain deficient for the gene you are interested in. You'll need to talk to someone much more familiar with yeast genetics than me to determine exactly what each notation means - I'm just remembering all this stuff from grad school 13 or 14 years ago...

Yeast strains have two mating types MATa (since it secretes a pheromone named 'a factor'), MATα (secretes pheromone 'α factor'). Both MATa and MATα strains are haploid and when they fuse together they form diploid zygote. A haploid yeast has only one set of genes and utilize chemicals like histidine and tryptophan (amino acids) and adenine (part of DNA, ATP and other molecules) for growing. Yeast strains mutant with any of genes to
make these chemicals they will not grow unless they can get these chemicals from their food (yeast media) or allowed to mate with strain having normal genes.
Interpreting the strain notation:
BY4743; MATa/MATα; ura3Δ0/ura3Δ0; leu2Δ0/leu2Δ0; his3Δ1/his3Δ1; Met15Δ0/MET15; LYS2/lys2Δ0; YKL019w/YKL019w::kanMX4
Strain name: BY4743
Genotype: MATa/MATα; ura3Δ0/ura3Δ0; leu2Δ0/leu2Δ0; his3Δ1/his3Δ1; Met15Δ0/MET15; LYS2/lys2Δ0; YKL019w/YKL019w::kanMX4
To understand clearly, you can dissect the genotype in individual strains
BY4743;MATa;ura3Δ0;leu2Δ0;his3Δ1;met15Δ0;LYS2;YKL019w/YKL019w
BY4743;MATα;ura3Δ0;leu2Δ0;his3Δ1;MET15;lys2Δ0;kanMX4
Yeast genetics nomenclature:

Normal or wildtype genes are written in capitalized form - MET15 in MATα
Mutated genes are symbolized with small letter and Δ - ura3Δ0
ura3Δ0/ura3Δ0 - allelic mutation:  mutation in same genes of both strains (MATa/MATα) - They are two mutant alleles in the same gene locus. Both alleles of same gene are knocked out, so even both strains mate, they need external source of uracil in media to grow. Defect in one strain is NOT complemented by the other.
Met15Δ0/MET15 & LYS2/lys2Δ0 - Non-allelic mutation: Defect in one strain is complemented by the other. MATa has Met15Δ0 (mutation in methionine gene) and MATα has wildtype MET15 gene, capable of met synthesis. Complementation works here.
YKL019w/YKL019w::kanMX4 - Critical aspect of yeast strain in functional complementation assays. In all commercially available yeast strains, one gene will be double knocked out (both alleles of same gene) and replaced with an auxotrophic markers like antibiotics - tetracycline, kanamycin, ampicillin - for selecting the diploid cells after mating two strains. It is similar to plating Kanamycin mixed LB media to pick E.coli colonies harboring Kanamycin resistance vector in it.

The gene that is replaced is the gene of interest, i.e. if I am looking to study role of putative PGPS in Plasmodium falciparum, I get yeast strain knocked out with yeast PGPS (pgsΔ). When I do complementation test, I provide external DNA template cloned with Plasmodium falciparum's PGPS to check whether it complements in yeast genome and yeast grows - gene essentiality study.
I am not sure of the gene YKL019w/YKL019w, but it implies that wildtype of YKL019 is replaced with Kanamycin - kanMX4.

Wow! That was an amazing answer. Thank you very much. I am still trying to digest all of it!


text:
What are respirasomes?
I have read wikipedia but don't understand it well. Do we mean Complex I, II,III and IV when we say respirasomes?

I have not heard of this term in so many years of studying biology. Whenever you are asking questions on terminology, always provide the context.

I could not add the context because it appeared as a question in one of our college exams.

@WYSIWYG Never heard of it either, sounds like it might be a 'kitchen table' terminology used by a handful (or just one!) researcher. Bit like 'quinary structure' which is meant to be assemblies of quaternary structures...

What the article is saying, is that there are several respirasomes, each of which consists of multiple other mitochondrial complexes or cytochromes. The article makes an example of three commonly observed respirasomes when it says:

The most common supercomplexes observed are Complex I/III, Complex
  I/III/IV, and Complex III/IV.

So, the short answer to your question is that a respirasome refers to a set of multiple cytochromes, whose combined action leads to respiration.
This paper goes into more detail, and reiterates that the term "respirasome" is used to describe multiple cytochrome supercomplexes.


text:
I need help identifying a completely unknown plant for my biology class
I know two things about this plant
1 is that it does not need to be watered for a long time because it has been able to survive in my schools greenhouse for quite some time without water and 2 my teacher says she "thinks" it blooms purple or pink flowers.
Thank you in advance for any help given!

Appears to be a succulent of some sort?

Any information on where it's native to?

"Succulent plant" means any plants that stores water inside their thickened  body-tissue. btw "succulent" is Not a "taxonomic-group" like "phanerogams", "cryptogams" etc. Succulents found in different-groups of plants. It is one-sort of adaptation against dryness. So, many desert plants  are succulent in nature.

I'm no expert on plants but it could be a kalanchoe. That's based mainly on the leaf characteristics and size.

There's some 120 or so species mainly originating from the old world. These are quite drought tolerant as yours seems to be. They are a common houseplant and there are ways to stimulate reflowering so that also makes it a good candidate.
Image source.

Awesome!! How is this done? Do you just happen to know them or you enter the characters or something in a key? Like, what is the std approach when you have no clue and youve got to identify?

@rg255 - JMusser will not get the ping unless he's posted in the thread. You might want to ping him in chat.

@Polisetty just persistence and searches!

Looks like a Kalanchoe to me, too! To answer @Polisetty 's question, you might go about identifying this by noting that it is a succulent ('juicy' leaves and does not need to be watered frequently), that it's opposite-leaved, that the leaf margins are jagged (I suppose maybe 'crenate' specifically), and that it has red flowers. This isn't going to help you much in using a botanical key, but might give you a start in google image-searching...

I was thinking of Sedum spectabile, another member of the Crassulaceae. But maybe Kalanchoe is better. @Polisetty Try to make it flower!


text:
What is proton leak?
I have some idea about it. Is it the wasteful back flow of H+ ions through uncoupling proteins during aerobic respiration?
Thank you

Short answer: yes.  It also includes unspecific leakage without the aid of uncoupling proteins, since the mitochondrial inner membrane is not entirely impermeable to protons. For example, protons might fall backward through the proton-pumping complexes, through other solute carriers, or through other openings or irregularities in the membrane.


text:
Get Parent GO terms of GO term vector?
I have a vector of GOIDs that are specific GO IDs outputted from an enrichment analysis. I want to cluster my GOIDs by their parent GOID term. I used GOstats to do my enrichment analysis, and I have noticed there is an inducedTermGraph, which outputs a graphNEL object of direct children and direction parents of the GOIDs you query. If you set parents=TRUE and children=FALSE, your graph includes only parent nodes which relate to your GOID query.
However, how can I extract the node names of these parent nodes??? See code below:
gene.ids <- c(51141, 84968, 140850, 388289, 406994, 677828, 693217, 100287428,
             100505685, 100506540, 101926966, 101927244, 101928659)
require(RnBeads)
uids <- rnb.get.annotation("genes")
uids <- sort(unique(as.numeric(na.omit(unlist(sapply(unlist(uids)$entrezID,
        function(i) strsplit(i, split=";")))))))
params <- new("GOHyperGParams", annotation = "org.Hs.eg.db", geneIds = gene.ids,
             universeGeneIds = uids, ontology = "BP", conditional = TRUE,
             testDirection = "over")

res <- tryCatch({
    hyper.genes <- hyperGTest(params)
  }, error = function(ee) {
    print("Errorfests.")
  })
go.ids <- summary(hyper.genes)[,"GOBPID"]
result <- inducedTermGraph(hyper.genes, id=go.ids, children=FALSE, parents=TRUE)
nAttrs <- list()
z <- attributes(result)$nodes
    names(z) <- nodes(result)
    nAttrs$label <- z
plot(result, nodeAttrs=nAttrs)

What is this code? Is that formatting break supposed to be there? There are long winded solutions I can think of with Biopython. Could you make your input clear, and what you want your output to be.

If you just want to know the parent nodes of a list of GO terms, you can use GOBPPARENTS in the Bioconductor package GO.db (which you use when using GOstats). This may be a better way to manipulate this information programmatically.

@ddiez do you have a code example of what you mean? for example if I have:  terms = c("GO:0001071","GO:0005886") I can't just run this: GOMFPARENTS$terms or GOMFPARENTS(terms).

@RickBeeloo see my answer below with some code. First problem you are mixing ontologies (GO:0001071 is for MF and GO:0005886 for CC). 2) You cannot access GOMFPARENTS with $ and a variable like that. 3) GOMFPARENTS is not a function so using () doesn't work either.

To answer @RickBeeloo's comment above I decided to include an answer with some detailed code. Basically to obtain the ancestors of any Gene Ontology (GO) term using the Bioconductor package GO.db we need a call to the AnnDbBimap object for the adequate ontology. For example if we want it for Molecular Function (MF) we would use GOMFANCESTOR like in the example:
library(GO.db)

terms <- c("GO:0008022","GO:0001071")
as.list(GOMFANCESTOR[terms])

$`GO:0008022`
[1] "GO:0005515" "GO:0003674" "GO:0005488" "all"

$`GO:0001071`
[1] "GO:0003674" "all"

Similar objects can be used for Biological process (BP) and Cellular compartment (CC): GOBPANCESTOR and GOCCANCESTOR. The only limiation is that you cannot mix terms from different ontologies (i.e. all BP, MF or CC). There are similar options to obtain the children of any given GO term (e.g. GOCCCHILDREN). The description of each term can be obtained with:
Term(GOTERM[terms])
                   GO:0008022                                           GO:0001071
 "protein C-terminus binding" "nucleic acid binding transcription factor activity"

All available mappings can be listed calling GO():
GO()

Quality control information for GO:

This package has the following mappings:

GOBPANCESTOR has 28477 mapped keys (of 28477 keys)
GOBPCHILDREN has 16829 mapped keys (of 28477 keys)
GOBPOFFSPRING has 16829 mapped keys (of 28477 keys)
GOBPPARENTS has 28477 mapped keys (of 28477 keys)
GOCCANCESTOR has 3897 mapped keys (of 3897 keys)
GOCCCHILDREN has 1317 mapped keys (of 3897 keys)
GOCCOFFSPRING has 1317 mapped keys (of 3897 keys)
GOCCPARENTS has 3897 mapped keys (of 3897 keys)
GOMFANCESTOR has 10021 mapped keys (of 10021 keys)
GOMFCHILDREN has 2046 mapped keys (of 10021 keys)
GOMFOFFSPRING has 2046 mapped keys (of 10021 keys)
GOMFPARENTS has 10021 mapped keys (of 10021 keys)
GOOBSOLETE has 2012 mapped keys (of 2012 keys)
GOTERM has 42396 mapped keys (of 42396 keys)

Additional Information about this package:

DB schema: GO_DB
DB schema version: 2.1
Date for GO data: 20160305

Thankyou! I have one question you use: as.list(GOMFANCESTOR[terms]) this will give two lines of output. But which of these lines is the parent of both of the terms? @ddiez

The result is a named list, the names are what follows $ in the result (e.g. $GO:0008022``). The names are the ids of the original GO terms in the variable terms. Each line shows the ancestors of the corresponding id. For example, for GO:0008022 (first id in terms) you get: "GO:0005515" "GO:0003674" "GO:0005488" "all".

So you have to compare those by hand to get the common parent of both IDs? @ddiez

I posted a question about this topic: http://stackoverflow.com/questions/39879936/r-bioconductor-go-terms-output-interpretation mabye you are interested in answering it @ddiez

It turns out if you set the font.size in the graphNEL object, you can see the node names in the plot of the inducedTermGraph.
Setting font.size to >20 worked for me!


text:
Does GC content determine codon bias or does codon bias determine GC content
I was wondering if someone knows the answer to this quenstion, because I can't find a clear answer, maybe there isn't a clear answer :).
question
Which of these two is right? or maybe both influence each other

GC% determines codon bias
codon bias determines GC%

Thankyou,

Think about it this way, the G-C content is averaged over the entire genome, and varies between different species.  Whether you are dealing with prokaryotes, with relatively compact genomes, or with eukaryotes, with lots of non-coding regions, the open reading frames will, in general, be influenced by the average G-C content across the genome. Therefore we would predict that in species with lower G-C their open reading frames would be biased to using the codons in the genetic code that are higher in A-T. N.B. this also means that their tRNAs should also favour anticodons higher in A-T. In contrast, we would predict that in species with high G-C content, the open reading frames would be biased, in general, to using codons that are higher in G-C.
That is all G-C bias in codons is; for some amino acids like Met and Trp, there is only a single codon, but for other amino acids there can be up to six codons that can each encode the same amino acid side chain. It is in these ones with a higher number of degenerate codons that you are going to see the effect of codon bias.

Thankyou for the answers, it cleared up a lott, but there is one thing I still don't get: I thought the GC bias is determined by the availibility of tRNA, so if a gene needs to be transcribed and translated to a protein very often like ribosomes, it prefers codons of which al lot of tRNA availible for, what am i missing here? @mdperry

This may be debatable (the cause of GC bias). If the abundance, or cellular concentration, of individual tRNAs is fixed, or pre-determined, then over many generations the individuals in the population who use more of the corresponding codons would be able to replicate faster, and over time, the G+C% of the species would appear to change. However, it is difficult for me to imagine a mechanism that would fix, or pre-determine, the concentrations of individual tRNAs in the cell. The concentrations are a combination of the rate of synthesis and the rate of decay. There is probably feedback.

Maybe the codon bias is determined by the GC% of the whole genome, so favoring the most GC rich codons. Futher, de codon usage is maybe determined by the availibility of tRNA, It's just what I think? @mdperry


text:
Does anyone know the explanation for branches with different flower colors (see picture)?
As you can see in the below picture, there's a branch with white-colored flowers, while the rest of the tree has pink flowers.

I googled a number of questions but it is a bit complicated to formulate in a search. Plus I have no background in botany or even biology.

I edited your post. Feel free to roll back if you don't like my edits

Many ornamental cherries are grown on a hardier root stock, that is, they are propagated by grafting onto hardy wild cherry saplings. This is because the ornamental variety will not produce offspring that are true to the parents, if they produce offspring at all.

All are grafted plants and mainly on wild cherry (gean) rootstock.  Such trees should be planted with the graft union above ground level.  Seed, rarely produced, will give rise to new hybrids.

This is a picture of an ornamental cherry of the pompom variety:

My guess is that the tree in your picture sent a shoot off the main trunk under the graft site, resulting in a branch of native cherry, which is mostly white and a much simpler flower than the ornamental variety that was grafter onto it. Another possibility is that two different specimens were grafted onto the same stock (but since the white blossoms are very simple - like a wild cherry - I would guess the former occurred.)
This is a picture of a wild cherry (gean):

So you have the grafted ornamental cherry blooming alongside of the rootstock cherry it was grafted to.
The rootstock (although usually wild cherry) can vary, so... can't identify with certainty the rootstock, but can explain what you're seeing.
It's not rare, but it's not usually desirable. Some newer growers are grafting several varietues of cherries onto the same rootstock to intentionally produce a tree with different kinds and colors of flowers. See, for example, this artist's work.
The Hamada Cherries

Wow! That's so intriguing. I suspected it to be a rootstock but I thought maybe there could be some other reason because that was on a small street where I live. Thanks!

There is a bougainvillea variety called 'Surprise', which puts out bracts either white or magenta in color, though I believe all of the actual flowers are white.

So, how does this point answer the question, even without a reference?


text:
'Obviously True' Statements that turned out to be false?
As someone who studies mathematics, there are plenty of examples by which some theorem that was considered as "obviously" true later turned out to be completely false. I was discussing this with my friend when she asked me to cite examples outside of math. The first thought that popped in my mind was the notion of spontaneous generation, but I'm not sure if it was so completely agreed on to be true that it was "obvious". As she is currently a biology undergraduate, I wish to tailor my examples to her interests.
In short, I'm wondering if there are any examples in the history of biology where some "fact" was so seemingly simple and obvious that researchers took it for granted, but it ended up being found to be completely false.


text:
What is the difference between hsa-miR-33a and hsa-miR-33b?
Does anyone know what is the difference between two miRNAs like hsa-miR-33a and hsa-miR-33b? The last letter in them shows what?
Also, if we know that hsa-miR-33a targets gene A, can we say that hsa-miR-33b targets gene A, too? or can we say that it is much probable that hsa-miR-33b targets gene A since hsa-miR-33a targets A?

They are paralogs i.e. they have high level of sequence homology. They may have the same seed sequence too (see this). The paralogs can have same targets if they have same seed sequence but it is not essential in all cases. However, the extent of homology required for this kind of classification is poorly defined. miRBase still follows the guidelines mentioned in this (quite old) article:

When such a candidate is so similar in sequence to the known miRNA
  that the probe designed to detect it would surely cross-hybridize with
  the known miRNA, criterion A need not be satisfied, and the candidate
  can be annotated as a variant form of the known miRNA, provided that
  the candidate itself meets criterion C, and there is also very high
  confidence that one of these paralogs is a confirmed miRNA (i.e., its
  classification is supported by at least three of the listed criteria).
  When there are two or more mismatches between the miRNA paralogs such
  that probes could differentiate between the species on Northern blots,
  criterion A must be satisfied experimentally. Sometimes partially
  overlapping cDNA sequences are identified from the same locus; these
  are assumed to represent differentially processed products from the
  gene.

mind that homology is a 0 or 1 term. I mean two sequences are homolog or not. Its better to use "similarity" instead of "homology".

@MySky not really. Percent homology is a commonly used term.

The term "percent homology" is often used to mean "sequence similarity". The percentage of identical residues (percent identity) or the percentage of residues conserved with similar physicochemical properties (percent similarity), e.g. leucine and isoleucine, is usually used to "quantify the homology". Based on the definition of homology specified above this terminology is incorrect since sequence similarity is the observation, homology is the conclusion. Sequences are either homologous or not.

look at this page: https://en.wikipedia.org/wiki/Sequence_homology


text:
Why doesn't blood remain on a mosquito's proboscis in quantities that could spread blood-borne diseases?
We know that HIV can't be transmitted by mosquitos, and nor can other highly virulent viruses that are transmitted through blood and bodily fluid exchanges, such as Ebola (thankfully!).
Marcus Junius Brutus asked an interesting question in a comment on that above-linked question's answer:

[Why can't] tiny droplets of blood remain on the proboscis of the mosquito long enough for said mosquito to inject its proboscis into the bloodstream of another person? In particular, in what physical aspects is the proboscis different than a needle or razor? I am not talking about blood sucked into the gut of the mosquito, I am talking about blood remaining on the proboscis

There's no doubt that dirty mosquito proboscises aren't a vector for blood-based viruses (if they were, Ebola would be completely uncontainable in West Africa), and I understand the explanation on the above linked answer that there's no route from the mosquito's stomach to its proboscis other than via saliva production, but given how tiny the amounts of blood are that are required for transmission of such highly virulent viruses, why does it never happen in a similar way to transmission from a dirty needle or razor?
I've never seen a mosquito put its proboscis in sterilising fluid or an autoclave between feedings...
My best guess would be that mosquitoes are very efficient at taking up all available fluid, and that surface tension means that at this scale it is possible to take up every last droplet - but that's just a guess.

I guess a spin on this question is: is one virus 'particle' enough to cause an infection (or what probability)? I understand that viruses are extremely small.

Doddy - I believe you're taking about virulence, which varies from pathogen to pathogen. Ebola and HIV I believe are extremely virulent, readily transferred via dirty needles etc, which is why I chose them as examples (since even they clearly aren't transmitted from a used probiscus)

Droplets might be the key to this. Apparently, the proboscis inner diameter can be something like 25 microns or so, while blood droplets are apparently around a milimeter or so (that's where the shape of the droplet is almost perfectly spherical, which means great surface tension). So it might very well be that no blood is "stuck" on the proboscis after a feeding. I'm quite interested in the actual answer, though :)

Always relevant videos for proboscis: one, two.

@Luaan I'm not an expert at all in this field, but I find it hard to believe that there's a 0% probability that just because a droplet of blood happened to be on the proboscis of a mosquito at one time means that it definitely cannot inject the virus into a subsequent victim. What does surface tension have to do with it? Can't virus particles stick to surfaces?

@Doddy There's no such thing as 0% probability, ever :) Surface tension is very important because it makes it harder for stuff to cross the surface of a liquid. Without a surfactant, there is very little contact between the tube and the droplet - the two repel each other quite strongly. Imagine a drop of water on an oily surface - you're not going to get a surface wet if it is hydrophobic, and if it doesn't get wet, it doesn't get dirty. Of course, assuming the "dirt" is polar - however since the envelope of HIV is sacharous, this should be a good description. It's just conjencture, though :)

That's right.  There is 0% probability of any 0% probability, ever. :)

What you're talking about is called mechanical transmission (at least in veterinary and medical circles; plant epidemiologists call it something different). There's a nice overview by Gray and Banerjee here, although it's a bit old.
The short answer is that blood-feeding insects can mechanically transmit a range of pathogens, including viruses. Mosquitoes specifically are thought not to be great mechanical vectors because of the small quantities of infectious material that could be transferred between feeds. Large biting flies such as tabanids are thought to be much better potential mechanical vectors as they are pool-feeders; they basically chew up an area of skin and then mop up blood from the wound with their mouths. The quantity of blood contaminating a horse fly's mouthparts after feeding is reckoned to be about 10 nanolitres (Foil et al. 1987), which while not much could contain an infectious dose for some viruses reaching high titres in the blood. They also feed frequently (and painfully, which means they are often interrupted).
However, a number of viruses do seem to be transmitted in the field or in a lab setting by mosquitoes, particularly poxviruses (lumpy skin disease virus, myxoma virus and fowlpox virus, for example). Equine infectious anaemia virus (a retrovirus) is also thought to be mechanically transmitted by large biting flies in some regions despite its relative fragility. Some parasitic and bacterial diseases are also mechanically transmitted by blood-feeding insects; Trypanosoma evansi for example (the causative agent of surra) has lost the capacity to be biologically transmitted by tsetse and is solely mechanically transmitted.
(suggestions for improving this answer extremely welcome; I'm fairly new to SE)

A mosquito's proboscis isn't like that of a butterfly, which could easily have nectar clinging to it when it is coiled up; instead, consider that the part of the mosquito's proboscis that enters a blood vessle is probably wiped clean when it is retracts outward through the epithelium. A a dirty needle or razor is many, many times larger than the sucking parts of a mosquito, and a razor is an unlikely vector of HIV.
Epithelial tissue consists of cells very tightly bound together; it has to be to prevent constant invasion by bacteria, fungi, etc. It takes some considerable force or sharpness to penetrate. If you've ever watched someone give you an injection (a vaccine, for example), the needle is never bloody upon withdrawal. You might get a bead of blood from the wound, but the needle itself will be quite clean. The reverse is also true due to essentially the same reasons: the likelihood of introducing a pathogen by dragging it from the surface into the subcutaneous area is so low that there is no absolute need to swab visibly clean skin before giving a subcutaneous injection:

Although skin that is visibly soiled or dirty must be washed, swabbing the clean skin of a patient before giving an injection is unnecessary. Studies suggest that there is no increased risk of infection when injections were given in the absence of skin preparation. (WHO Bulletin)

HIV is the most serious virus (aside from Ebola, about which much is still unknown) which can be transmitted by needlestick. Sharps injuries - needles, suture needles, scalpels, lancets, etc. - are very common in the medical field, estimated to be much higher than 350,000/year due to underreporting and occurrence in non-hospital settings, e.g. nursing homes, etc. Of course, in the majority of sharps injuries, the sharp wasn't likely to have been used on someone with HIV. Still. HIV is not rare.
Even with a potential half-million exposures a year to sharps, as of December 31, 2013, only 58 confirmed occupational transmissions of HIV and 150 possible transmissions had been reported in the United States. Of these, the vast majority follow hollow needle sticks (88%), where blood drawn from a patient still remains in the bore of the needle which can be reinjected into the unfortunate recipient. If the patient is terminally ill with AIDS, the incidence of transmission by hollow needlestick is increased, meaning the viral load in the blood is important. A solid needle, even a bloody one, presents a very low risk (the risk is, in fact, unknown*.) Getting blood splashed in the eye is a higher risk than a sharp solid (i.e. suture or lancet) needle.
The piercing mouthparts (The mandibles and the maxillae) are solid, akin to a solid sharp. Only the twin tubes (the hypopharynx and the labrum) actually reach blood.
So, given the combined factors of limited survival of HIV on exposed surfaces, the small size of the proboscis (compared to a suturing needle or a lancet, both of which have a higher surface area, yet not known for certain ever to have transmitted HIV), the low probability that the mouth parts have HIV-laden droplets of blood on it, the fact that only the tip of the hypopharynx and labrum encounter blood (the fluid most likely to contain virus) and the extremely low probability that there are enough actual HIV viruses to cause an infection anywhere on the proboscis, I hope this answers your question.
Edited to add: I've focused on HIV here, because it's not known to infect mosquitoes. Mosquitoes are considered by many to be the most dangerous animal in the world. They transmit a significant number of viruses and parasites (like dog heartworm, elephantiasis, dengue fever, equine encephalitis, etc.), but (hypothesized from those diseases that have been studied in mosquitoes) only after being infected by the pathogens themselves. Some die of the infection; some die before the infection spreads through the mosquito's body, some don't harm the mosquito. But transmission is from infected saliva injected into or onto the bite site, not virus particles on the proboscis, as evidenced by the need for adequate incubation time between the bite that takes up the virus to the bite that transmits the virus. If there was sufficient virus on the surface of the proboscis, that incubation time would not be necessary.
Best infection control practices for intradermal, subcutaneous, and intramuscular needle injections
Workbook for Designing, Implementing and Evaluating a Sharps Injury Prevention Program
Occupational HIV infection among health care workers exposed to blood and body fluids in Brazil
Needlesticks: What you must know

Great answer! The only thing this leaves me wondering is, how does sharing needles lead to virus transmission? I believe it's common among drug users (especially hepatitis I believe?). I guess hypodermic needles can suck small amounts of blood inside the tip?

Hepatitis B is much more easily transmitted by sharps and needlesticks than HIV. In terms of needle sharing, some of it has to do with withdrawing a small amount of blood into the syringe before injecting the drug, guaranteeing that some blood will be in the syringe shared with the next person, and the fact that it's a hollow-bore needle.

I assume the "withdrawing a small amount of blood" is accidental and related to untrained needle use (e.g. allowing the plunger to move out slightly before withdrawing the needle)? I guess the obvious difference with a mosquito is, that any remaining inside their proboscis will then be sucked into their stomach, whereas with a shared needle it'll be mixed with the next injection.

I have never injected drugs into myself, but the usual procedure insuring that the needle is in the vein is to withdraw the plunger a bit until you get "venous return" (blood tinging the fluid in the hub if not the barrel of the syringe.) If you don't do this, you might inject the drug into subcutaneous tissue instead of the blood stream, which would be pretty much a waste of the drug.

@user568458 anongoodnurse is, of course, correct, but I'd just add: IV needle sharing involves repeated direct injection into a vein. The direct injection into a vein makes it a much more efficient method for transmitting any bloodborne pathogen than a single prick of the skin. And yes, the transmission efficiency of HBV > HCV > HIV, but when I had my sleep deprived accidental stick with a sharp used on an HIV+ patient, I surely didn't inject it into my vein.


text:
Structure of proteins
Regarding the secondary structure of proteins, I know that there are 3 main types. The beta sheet formation is made up of beta strands stabilized by hydrogen bonds to form an anti parallel or a parallel structure. I learned that these beta strands are a zigzag sequence of amino acids, but what traits of beta strands differentiate it from the primary structure? Or are the beta strands just primary structures that link together to make beta sheets?

Primary structure when talking about proteins refers only to the aminoacid sequence, it does not refer to any spacial/3D structures like beta strands..

This is a little confused. Secondary structure usually refers to helices and sheets. Sheets are made up of strands that can be either parallel or anti-parallel.

As @gilleain said secondary structure is the Beta pleated sheet and not the Beta strands.

primary structure
focus = peptide bonds (because these link the amino acids
The sequence of amino acids, for example AGGVHIL..

secondary structure
focus = H-bonds between the parts of the backbone
 There are several different types of secondary structure (α-helices, β-sheets, etc.). However the most import thing to remember is that the secondary structure refers to the the patterns of hydrogen bonds formed between amine hydrogen and carbonyl oxygen atoms contained in the backbone peptide bonds of the protein

your confusion
You are partly correct from a very simple perspective you can see the secondary structure of β-Sheets just as connected primary structures. However when talking about a piece of secondary structure you have to take the hydrogen bonding into consideration as this is what connects your primary structure parts (β-strands) to form a β-sheet.


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Runs of homozygosity - degree of inbreeding and disease associations
Been reading recently about methods to determine how inbred a particular person is by measuring their "runs of homozygosity." Loosly, these are defined as regions of the genome (typically >1Mb) where the person is homozygous for all polymorphisms, suggesting their parents were identical for this region. If a person has 'many' of these regions, it suggests their parents were closely related.
A study in 2015 [1] found some evidence that people with more regions of homozygosity had higher risk of heart disease.
My question firstly relates to the amount of homozygosity you might expect in a 'normal' out-bred person, compared to an in-bred population (e.g. small community), and then to 'extreme' examples of relatedness (parent/child offspring). In my searching I didn't see any cut-offs, if they exist, or whether this is even the right way to be thinking about it. And secondly, just how bad is it to have these runs?

Christofidou P, et al. Runs of Homozygosity: Association with Coronary Artery Disease and Gene Expression in Monocytes and Macrophages. Am J Hum Genet. 2015; 97:228–237. PMID: 26166477.

FIRST QUESTION: It all depends on the allele frequency in the population you consider. Under the Hardy-Weinberg assumption, the probability of two randomly picked allele to be identical by descent is $\sum_i x_i^2$, where $x_i$ is the frequency of the $i^{th}$ allele. If you look at a region that is under strong purifying selection in a large population, then most SNPs will have very low minor allele frequency and very low heterozygosity and therefore you would see very long runs of homozygosity.

SECOND QUESTION: The article you cite is probably one of the best place to go to ask "how bad are those runs". They probably report an effect size at some point.


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Is EGF-mediated proliferation symmetric?
It's known that the MAPK signaling cascade (say, ERK) is downstream of EGFR in epithelial cells, and that EGFR activation can cause proliferation in some cell types in some situations. My question is the following: if an epithelial cell with active EGFR (and hence active ERK activity) divides, will the two daughter cells have the same amount of ERK activity as the parent, both have half as much ERK activity as the parent, or divide asymmetrically? I suppose ERK activity should be defined here as ERK phosphorylation... though I would certainly welcome better definitions!
If you need better context, I would be considering wound healing of mammalian epidermal skin. There are plenty of sources suggesting that in response to  a wound puncture, EGF is released and stimulates proliferation.
Thank you!


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Amount of Na+ needed to be transfered in order to depolarize the membrane?
I found out that the number of $Na^+$ ions that is needed to be transfered across the membrane to make it depolarized is a small number.
In what way its proved? (Goldman equation maybe?)

You mean how the exact number of ions passing the membrane is measured?

One ion is enough to depolarize it. It depends on how much depolarization you are looking for and on the areal surface you want to depolarize and on the exact physiological ionic composition in and out of the cell at that time


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Concentration gradients across membranes with different ions
I'm trying to gain an intuition for the dynamics of across neuronal membranes. The overarching idea here is they are controlled by ion concentration gradients across the membrane (which we can describe mathematically).
I'm looking for someone to delineate every present concentration gradient across neuronal membranes that are relevant here(involving $Na^+$, $Ca^{2+}$, $K^-$, and $Cl^-$).
It's unclear to me what creates a concentration gradient:

Are the concentrations of each type of ion independent from eachother, i.e. in a world without charge, diffusion across the membrane is individual to the concentration of each ion, or, is mediated by the net concentrations of mass (which makes less sense)?
Is the flow of ions across the membrane driven by net charge on each side, or the charge concentrations of each individual ion?

Hmm.. chemical gradients are individual while for the electric, we take the over all charge, or rather the potential difference. This is what we are actually doing in the Nernst equation right.. We equate the chemical potential to the electric potential difference to see, at which voltage it would balance out. So finally, chemical gradients of individual ions and net charge (implying potential). But still, lets wait for a well structured answer!

Ok thanks. that's what I was hoping it would be; otherwise Id be really confused. On that last point, I don't understand why chemical gradients work on individual ions – I'd think it's about the net chemical concentrations. What am I missing in my mental model?

I try to answer your two questions briefly:

Ion gradients are dependent on charge, but there exist independent transport mechanisms, extending diffusion. Trans-membrane transport proteins can specifically move only one sort of ions. Also symport or antiport exists, that can depend on gradients of other (e.g. non-charged molecules). In addition, the mentioned inorganic ions can form chemical bonding to organic ions for example, which neutralizes the electrical charge.
Beside an electrical potential, also chemical (concentration) potential can act as force on ios. In addition active transport, inactivation as mentioned above and other factors have an influence on the molecule flow.

You don't mention the Nernst equation at all here. Isn't that somewhat important?


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Use of sunlight in biological processes
Sunlight is used by green plants in photosynthesis, but it is also used by animals in the synthesis of Vitamin D. Are there any similarities between the two processes and how is the light energy actually used?

It's synthesized from a type of cholesterol that is converted to vitamin D by uvb exposture. So nothing like photosynthesis really. See https://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional/#h3 for more.

Radiation being the source of energy for photosynthesis and vitamin D synthesis seems a reasonable correlation to someone having obviously very limited knowledge about the most important biochemical reaction.

This source explains it really nicely if you have the science background to understand it. Basically, the ultraviolet light of a certain wavelength - or high energy photons - breaks a particular bond in a precursor normally made in the skin. From there, the body takes over.

We don't get it from the sun, it's synthesized.
Humans can get it...

via nutrition.
via synthesis in the skin, which depends on UV radiation. Sun is the major source of it (the radiation, not the vitamin), and synthesis in the skin the major source of the vitamin. However, it needs further modification in the liver or kidney to become bioactive. UV radiation is necessary and directly causing the opening of a cyclic molecule structure, changing a cholesterol to a previtamin D3.

For more details see chapter 'Biosynthesis' at https://en.wikipedia.org/wiki/Vitamin_D

What is the down vote about?

At a guess, it's because you start by saying we don't get vitamin D from the sun, then go on to explain how the body makes it.  Maybe it's just bad wording: of course vitamin D molecules aren't literally part of the solar wind :-)

@jamesqf I think it's legitimate to re-use the phrase from the question and to point out that things are different.

Similarities
Despite major overall differences, there are some basic similarities in the two processes:

Light energy excites an electron to a higher energy level.
A covalent bond is broken as the electron moves elsewhere. This
process is called ‘photolysis’ and is purely chemical.

Differences
The difference is in what happens to the excited electron and the extent of involvement of cellular proteins and lipids:

In Vitamin D synthesis the electron just moves ‘spontaneously’ to
another bond in the new molecule that is formed. That is the end of
the matter and enzymes are not involved in this reaction.
In photosynthesis the light is first captured by photoreceptors and
funnelled to the site of photolysis. After photolysis, the
co-operation of many proteins in a complex process within a
membrane-bond system ensures that the excited electron is transferred
to NAD+, forming NADH, the reducing power for then subsequent
conversion of carbon dioxide to phosphoglycerate. (An
electrochemical membrane potential is also generated, allowing ADP to
be converted to ATP, the hydrolysis of which is used for formation of
the C-C bonds of the phosphoglycerate.)

Vitamin D synthesis
The photolysis step in Vitamin D synthesis is shown below:

The precursor molecule is formed from cholesterol in a series of enzymic reactions and the Vitamin D3 produced (actually resulting from a spontaneous rearrangement of the initial product molecule) may be metabolized further in enzymic processes (see Berg et al. for more detail). However the photolysis of the bond indicated in red is purely chemical.
One may ask why no other electrons are raised to a higher energy level and the  corresponding bonds broken. Other electrons may conceivably be excited, but in the absence of a suitable reaction pathway to a compound of lower thermodynamic free energy the electron will fall back to its original energy level, liberating heat. In the case of 7-dehydrocholesterol the co-ordinated double-bond system provides a suitable reaction pathway to a product of lower free energy. One can think of light (of appropriate wavelength) providing the activation energy of the reaction (overcoming the energy barrier resulting from the higher free energy of the reaction intermediate).
Photosynthesis
The reactions of photosynthesis that utilize light energy (the so-called ‘light reactions’) involve two complex photosystems that are described in standard texts, e.g. Berg et al.. The simplified diagram deals only with the overall photolytic process.

The molecule undergoing photolysis here is water — the two H–O bonds are broken and oxygen is produced. However in this case the product is incidental to enabling the electron to reduce NAD+. (Chemically oxidation is removal of electrons, and reduction their addition.) As mentioned above, this complex series of reactions also results in an electrochemical gradient within the chloroplast. The movement of hydrogen ions through an ATP synthase in the thylakoid membrane of the chloroplast stroma converts ADP to ATP (in a similar manner to that of oxidative phosphorylation).
The result of the photolysis in this case is the provision of molecular reducing power and ‘energy’ that will be used to convert 1-C carbon dioxide to the 3-C reduced sugar in a separate series of reactions that do not themselves involve light energy (these are referred to as ‘dark reactions’, although they obviously do not have to take place in the dark).
Coda
Although one often hears loose reference to light energy being used to ‘make’ Vitamin D or sugars, this can be quite misleading. I would suggest that it is better to express what the light energy is achieving in chemical terms and then place this in the context of the relevant synthetic process.


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Did toads evolve from frogs?
I know frogs still exist but that doesn't mean there wasn't ever a frog population that evolved into toads. Did frogs evolve into toads because their available swamp slowly went away and toads could survive better without water? Did frogs and toads evolve independently from similar selection pressure for shape?

I think you're mixed up; tadpoles are the baby form of frogs, not toads.

Oops... That was a translation issue. Sorry about that. I removed my comments.

"Toads", as commonly used, are not a monophyletic grouping - that is, all toads do not descend from a single common ancestor which only produced other toads. Instead, it's a polyphyletic grouping of those frog species which show common morphological characteristics related to a primarily terrestrial lifestyle. As a polyphyletic group, the parsimonious assumption is that various species of toads evolved from frogs on multiple occasions.
There's several possibilities for similar morphological features in the different toad lineages. The first is convergent evolution - similar selection pressure in the shared terrestrial environment selected for novel generation of similar features. Another is that the common ancestor of frogs and toads had morphological aspects that were a blend between frogs and toads, and depending on environment "toad-like" or "frog-like" features become more prominent or recessive - that is, "toad" genes are sitting dormant in the DNA of most frog species, waiting for the right environment to be expressed. In all likelihood the true explanation probably will be a combination of the two.
By the way, most toad species still depend on bodies of water, particularly for breeding. For example, the common toad (Bufo bufo) will go to a pond to lay its eggs, where the young toads will spend time as aquatic tadpoles before they metamorphosize into the adult form. So when thinking about toad evolution, it's probably incorrect to view it strictly as frogs compensating for losing access to water (though that might have happened for some species), but rather toads evolving to take advantage of the opportunities presented by a terrestrial habitat that's coexisting alongside watery environments.

It is more important to understand the entire argument of evolutionary assumption. For instance, we have no solid observational, repeatable or testable evidence that the frog or toad evolved into one or the other.
We are assuming a lot in this instance. Convergent Evolution is totally crazy.
We hinge a lot of belief upon 'possibilities' and unobserved 'data' through computer generation, and uniformity.
The problem is no one considers that the genetic code will not and can not add information to the gene pool (such as teeth to no teeth, hard skin, or wet skin,) some mutations and adaptations can improve a kind of life form but it has its limits in the DNA.
The truth is, we cannot say that frogs and toads evolved into anything because we have not observed this ever.
We have observed species varying among kinds. However, the toad and the frog are different kinds of reptiles just as the lizard differs from the tortoise.
Always go by fact question assumption.

Convergent evolution is amply demonstrated, e.g. ichthyosaurs/swordfish &c/dolphin, pterosaurs/birds/bats.  Nor are toads and frogs reptiles, they are amphibians.

Although I think there is a positive contribution contained within this answer, namely that people should understand where scientific conclusions come from, I think this answer overall misunderstands the tools that are available and is outright misleading in several ways.


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Do Class A biosolids count as organic fertiliser?
Does Human Waste, which has been treated at least twice to remove pathogens & remove stink, still count as organic despite it passing the EPA's class A standard?
If so, does this mean that none-GMO crops grown in this fertiliser are still organic?
Thank you to those that take the time to answer.

Definition of "organic" in Science
In science (esp. in chemistry), organic matter loosely refers to matter that eventually make up living beings are are remains of living beings. Typically organic matter consists of long chains of carbon surrounded by hydrogen atoms and a few oxygens and nitrogens (and eventually other things such as sulfur and phosophorus).
Can we eat something that is not organic?
Unlike plants, we (all animals and fungi) are heterotrophs (feed on organic matter only). As a consequence, there is no such thing one could call food that would not be organic.
The (mis)use of the term "organic" in popular culture
In the popular culture organic is a term that tries to refer to certain type of food that are grown under certain conditions and treated a certain way. However, there is really no good definition of organic in the popular culture and there exists no objective definition that would satisfy someone that wishes to categorize food into what they like to call "organic food" and "not organic food". Similarly there is no good objective definition of GMO either.
Some organization may make up definitions of "GMO" or "organic food" but those definitions rely on a long list of products rather than to an actual definition.
I just want to attract the attention of the naive reader that I am not saying that the term organic as used in the popular culture is healthy/not healthy or good/bad. Arguments concerning whether it is ethical to buy organic food goes both ways and it is not the job of a science website to discuss questions of ethics.
Are GMO safe to eat?
You are not asking this question here. But in case you wonder you might want to have a look at the Skeptics.SE post: Is Genetically Modified food safe to consume?

no - USDA organic designation does not allow ANY biosolids of any class to be used on the land - and way not?? Because even class A still contains thousands of toxins - hardly any tested for. To call Biosolids organic matter is to do violence to the language - would you call a substance made up of 40% toxins (by weight) ORGANIC .....no.

can you add some citations to support your claims?


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How can I obtain a computer readable model of Dr. Gerhard Michal's biological pathways map?
I want to run simulations of various metabolic pathways – the project could end up becoming quite large, and having a machine readable chart would make thing a lot easier. Does anyone know if there is a machine readable file of Dr. Gerhard Michal's famous metabolic pathways chart?

Can you think of any format you would like this map to be in?

If yes, you could maybe email ROCHE directly to ask. I am not so familiar with the standard methods used in numerical simulation of metabolic pathway to know whether there is such thing as a standard format for this kind of data.

Can you give more details about the sort of simulations you want to run?

Roche's Biochemical Pathways works as a big png image and just put labels on the map. But you could try to extract data using queries like http://biochemical-pathways.com/pol/fts/query?query=Glutarate
It seems to be legal as it's not prohibited.
Escher is a good pathway visualization tool where you can save map in JSON or SVG.
Another choice is VMH (Virtual Metabolic Human) - the virtual metabolic human database provides literature-derived information on human metabolism, gut microbial metabolism, nutrition, and diseases.
Reactome has two layer map - first layer is biological interactions, second layer is pathways.


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What is the difference between multiple allelism and polymorphism?
From the Scott Freeman textbook Biological Science 4th Edition:
https://www.amazon.com/Biological-Science-4th-Scott-Freeman/dp/0321598202,
Multiple allelism is defined as "the existence of more than two alleles of the same gene within a population."
Polymorphism is defined as "the occurrence of more than two distinct phenotypes of a trait in a population."
I don't really understand the difference - unless it means that two alleles may not result in two different phenotypes?
Additionally, another definition of polymorphism also in the textbook was "the existence of more than one allele at a certain genetic locus."
What does this mean? I was under the impression that all genes had at least two alleles.

can you cite where you are getting your definitions?

There are many different meanings of polymorphism and not all involve different phenotypes. Please [edit] your question and give us more context. Neither of the definitions you use are really correct.

Well, my original definitions came from my teacher, but the definitions provided in my textbook have both cleared up some confusion AND yet further confused me. Which definition of polymorphism is most common?

Can you please indicate what is your textbook and indicate on what page you found these definitions?

The name of the textbook was already given above, but for further detail it is the 4th edition (2011). The definitions were part of the glossary, on pages G:19 and G:23.

The term polymorphism is broad and can have different meanings. Here are your definitions

Multiple Allelism: The existence of more than two alleles of the same gene within a population.
Polymorphism: the occurrence of more than two distinct phenotypes of a trait in a population.

Considering your definitions only, then multiple allelism has to do with genetics while polymorphism has to do with the phenotype.
Most loci (=position in the genome) that contain more than one allele (=genetic variant) have no effect on the phenotype. So multiple allelism does not necessarily yield to phenotypic polymorphism.
On the other hand, plenty of phenotypic variation in a population is due to environmental variation (including what an individual eats) and not to genetic variation. So phenotypic polymorphism is not necessarily caused by a case of multiple allelism.

This answer refers to polymorphism within genetics (for clarification), which as far as I know is the more common use of the term (but that could just be because I'm a geneticist).
Polymorphism in general refers to genetic variation of traits within a population (or species), due to mutations.
A 'single nucleotide polymorphism' is a single change in the DNA sequence of an organism at some point. So:
A -> C
or
T -> G
Or some other combination of these. It is simply a change of a single nucleotide. More specifically, a SNP is present in at least 1% of a given population.
As these mutations (and other types of mutations) accumulate it results in multiple allele variants of a gene.
Here is a good reference: http://www.nature.com/scitable/search-scitable?criteria=Polymorphism
You are right to say that not all alleles will yield a different phenotype.
Finally, in principle, genes do not necessarily have to have more than one allele, it is the result of mutations that cause this.

Please add references to your answer.

My apologies. Reference has just been added.

Is a slightly difference:

polymorphism is a variation in an allele at the sequence level. A common one is Single Mutation Polymorphisms SNPs.
Multiple allelism means that in a population there are more than one alleles for a certain gene.

Please add references to your answer.

My genetic Professor

Welcome to Biology.SE. Please provide non-anecdotal references for your claims, i.e. information that can be checked by others as well. Also take a look at the guidelines on how to provide good answer and consider taking the tour. Have fun on Biology.SE!

unless it means that two alleles may not result in two different phenotypes?

That is correct. Due to codon degeneracy.. ie one amino acid can be encoded by more than one set of 3 DNA base pairs... you can a difference in DNA but no difference in the protein. This synonymous base changes leads to no phenotype.
Also it is possible for an amino acid change to occur in a protein and cause no phenotype either, as the change may occur in a region that has no over effect on the protein function, folding and interaction with other proteins.
So as you have eluded too, not all allelic variation leads to a phenotypic  variation.


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Question about radiation and how it affects biological systems
I'm doing research on the effects of radiation, and specifically UV, X-Ray and Gamma radiation, on biological systems at the cellular level and beyond. I understand that radiation types can be classified by their wavelength, with the gamma radiation being of the shortest wavelength and thus highest energy.
How does this measure of wavelength relate to the unit rads, or radiation dosage? And how do they both affect the survivability of cells? I can understand that the lower the wavelength, the higher the energy and it will affect the cells more adversely at those levels, but how does rads relate to that?

The absorbed dose describes the amount of radiation absorbed by an object or person, i.e., the amount of energy that radioactive sources deposit in materials through which they pass. The units for absorbed dose are the radiation absorbed dose (rad), or better: the gray (Gy) unit.
One gray dose is equivalent to one joule radiation energy absorbed per kilogram of organ or tissue weight. Rad is the old and still used unit of absorbed dose. One gray is equivalent to 100 rads.
1 Gy = 100 rads
Equal doses of all types of ionizing radiation are not equally harmful. Alpha particles, for example, produce greater harm than do beta particles, gamma rays and X rays for a given absorbed dose. Alpha radiation is the most dangerous because it is easily absorbed by cells. Beta, gamma an X radiation are not as dangerous because they are less likely to be absorbed by a cell and will usually just pass right through it (source: BBC).
To account for this difference, radiation dose is expressed as equivalent dose in units of sievert (Sv). The dose in Sv is equal to absorbed dose" multiplied by a radiation weighting factor (WR - see Table 1 below). Prior to 1990, this weighting factor was referred to as Quality Factor (QF).
Note that the heaviness of the alpha particle makes its penetration rates very low. Hence, it will not easily penetrate through the outer layers of the skin.

Table 1. Recommended Radiation Weighting Factors. source: Canadian Centre for Occupational Health and Safety
Now to your question:
Ionizing radiation has more energy than non-ionizing radiation. Ionizing radiation can cause chemical changes by breaking chemical bonds and damage living tissues.
Shorter wavelength UV begins to have enough energy to break chemical bonds. X-ray and gamma ray radiation, which are at the upper end of the EM spectrum, have high frequencies (~100 billion billion hertz). Radiation in this range has high energy and it can strip electrons from an atom or even break up the nucleus of the atom.
The process in which an electron is given enough energy to break away from an atom is called ionization. It results in the formation of two ions: the molecule with a net positive charge, and the free electron with a negative charge. Each ionization releases a large amount of energy which is absorbed by the surrounding tissues.
There are three main kinds of ionizing radiation:
Alpha particles, which include two protons and two neutrons; beta particles, which are essentially electrons; and gamma rays and x-rays are photons. Alpha particles, beta particles and neurons are not part of the EM as they are energetic particles as opposed to pure energy bundles (photons) (source: ARPANSA Australia).
So in the EM realm, frequency is proportional to energy and hence to tissue damage (Fig. 2) and hence to rads.

Fig. 2. EM spectrum. source: ARPANSA


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Why the name hypopharynx?
Why the tongue (like structure) in cockroach (or other insects) is called hypopharynx? In humans I know it's the lower part of pharynx, not a structure. Isn't this anatomical name misleading? Are there other ambiguous terms like this?


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Why is active transport needed in repolarization?
During the repolarization phase of an action potential, the potassium ions diffuse out of the cell, and active transport begins.
What I do not understand is why active transport is needed when the movement of ions is not against their concentration gradient?
Since the potassium ions have diffused out in repolarization, only the sodium ions are left in the intracellular space.
The sodium/potassium pump is used to pump 3 sodium ions out and 2 potassium ions in. However, isn't there a concentration gradient as the sodium ions are moving out of the cell, where there are no sodium ions, and thus from a high concentration to a low concentration?
Is it because the active transport allows the imbalance to occur (3 out and 2 in)?

...when the movement of ions is not against their concentration gradient...

This assumption is incorrect: Na+ has to be pumped out of the cell against its chemical gradient (table 1) and against its electrical gradient, given that the inside of the cell is negative (Fig. 1).

...potassium ions have diffused out in repolarization, only the sodium ions are left in the intracellular space

This is incorrect: There are heaps of K+ ions in the cell, also after repolarization. A tiny fraction exits the cell during repolarization.

...moving out of the cell where there are no sodium ions...

This is incorrect; there are Na+ ions out of the cell, heaps in fact. You should be aware that the flux of ions is not an all-or-nothing phenomenon. It is a flux of relatively few ions out of a pool of them. Action potential formation and ion gradients are membrane-bound phenomena. While Na+ may enter the cell during an action potential, there is still a nearly infinite large amount of Na+ left in the intercellular space.

Table 1. approximate ion concentrations in and out of the cell. source: Med Quarterly

Fig. 1. Action potential. source: UC Davis

Okay. Regarding the fact that the movement of ions is "not all or nothing", as during depolarization the intracellular space is momentarily positive compared to the extracellular space, although not all of the sodium ions have diffused into the cell, there is enough to create a positive charge within in addition to the positive charge of the potassium ions?

And so even with the pump actively transporting 3 sodium out and 2 potassium in during the resting potential, there will never be only potassium in the inside and sodium on the outside correct?

@city7lights that is correct


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Measuring tumor heterogeneity
I would like to ask if there's any method (established or not) in order to quantify heterogeneity found in mutations occuring in primary neoplasms and metastatic lesions (either common or private) and potentially correlate this number to standard clinicopathologic traits.

What kind of heterogeneity: genetic, morphological, biochemical?

The methods that come immediately to mind are mostly related to next-generation sequencing. You can do deep sequencing on your sample, which is just increasing the coverage as much as possible to find rare events. You can do RNA-seq to look at the transcriptome, ChIP-seq to look at chromatin modifications, and single-cell sequencing (a form of deep sequencing operating on individual cells) to get truly cell-by-cell data, either from the genome (DNA) or transcriptome (RNA).
If you are purely looking at phenotypes, flow cytometry is quite useful for analyzing relative expression levels of proteins, using both extracellular and intracellular markers and stains. FACS is an extension of flow cytometry that allows for the sorting of various cell populations into separate containers. These "purified" samples can then be used in any of the methods listed above.