text:
Madrid, Noise by the river: Bird or cricket?
I currently live in Madrid, Spain. In July there was a loud animal near the river, in an out of town area surrounded by grassland, with trees along the river.
It's continued into August, though it has reduced.
It sounds like a cricket in general tone and rhythm, but it is always high in the trees, and sounds too deep to be an insect. It's in the frequency range of a squawking bird, so if it's a cricket it must be huge.
On the other hand, if it was a bird, I should have been able to spot one.
Does anyone have any idea what it is?
The sound is rhythmic, rasping note, with two beats of equal duration but slighly different tone, repeated over and over again without any pause.  The animal that makes it calls continuously for long periods.
EDIT: thanks to AliceD for the comment, I didn't realise we had cicadas in Europe. It could be a cicada, but it's deeper and more consistent / regular in its song than this one:
https://www.youtube.com/watch?v=DSdxm52VwOg

Sounds like a cicada to me https://en.wikipedia.org/wiki/Cicada. Btwo: with frequency range I presume you mean "loudness"? They are two very different things.

@AliceD Thanks, it could be a cicada, though of a different species than the ones in the wikipedia article and the one in the video I've added to the question. This thing is loud, but what most impresses me is how deep it is, definitely deeper than recordings in the above mentioned media. In July there were loads of them and I assumed they were birds. Now that there's less of them and I can differentiate individuals, I'm impressed by how monotonous and consistent they are - bird song is  normally more sophisticated. Also they like water, I only ever hear these things by one stretch of river.

Have you heard of the proposed Bioacoustics Stack Exchange? It seems like you might be a valuable member of that community. Please consider committing to the page so we can get closer to making it to the Beta stage. Cheers!
https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=YjZmYjUxYzJkNDI1YmY5NDk3NzdhMzViMmZlNzI4ZDdiYTAyMWQxNTM5ZWFiNzRhODNkMmFiMzIxZjI3MmY1N_gFvrICTvBsmYNJ2ptRM6lIZEAV-VGkXtIwNyVDja680

In this case i am going to agree with AliceD, because I live in Greece and here we hear cicadas everywhere. But in Madrid, there is a other kind of cicada that its "song" is more noisy and more deep.In this video you can hear how your cicada sings.https://youtu.be/mah26og11ms

Thanks, but that is not my cicada, the rhythm of the song is different. The closest I have found is the one in the video in the question. Also the people talking on your video have an American accent, but I wouldnt discount the possibility that we have American cicadas in Madrid. It is a very cosmopolitan city with many connections to Latin America, so cicadas could be introduced. You can hear some Greek cicadas in one of the audio tracks in the Wikipedia article that AliceD linked. They are indeed much more high pitched.

That said, I was just in the park and heard a noise very much like your linked video. So I guess we have at least 2 species of cicada where I live.

Just to be clear – the cicada in the video linked just above (https://youtu.be/mah26og11ms) is Neotibicen tibicen, a genus found only in eastern North America.  See here at Wikipedia.  Sound recording on this page.

As suggested by AliceD, it does indeed appear to be some kind of cicada. I went down the river and heard one calling, unusually far from the river (30m) where there are lower, newly planted trees. I was able to approach it and take this photo which unfortunately isn't very good.
It's possible that it's even the same species as the video I added to the question. It may be that the cicada in the video did not sing with a regular pattern because it was disturbed by the observers. My cicada refused to sing at all while I was watching him, preferring not to draw attention to himself. I took 3 photos before he began to walk up the tree. On my fourth photo he became startled, flew off, and immediately resumed singing elsewhere.
The cicada in the video sounds more tinny than the ones by my river. That may be an audio effect.

The originally posted song and video suggest a cicada in the genus Cicada (the type genus of the family Cicadidae, which is known from southern Europe, eastern Asia, and north Africa); some identified recordings of this genus can be found at this page on European cicadas.  So far I can only find references to C. orni and C. barbara in Spain, but the recordings of those species given on the European cicadas site don't exactly match, although the physical appearance does suggest C. orni (keeping in mind that the white waxiness often gets rubbed off adult cicadas over time).  Since the orni recording on the website is from Slovenia, it may just be that the cadence of the song in that location differs from that of Spain (or in different temperatures, or in different courtship contexts). There are a few other Youtube videos described as orni from Spain with similar sounds (e.g., https://www.youtube.com/watch?v=3Z4STY71C-8). I don't know if there are other candidates besides orni and barbara in Spain.


text:
How to get rid of mosquitoes in a small lake
I own a small lake. Give or take it is about 50 meters wide and 100 meters long (or 160 feet wide, 320 feet long), with a max depth of around 2 meters / 6.5 feet. One third of the lake is surrounded by forest, the rest is grass / small enclaves of tress. The lake absorbes only rainwater from the surrounding residential area. There is a small outlet towards a much larger lake close by. The lake was recently dredge to remove many years of plantlife that had almost turned it into a swamp.
The lake has a large number of mosquitoes. There is also quite many frogs and a few birds that live near the lake.
What can I do to decrease the amount of mosquitoes in the lake?
For example, can I set up certain nesting boxes that will attract birds or bats that will eat a large number of mosquitoes?
Can I release certain fish that thrive on mosquites?
It is in Scandinavia.
EDIT
The shorelines are sharp and most of the vegatation has recently been removed. The lake was recently completely emptied and about 2 meters (or more) of vegatation and soil was removed. The lake has previously been contaminated which was cleaned away. I guess this means that a very large part of the ecosystem has been removed, a few fish did manage to survive, but not very many.

Salitifing the water will terminate larva before developing into mosquitoes.

What does the shoreline look like? Is it "sharp" or does it merge into wetland areas that are flooded during spring? The latter will most often lead to more mosquites, since they are usually found in stagnant waters.

Maybe you can find help at gardening SE? It's not about plants, but I would guess quite some gardeners have faced this problem before.

If the lake was a lot smaller I could suggest tablets of bacillus thuringiensis that you can actually toss into the water and you let the bacteria control the mosquito larvae. For a lake that large though, this would entail quite a bit of control. You maybe want to try and get small top-feeding fish in there, almost like minnows, that will eat the mosquito larva. Other solutions I can think of are tightly regulated or available only to approved agencies/providers in the US or basically otherwise require special handling, or harm other insects/plants.

Bear in mind most solutions refer to owners of small artificial ponds, and local wildlife authorities normally do mosquito control (again speaking from the USA) in larger bodies.

Gah - I knew someone else would add Bti while I was writing my answer! :(

I recommend getting a Mosquito Laser :-)

The Guppy fish is good at eating the larvae. But you'd have to investigate if its introduction into your ecosystem is OK or forbidden.

There are a number of environmentally destructive methods that would be effective, including draining the lake, covering the surface with a continuous layer of oil, or adding toxins to the water, but I'm assuming you're looking for a method that will have the minimum possible off-target effect.
Different mosquito species breed in different habitats and are thus susceptible to different control strategies, so good photos of some adults might help, but I'm assuming here that you've correctly identified the lake as the breeding site. If there are any other possible breeding sites in the area please add them to your question.
If the assumptions above are correct then, broadly speaking, your best options are habitat modification or biological control. I'm not going to go into chemical control here since as stated above I assume you want low environmental and financial cost; if this is incorrect let me know.

Habitat modification: regularly removing
plant growth within the lake and trimming vegetation overhanging the edges will limit the ability of mosquito larvae to escape predators and may have some effect. However, the recent management you describe has
probably gone some way towards this (did you
notice whether the mosquito problem got any better after the plants
were removed?)
Biological control: introduce predators or parasites into the environment. Plenty of species eat adult mosquitoes but there aren't really any that primarily feed on them (unless they're the only food source available) and many adult mosquitoes will have laid eggs already - the most effective strategy will be to target the immature population. Larvivorous fish have been shown to be effective in many parts of the world, for example fish in the genus Gambusia ('mosquito fish'). I don't know of any that have been shown to be effective and can thrive as far north as Scandinavia, but if you stock the lake with fish (combined with managing vegetation as above) I'd be surprised if you don't see some improvement.
Biological control, part 2: Use Bti (Bacillus thuringiensis var. israelensis). This is a bacterium that produces toxins which are highly specific to dipterans and don't really affect anything else. You can buy the bacterium in various formulations including sprays, tablets etc. I'm mainly familar with its use for controlling container-breeding mosquitoes, but this paper describes its use in large lakes so should give you some idea of dose required, optimal application method and time to reapplication.

Without knowing more about your budget, available time/manpower etc I can't really help you choose between these but I suspect #3 is your best bet.

My suggestions, based on mosquitoe projects I've heard about in Sweden, would be to:

Thin vegetation along the shores
Remove accumulated detritus
Manage grasslands along the shore, by grazing if possible.

The idea here is to remove the stagnant pools where mosquitoes develop, either coming from rainfall or spring flooding/snowmelt. By removing pools and increasing sun exposture you will probably decrease habitats and larval survival. Continously managing grasslands usually also helps, since it removes excess plant materials and kills mosquitoe larvae by trampling (if grazing is used). To introduce grazing by e.g. sheep (if possible) will probably also have positive conservation effects. Stocking of fish might help, but I suspect that the mosquitoes mainly comes from adjacent waters and edge pools and not the main water body. I doubt that birds and bats can control the mosquito population to any larger extent, but don't have anything specific to back-up this statement.
Also note that actions depend on the types of mosquitoes found in the area. There are both "forest mosquitoes" and "flood mosquitoes" in Sweden, but most perceived problems come from the latter kind, and since you are referring to mosquitoes from the lake/pond I suspect you are dealing with the latter kind. You should try to determine the most common species found there though. Treatment with Vectobac G (Bacillus thuringiensis israelensis) might be an option, but I don't know what kind of retrictions there are on using it privately.
You might be interested in this report from a Swedish county board, since it mentions ways to control mosquitos (in Swedish):
Lundqvist et al. 2013. Förslag till hur myggproblemet vid Nedre Dalälven kan hanteras på lång sikt. Länsstyrelsen Gävleborg ("Suggestions for how to handle the mosquito problem at Lower Dalälven over the long-term" freely translated).

Don't salinate the lake. It'll be a nightmare to maintain.
The 'standard' biocontrol measure is to release 'mosquitofish', but outside their native range they're almost as good at killing native mosquito-eating fish as they are at eating mosquitoes.
Find some native fish(perhaps in the bigger lake?) and stock your pond with them. Small fish are probably better for this purpose. If your pond freezes all the way through in the winter(it almost certainly does not, but it depends where you are in Scandinavia) you'll have to find something else. If it just freezes over lots of fish can handle being under an icecap for a few months.
If you have a local fish and game authority they will probably have advice about stocking your pond, or at least handled that question before.

And please: Do not release any fish and mess up the eco system of the lake.

There are some native fish in Scandinavia, such as the crucian carp (ruda in Swedish), that can survive even in ponds that freeze (nearly) to the bottom in winter. They'll eat pretty much everything, including insect larvae, so they should be at least some help in controlling mosquitoes. Do note that crucian carp tend to outcompete other fish in small ponds, and can be hard to eradicate once present. If your pond already has an existing fish population, think twice before introducing them.

According to http://baliadvertiser.biz/mosquitoes/, more specifically the 3rd paragraph:

The next easiest solution is to add a submersible pump, a waterfall or fountain. Flowing water is pleasant and will also enhance the water quality. If it is possible keep the water flowing at all times. Mosquito larvae can only survive in stagnant water. Newly hatched mosquitoes must rest on the surface for a few minutes to let their wings dry, because of this they will not lay eggs in water that is constantly moving.

Mosquitos don't breed in moving water, because their larvae have to rest on stagnant water for a few minutes so their wings can dry. Flowing water will also improve the water quality by adding extra oxygen.
The trick is that you likely want a way to get rid of the mosquitoes that doesn't require maintenance, which rules out most mechanized methods that you could use to make the water move like wave generators, pumps or bubble generators. In theory, you can just let it run during the breeding season so they can't lay their eggs. The best solution will probably depend on how much effort you're willing to put into it. Maybe you can promote the pond as a nice place to play with remote controlled boats during the spring and early summer?

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
How do you create a .snp datafile?
I'm looking to use the software DIYABC 2.1.0 to apply approximate bayesian computing (ABC) to some resequenced data that I have.
The resequenced data is in FASTA format however, and the software requires an SNP datafile format (.snp). How do I generate such a file from FASTA formatted data? Is it possible?

I don't know either piece of software.  Hopefully, someone will have written a utility to do the conversion you need, or maybe there is a set of utilities, so that you can convert from format A, to B, to C, etc.  However, sometimes you have to write your own genetic data file conversion program (in Python, Perl, etc.--whatever you like).  It's probably conceptually easy--you're just rearranging or recoding the same data--although the routines can require some care.  If you know enough to get started, but get stuck along the way, Stackoverflow.com would be relevant.  Maybe none of this is news.

You will have to detect SNPs. You can get the vcf by aligning your resequenced fastA to the reference genome (or previously sequenced genome) and use a Variant Calling method of your liking. Then there is this tool to convert vcf to the required .snp file: https://github.com/loire/vcf2DIYABC.py

@Mars That's very helpful, thank you. I'm very much a novice, so any input is appreciated!

@skymningen Great, I shall try and produce that intermediate vcf file. I did try using PGDSpider to convert the files, but there was obviously something else that had to be done. Cheers!

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
What genetic distance model should be used when calculating genetic differences in Arelquin?
I'm using Arelquin to look at the genetic structure between a number of different populations. I  want to compare the populations by producing pairwise FST values, however I don't know what model for the genetic distances I should use.
The two models provided are Slatkin's distance or Reynold's distance. They both aim to linearize the FST values by transforming them [Slatkin's = FST/(1-FST), Reynold's = -ln(1-FST)].
How do I know if the FST values need to be transformed, and if they do need to be transformed, what model should I use?


text:
How do you convert mtDNA sequences in FASTA to FSTAT format?
I've got control region sequence data from a population of shark and I'm looking to convert this from FASTA to FSTAT in order to calculated the effective population size of females. The software I want to use only accepts FSTAT or Genepop files.
Is it possible to convert FASTA to FSTAT or even Genepop?

Check out PGDSpider. The inputs and outputs table indicates that it supports conversion between FASTA and FSTAT formats, among many others.

I tried this, but the output file only showed that there was one locus. This is what made me wonder if it was possible to convert the file in the first place.

@WillPerry can you post an example of your FASTA? have you confirmed that it's formatted as expected? The manual might be helpful: http://www.cmpg.unibe.ch/software/PGDSpider/PGDSpider%20manual_vers%202-1-1-5.pdf

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


text:
How to calculate the number of sterile insects that must be released in SIT?
The sterile insect technique (SIT) is used to control insect pests through overwhelming the population in sterile males. The increase in sterile males released into an environment causes the increase in infertile matings. This, in theory, would reduce the population.
However, how would you calculate the number of sterile flies needed to be released in order to be effective? It would be dependent on the reproduction rate of the insect, initial density, and sex ratio in the young, but is there an equation to express this? Or is there simply a generic ratio of the target population that is used?
I'm looking at the example of the New World Screwworm fly, and the eradication in Central America.

You might also want to consider the relative reproductive capacity of a sterilised vs a wild type fly.


text:
Why do the fastest runners tend to be black?
If you watched the last Olympics like me you probably also observed that most medallists in running events were black. Why is that? I discussed this with university grad friends and researchers and we only came up with hypotheses but nobody had an actual explanation. Is it cultural, genetic, other reasons or nobody really know?
Update:
Sprint and distance running requiring different attributes for being the best, let separate this question in two parts: 1) Sprint (i.e. 100m) and 2) Distance running (@Forest already provided a great answer for this).
Note: I know this question can potentially bring disrespectful answers/comments, but I'm hopeful that this site and its members can answer this interesting question. Otherwise, I'll simply erase my question.

Related post: Athletes: nature vs. nurture?

Matthew Syed covers this in his book "Bounce", which I highly recommend. In summary: Many of the fastest runners are not only black, but also Kenyan, and not only Kenyan but from a specific village in Kenya. This village has a training track at a high altitude, and also the entire village hero-worships all fast runners, which encourages people to really give it their all from a young age.
Your question is more general, but I imagine there are many effects like this in many communities of people (Syed also points out that all the top UK Table Tennis players are from one neighbourhood)

I wanted to know why 0 swimmers were black. My darker friend said he'd ask at the next meeting of black folk, but he hasn't gotten back to me yet.

@Chloe luckily for you the scientific paper I've quoted in my answer (see below) also talks about the swimming disadvantage for black people. See http://www.witpress.com/elibrary/dne-volumes/5/3/454 Whether it's right or wrong is another story but that's an hypothesis.

@Chloe uh, a black American won gold in swimming.

The title of this question isn't asking the same thing as the body of the question. "The fastest runners tend to be black" is not the same as "Black people tend to be fast runners".

@Chloe: See also Why Simone Manuel’s gold-medal swim in Rio was so historic -- "Manuel overcame a fraught history between Black people and water, which ripples across nations."  Apparently part of it stems from people thinking segregation in pools was easier to justify than in other places, because pool water could spread ... stuff ... between people.

@PeterCordes OK but that was the 50's & 60's. How does it explain why there aren't more recently? It seems the peak athlete age is 20, so anyone born after 1996 would have pool access. What about NBA or NFL? Darker skins dominate that sport for decades. And what about other countries, like Jamaica? @ BruceWayne Cool.

@Chloe: read the article. Cultural inertia takes a while to overcome.  If your parents don't swim at all, they're less likely to sign you up for swimming lessons, etc. etc.  Also, I said "part of it is...", because there are of course other factors.  e.g. some sports cost more to participate in, and wealth inequality is racially biased.  And sports heros of your own race and/or background might be more likely to inspire you to take up a sport.  And other factors beyond that.

Specifying between sprint and distance running would be helpful, the attributes for being the best are very different between the disciplines - as it stands it's a little broad hence is attracting answers that make sloppy generalised statements rather than providing useful evidence and theory

It's an interesting question and one that has been asked before. NPR did a story in 2013 on this topic, but their question was a bit more focused than just "why are so many black people good runners?"
The observation that led to their story wasn't just that black people in general were over-represented among long-distance running medalists, but that Kenyans in particular were over-represented. Digging deeper, the story's investigators found that the best runners in Kenya also tended to come from the same tribal group: the Kalenjin.
I'm not going to repeat all the details in that story (which I encourage you to read), but the working answer that the investigators came up with is that there are both genetic traits and certain cultural practices that contribute to this tribe's success on the track. Unfortunately, from the point of view of someone who wants a concise answer, it is very difficult to separate and quantify the exact contributions that each genetic and cultural modification makes to the runners' successes.
Pubmed also has a number of peer-reviewed papers detailing the Kalenjin running phenomenon, but I could only find two with free full-access and neither had the promising title of "Analysis of the Kenyan distance-running phenomenon," for which you have to pay. Insert annoyed frowning face here.
I did a quick search of some Kenyan gold medalist runners in the 2016 Olympics and sure enough, several (though certainly not all) are Kalenjin. I'm less sure about the Ethiopian runners, since most research that I found online seems to focus on the Kenyans, but I'd feel safe hypothesizing that something similar can explain their dominance at the podium.
So, the short answer to your question is that it's not just "black people" who dominate the world of competitive long-distance running, but that very specific subsets of people (who, as it turns out, are black) do display a competitive advantage and that both genetics and culture account for much of this advantage.

Nice answer, I did listen at the Radio Lab podcast (http://www.radiolab.org/story/runners/) about this story few years ago and this is actually what sparkled my interest. It answers the long distance running, however my question is more related to the sprints (i.e. 100m). In Rio, male and female medallists were black but none of them were from Africa (Males = 1st Jam, 2nd USA, 3rd Can; Females = 1st Jam, 2nd USA, 3rd Jam). Maybe we'll need more studies about Jamaican sprinters?

@MudWarrior Gotcha - I didn't look into the sprinters. At a passing glance, I don't see a trend similar to the Kalenjin/distance runner effect. Would have to do a bit of research to even see what hypotheses to look into. Eeeenteresting...(mad scientist laugh)

Very nice answer for a question that could turn ugly very quick.

@gaborous Thanks! I try to keep things classy and on-point. Partly, it comes with the terrain. I'm a science journalist, which demands some tact when reporting certain topics. :-)

@MudWarrior - Jamaica is not necessarily a meaningful factor - the genetic lines that affect things likely far predate the arrival of ancestors of those runners to Jamaica within last 500 years, and you can't know if the specific winners actually did ultimately descend from Kalenjin ancestry just by where they are born in 21st century.

@Forest I found a source for the paper you mentioned: https://www.researchgate.net/publication/264745551_Analysis_of_the_Kenyan_Distance-Running_Phenomenon

@DVK This has nothing to do with Kalenjin, sprints and long distance running are absolutely different. Sprinters are descendant of West African people (often brought as slaves to America).

@Koga Thanks & good find! The paper provides some nice quantitative background to the Kalenjin/Kenyan/Ethiopian distance runner story. It would be really nice to find something that integrated these results with some of the cultural practices that probably contribute to the Kalenjin's (and others) success. That would be a pretty interesting read.

Take a look at Will Grover's answer here, I will cite the genetic diveristy explantion here, I think that sounds the most logical:

Genetic Diversity
  This is my favorite answer, and the one that makes the most sense to me: Africans are more genetically diverse than other groups; in fact, they find that the further you are from Africa, generally the less genetically diverse you are. So you would expect to see some groups who are faster than others, or slower, stronger, smaller etc. Massive Genetic Study Supports "Out of Africa" Theory. There is a great Fresh Air podcast that describes this as well (thank you Jay Hobson for providing the link!) Talent Or Skill?: Homing In On The Elusive 'Sports Gene'

Because of more genetic diversity you will have more "choice" when it comes to natural selection. Maybe because those people were there first they were exposed to threats which required more strength or speed. So maybe that's the cause— I'm just guessing.
Update
I Found another interesting theory:
African people have most of the time another type of muscle fiber(Type II) instead of Type I. Appeareantly Type II is more reddisch --> more hemoglobin --> more oxygen --> more endurance. take a look at this article.

Good suggestion @Rick Beeloo. I also found another hypothesis (see my answer below).

Interesting theory, but wouldn't we then expect that they would dominate other sports that can be "found" in primitive societies? I wouldn't argue that it will help soccer or pentathlon, but various throws, jumps, swims and perhaps weightlifting should be affected as well, no?

@Ordous, increased variation means you're more likely to find somebody with genetics appropriate for the task; reduced variation means that if the local genetics are appropriate for the task, you've got a larger pool to draw from (and are more likely to find someone who's especially good at the task).

How does the genetic diversity of Western black people (say Jamaicans) compare to that of Western whites (e.g. Americans)... Black populations outside of Africa often come from recently bottlenecked populations

Also your answer is mainly just text lifted from elsewhere with a guess pinned to the end of it, so it's a downvote from me as I don't think it's a good quality answer (if you improve it I am happy to make it an upvote)

Every answer is based on text elsewhere no one knows everything at birth right? But I understand your critic. @rg255

I had heard rumours that most people don't know much at birth, but that doesn't make the text good quality or useful in the context - the text is not particularly good at providing any explanation

Although if we overgeneralize, the genetic diversity argument may be true, it is so bland that in any other case, we would not accept it. Problem with genetic diversity is that most of it is in neutral alleles. When speaking about particular trait, this answer is just not sufficient. One group with higher genetic diversity could have low diversity in particular trait, while other group with smaller overall genetic diversity could be highly diverse. It depends on particular evolutionary pressures.

@FloriOn Edits are always welcome, but do not remove critical content. Now the reader needs to lookup the article and even search the corresponding text which makes it really cubersome. Further everything is coming from a source, then you could just write see: this, this and this, doesn't make sense right?

@RickBeeloo Still better than reading straight up false informations. Also, I think you have linked the wrong article, as it doesn't have to do anything with the topic you wrote.

I also found this hypothesis from a scientific paper which suggests that asian and white people have a lower center of gravity than black people. See the general explanation:

Blacks tend to have longer limbs with smaller circumferences, meaning that their centers of gravity are higher compared to whites of the
  same height," said Adrian Bejan, Jones' co-author, an engineering
  professor at Duke University. "Asians and whites tend to have longer
  torsos, so their centers of gravity are lower."

Update:
Here's an excerpt from the abstract that explains this idea:

The world records in running tend to be set by black athletes and in swimming by white athletes. We show that this phenomenon is predictable from physics. Locomotion is a ‘falling-forward’ cycle, in which body mass falls forward and then rises again. Mass that falls from a higher altitude falls faster, down and forward. In running, the altitude (L1) is set by the position of the center of mass above the ground. In swimming, the altitude is set by the upper body rising above the water, and it is proportional to H – L1, where H is the height of the athlete. The anthropometric literature shows that the center of mass in blacks is 3 percent higher above the ground than in whites. This means that blacks hold a 1.5 percent speed advantage in running, and whites hold a 1.5 percent speed advantage in swimming. Among athletes of the same height Asians are even more favored than whites in swimming but they are not setting records because they are not as tall.

That link (and the link therein) don't actually provide any evidence that center of gravity affects running speed, or why it would. The hyperlink that should point to an article about center of gravity height and foot speed actually links to an article about joint stress and running shoes.

Thanks @Matt I didn't clicked the links while reading it. It's fixed now, I've added the actual study link and it's even open access!

I thought it was generally accepted that the reason fast people run fast is because of a greater proportion of fast-twitch muscle fibres.  Why this appears to be more common in black people I do not know - maybe Rick Beeloo's answer is correct??  Any suggestion that it's to do with body geometry is heading down a very murky path in my opinion.

Also note that, up until Bolt's success, it was generally accepted that a sprinter shouldn't be too tall - tall athletes cannot accelerate out of the blocks as quickly and, in the 200m, cannot run the bend as successfully.  Most top sprinters are around 6ft (Johan Blake 5'11", Justin Gatlin 6'1"), Bolt at 6'5" is several inches taller than almost all of his competitors.

@Mr_Thyroid Thanks for your input, it's not my intention to head down a murky path. I only wanted to point a published study from (what seems to me) a well-known and respectable scientist. I didn't hear about the fast-twitch muscle fibres yet, if you have time, can you make it an actual answer (including references)? This could be a quite useful input to this discussion.

You relate limb length with center of gravity, but... one might think that speed would correlate with length of stride which would correlate with limb length, and speed would also correlate with step rate which would correlate (inversely) with mass at the extremities. In other words, longer lighter limbs can be moved through each step more quickly and cover a greater stride with each step, adding up to a faster run.

@AnthonyX I think you should look at the abstract of the scientific paper I've cited, it's pretty self-explanatory. But you're right, the quote from the "news paper" I used is somewhat confusing.

And that helps or hinders how?

@BobJarvis I've updated my answer to better explain this idea.

Scientists say it is because coloured people have higher centre of gravity in comparison to their white counterpart.
Using law of locomotion,researchers found that black sprinters have 0.15 seconds advantage over their white rivals due to higher centre of gravity,meaning they fall to the ground more quickly between each stride.
Conversely, having a lower than average centre of gravity helps white swimmers as their speed is determined by height they can get above the water
Source:Physics Spectrum Magazine edition April,2016, Arihant publication
           Page number:45

authors: Bob Jarvis - Слава Україні

authors: Vladimir F Героям слава


text:
What animal is this track from?
Last week I noticed this odd track made of "squiggly triangle footprints" on the outside surface of a dirty skylight in my home in the northern Netherlands, and I found it odd that I can't imagine what kind of animal this track would have come from. I assume it's animal since the movement seems very intentional and the triangle shapes are periodic, rather than being a continuous smudge that might be caused by a tiny leaf blown in the wind for example. Each tiny triangular "footprint" is around 3mm wide. Any pointers on how to identify what caused this track?

My guess is a rocking and rolling pinecone.

any kind of close up would be a huge help, I can't see any detail.

Yeah I thought of a pinecone-like object being blown around, but note that it appears to all be a single track which moves up and down and around in a very consistent pattern, no skips. Also note that this is a pretty steep skylight; I wouldn't expect even a very fortuitous wind to keep a roundish object in place long enough to do such an intricate pattern. @John sorry that's the only image I grabbed before I washed the offending window :-) but a reasonable amount of detail is visible if you zoom in.

@TopherHunt Is there a coniferous plant above the window? Have you tried taking one of the cones and reproducing the pattern? Perhaps if the cone is not roundish, but more cylindrical or cone-like shaped, this could explain the left-to-right wiggly pattern of its descent ...

Snail feeding.
It is really obvious if you have seen it before. It is the track left by a feeding snail.
Here is the grazing pattern of the common snail.

https://commons.wikimedia.org/wiki/File:Land_Snail_radula_tracks.jpg
https://alexhyde.photoshelter.com/image/I0000oboo93ZzSEI

YES thank you. And that fits because Friesland is teeming with snails and slugs. Allegedly they don't have many predators here.

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


text:
Binomial nomenclature: Why am I seeing different genera with the same species name?
I have looked online but still do not understand how two organisms can have the the same species names but be in different genera?
Do all genera share common species names?
Also which would be more closely related, two organisms with the same genus name but different species name or two organisms with different genus names but the same species name?
According to a textbook, the two with the same genus are more closely related, but I do not understand why?

For a very simple analogy, consider the Genus name to be like a person's last name and the Species name to be like their first name. John Smith is more closely related to his brother Bob Smith than he is to his neighbor, John Brown.

@CactusWoman, good analogy, unless of course John Brown and John Smith's mom, well, you know... John Jr....

I assume that you are talking about the second part of the binomial name when you write 'species name', which is in fact called 'species epithet' (or 'specific epithet'). 'Species name' is referring to the full binomial name in binomial nomenclature.

Two different species can have the same species epithet if they belong to different genera ('species name' is referring to the full binomial name). Consider for example Pinus glabra and Ilex glabra
P. glabra

I. glabra

Two species can be have the same genus name (meaning they belong to the same genus) and will therefore necessarily have different species epithets (otherwise we would name them exactly the same way which would be very confusing). Consider for example Pinus glabra (again) and Pinus resionosa
P.glabra

P. resinosa

As a consequence, if two species share the same species epithet then it tells you nothing about how closely related they are. If they share the same genus name, then they belong to the same genus (except exceptions probably!).
For the above examples, the term glabra comes from "glaber" (latin) which means "Hairless". So the only thing you can tell from P. glabra and I. glabra is that they are probably both hairless when you compare them with their respective closely related species.

Could the analogy be used for two organisms with different family and same genus? (I am aware that this is no longer binomial nomenclature). So, they would be less closely related compared to two organisms with same family, different genus? In simple terms, the category that comes first should be prioritised when deciding how closely related they are? (if that makes sense).

Yes indeed. Extending on @CactusWoman nice analogy (which is almost more than just an analogy): If the species is a first name, then genus is the family name and family is the ethnical origin and so on... A case could exist where two individuals of different ethnic groups would have the same family name but that would not be due to common descent but only to "chance".

I corrected your use of 'species name' to 'species epithet', since this is the term for the second part of the binomial name (also 'specific epithet' or 'specific name').  'Species name' is referring to the full binomial name.

And then there are cases when completely different organisms have the exact same genus and specific epithet, such as Orestias elegans Ridl. and Orestias elegans Garman, 1895.

This is a widespread issue amongst binomial names. Only the full binomial name has to be unique in nomenclature, and therefore many genera contain different organisms with the same specific epithet. As Remi.b has already mentioned, two organisms with binomial names that have the same species but different genus are very likely more different from each other than two organisms that share a genus but have a different specific epithet.
For example, the Wikipedia page on the specific epithet "Officinalis" lists dozens of organisms with a variant of that specific epithet conforming to the Latin declension of its genus.
This list consists of organisms which are completely unrelated to each other, containing fungi, plants and animals.
Althaea officinalis (marshmallow)
Anchusa officinalis (bugloss)
Archangelica officinalis (angelica)
Asparagus officinalis (asparagus)
Avicennia officinalis (mangrove)
Bistorta officinalis (European bistort)
Borago officinalis (borage)
Buddleja officinalis (pole butterflybush)
Calendula officinalis (pot marigold)
Cinchona officinalis (quinine)
Cochlearia officinalis (scurvygrass)
Corallina officinalis (a seaweed)
Cornus officinalis (cornelian cherry)
Cyathula officinalis (ox knee)
Cynoglossum officinale (houndstongue)
Euphrasia officinalis (eyebright)
Fumaria officinalis (fumitory)
Galega officinalis (goat's rue)
Gratiola officinalis (hedge hyssop)
Guaiacum officinale (lignum vitae)
Hyssopus officinalis (hyssop)
Jasminum officinale (jasmine)
Laricifomes officinalis (a wood fungus)
Lavandula officinalis (lavender)
Levisticum officinale (lovage)
Lithospermum officinale (gromwell)
Magnolia officinalis (magnolia)
Melilotus officinalis (ribbed melilot)
Melissa officinalis (lemon balm)
Morinda officinalis (Indian mulberry)
Nasturtium officinale (watercress)
Paeonia officinalis (common paeony)
Parietaria officinalis (upright pellitory)
Primula officinalis (cowslip)
Pulmonaria officinalis (lungwort)
Rheum officinale (a rhubarb)
Rosa gallica 'Officinalis' (apothecary rose)
Rosmarinus officinalis (rosemary)
Salvia officinalis (sage)
Sanguisorba officinalis (great burnet)
Saponaria officinalis (soapwort)
Sepia officinalis (cuttlefish)
Sisymbrium officinale (hedge mustard)
Spongia officinalis (bath sponge)
Stachys officinalis (betony)
Styrax officinalis (drug snowbell)
Symphytum officinale (comfrey)
Taraxacum officinale (dandelion)
Tormentilla officinalis (tormentil)
Valeriana officinalis (valerian)
Verbena officinalis (vervain)
Veronica officinalis (speedwell)
Zingiber officinale (ginger)


text:
Organic battery?
Similar to the Matrix movie where humans were used as a source of electricity but different by using electric eels. Farmed like tuna what would be the electricity exchange to the food they eat?

I don't have the math at hand for the actually energy efficiency, but let's just start from the storage capacity.
Basically, an electric eel wouldn't make a very good battery. They could be a decent, albeit fairly inefficient capacitor, but they actually store little energy. Using data from Wikipedia on Electric Eels it works out to something less than 2 joules (less than 1kilowatt over 2 ms), whereas an AA battery is around 12000 joules.
You're going to need a very, very big tank to store any appreciable amount of energy, before you even worry about how much food it will take you, let alone the animal welfare concerns with forcefully discharging a tank of eels at your whim.

What if they where grown like farmed tuna?

(side note: this could make an excellent question for Randall Munroe at XKCD's What If if you phrased it in the form of "how much would I have to feed a tank of electric eels sufficient to power the world's energy grid")

@Muze How you farm them doesn't change the basic math that you will need 6000 of them to equal a single AA battery. (and by the way, tuna is probably not the best example for farming - it is quite difficult to farm tuna and only recently achieved) I think it's off-topic to discuss here the sustainability of AA battery production but I am confident I can get one from the local supermarket for less cost than you will ever be able to feed and house 6000 fish.


text:
What is enantiostasis?
I have searched around and read my textbook but I am failing to understand how enantiostasis is different to homeostasis. For reference, Wikipedia definition is as follows:

Enantiostasis is the ability of an open system, especially a living organism, to maintain and conserve its metabolic and physiological functions in response to variations in an unstable environment. Estuarine organisms typically undergo enantiostasis in order to survive with constantly changing salt concentrations.

http://www.hsc.csu.edu.au/biology/core/balance/9_2_3/923net.html towards the bottom of the page.

Welcome to Biology.SE. You are citing the wikipedia definition, not the Google definition

The Wikipedia page you're referring to more or less has the answer: "Enantiostasis is not a form of classical homeostasis, meaning "standing at a similar level," which focused on maintenance of internal body conditions such as pH, oxygen levels, and ion concentrations. Rather than maintaining homeostatic (stable ideal) conditions, enantiostasis involves maintaining only functionality in spite of external fluctuations"

Both are ways for an organism to adapt to the environment, but enantiostasis focuses on maintaining functionality while homeostasis focuses on maintaining a stable internal environment.
For example, if the organism has to deal with changing salt concentration in water, it can do it in two ways:

Homeostasis : the organism will adapt itself so that its internal conditions do not change despite the change in the external environment (the focus is on not changing these conditions). This could mean stopping or reducing other activities because of this adaptation, but, in this example, the internal conditions (salt concentration inside the organism) will not change.
Enantiostasis : the organism adapt itself so that its functionality is preserved, at the possible expanse of stable internal conditions. This could mean the salt concentration in the organism will change, but the organism's functions will not stop or be reduced because of it. Enantiostasis can be realized either by avoiding external changes (for example, absorbing more water when the salt concentration is high and less when it's low) or tolerating it with a wide range of possible conditions.

(Source : detailed explanation on this subject as a commentary on a university course)


text:
How does the immune system fight scabies mites?
After a distressing episode involving my elderly mother and a nursing home, I've been reading up on scabies. It seems that in healthy people, the immune system limits the mite population to around 10 of the creatures at any one time; elderly and immunocompromised people can be infested by many more - thousands, even millions of mites (shudder).
So my question is, given that the mites burrow in the top, dead, layer of the skin, how does the immune system detect them and suppress them at all?
Conversely, if the immune system can limit the mite population so effectively, why doesn't it wipe them out entirely?

Welcome to Biology.SE! I think this is a very good question and made some edits to clarify it. Please feel free to further edit!

@Alex Thanks. I have only reverted the 'S' in the question, b/c I believe 'scabies' isn't a plural - same as eg 'measles'

Did you do any reaearch, say, into the immunology of susceptibility and resistance to scabies? If so, what did you find? On this site, some attempt to answer the question, even if the research doesn't help, is expected and appreciated. (Btw, I never heard that number. And from the numbers of healthy people I've had to treat for scabies - and having suffered a bad infection myself in early adolescence [an unforgettible experience] - I'd say the immune system is not all that great at suppressing the infection.)

@anongoodnurse  As in my OP, my research consisted of googling 'scabies', the results of which led me to those figures. (eg Wikipedia suggests a number as high as 2 million mites for encrusted scabies.)  I don't really have access to anything more specialised, which is why I posed the question on here.

while it seems that you're getting answers here, it's likely that SE Medical Sciences is a more appropriate forum for this question.

Found from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3535073/
In addition to being a physical barrier, the skin is an immunological barrier63. The skin immune response is vital in wounding and infection and also modulates the commensal microbiota that colonizes the skin. Keratinocytes continuously sample the microbiota colonizing the skin surface through pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs), mannose receptors and the NOD-like receptors. These receptors recognize pathogen-associated molecular patterns (PAMPs) including flagellin and nucleic acids, as well as lipopolysaccharide from Gram-negative bacteria, mannan and zymosin from fungal cell walls, and peptidoglycan and lipoteichoic acid from Gram-positive bacteria. The activation of keratinocyte PRRs by PAMPs immediately initiates the innate immune response, resulting in the secretion of antimicrobial peptides (AMPs), cytokines and chemokines. Beyond effecting an adaptive immune response, AMPs also directly kill bacteria, fungi and enveloped viruses64. Therefore, there is a constant interplay among keratinocytes, immune cells and microorganisms that is modulated by AMPs, cytokines, chemokines and microbial peptides.
While mites certainly are not fungal, viral, or bacterial, you can extrapolate the mechanisms required to prevent mite infestation being similar to those referenced above. Hope this helps!

This is an excellent question. We mostly hear about parasites being attacked by white blood cells, but mites are obviously too large to be phagocytosed, and furthermore the white blood cells are in the mite's stomach by the time they come into contact with the mite. Yet, mites are usually too small for us to see, so we can't crush them like we crush fleas. I know that aphids are eaten by other insects, but they are macroscopic, and I don't have any macroscopic insects on my skin. At the same time, when people get sick they start to be at risk for mite infestations. Also, sometimes one individual who is asymptomatic will give a mite infection to another individual, through close contact, which then causes a visible immune reaction in the victim: small red bumps indicating the locations of bites. This suggests that the immune system might be involved.
One theory is that we are looking for something like a mobile bacterium, which could live inside human white blood cells. Normally the bacterium would be dormant, but when white blood cells are ingested by a flea or a mite, the bacterium would start reproducing and releasing chemicals to counteract digestion by the parasite. Eventually the bacterium, if clever enough, would release enough chemicals to kill the mite that ingested it. However, mites have short lifespans and therefore evolve much more quickly than humans do. Unless your body can upgrade its defenses at the same pace, it will fall behind and mites will evolve resistance to the bacteria and its chemicals. The bacteria could evolve within the body, but we have no way to measure their fitness until after they are swallowed by the mite. So how could your immune system keep track of which bacteria are still effective against your mites? How does it know which bacteria should multiply and be deployed against future mites, and which ones are no longer useful?
From an information theoretic standpoint, in order for coevolution to occur, there needs to be some way for the bacterium to get back to the original host after living inside the mite. One way to accomplish this is if the bacteria kill mites by crawling up their throats and blocking them. Then when the mites try to feed a second time, some of the bacteria will get regurgitated back into the blood of the host, where it could be scavenged and returned to the lymph nodes for selection and review by the immune system.
Such a bacterium exists. Let's give it an alias: Bacterium X. Bacterium X blocks the throats of many kinds of fleas, as is well known. It can live inside white blood cells, usually being dormant in lymph nodes. Mites are observed to feed poorly on mice that are infected with Bacterium X, although they feed well on healthy mice. Fleas can transmit Bacterium X to new hosts both before and after they become blocked. Blockage in susceptible fleas leads to death by starvation. The bacteria is endemic in rodents worldwide, and normally harmless. However, when a pandemic strain emerges then it can be exceptionally virulent, producing lethal bacteremia in both human and rodent hosts. The Bacterium X disease condition is often characterized by swelling of the lymph nodes where the bacterium resides. Presumably, some of the high infectivity of pathogenic strains of Bacterium X could be due to its role as an endosymbiont, and the immune system's consequent eagerness to scavenge it from the environment so that co-evolution may happen.
The relationship of Bacterium X with mites is not well studied, perhaps partly because mites haven't been observed to transmit it between rodents, as fleas do. But many of X's traits in mites could be expected to generalize from its behavior in fleas; for example, smaller-sized species of flea are more susceptible to blockage, suggesting that mites, which are smaller than fleas, should be even more vulnerable to attack by Bacterium X.
I haven't given the actual name of Bacterium X because I wanted others to have the chance to figure it out. However, it is known that human white blood cells can contain multiple species of bacteria capable of killing fleas, in addition to the particular one I described. For me, an interesting question here is whether these bacteria are doing this on purpose, and if so, how the body keeps them evolving so that it can win the biological arms race against mites. However, I have trouble finding actual discussion of these ideas in the scientific literature. It seems possible that we have a tendency to want to view inter-species interactions as primarily hostile or pathological rather than potentially cooperative. Perhaps there is some other reason why evidences of symbiosis seems to go unremarked-upon, even when they seem fairly apparent: an ability for a bacterium to reproduce inside human and rodent macrophages, for example, or to kill a common insect parasite...

"mites are usually too small for us to see, so we can't crush them like we crush fleas."
Ah, you raise an interesting point - has anyone really tried ? I had scabies once, it was truly horrid and I scratched till I bled, which didn't stop the itching. Problem is that dead mites are just as provocative to the immune system as live ones. But I wonder if you could kill them by skin pressure before they proliferate ? I think they are probably evolved to survive pressure, but who knows ?

@JimmyWiddle Thanks for sharing. Yeah, if mites are anything like fleas ... fleas are almost indestructible. You said "I scratched till I bled" - maybe that is another way to encourage contact between skin parasites and the immune system. Mother always said "don't scratch, that will only make it worse", but I suspected this of being bad advice.


text:
Counting the number of hydrogen bonds of multiple PDB files
I've been trying to figure out a systematic way to count the number of hydrogen bonds for multiple PDB files.
DSSP shows me the total number of hydrogen bonds when I make dssp.exe 1A11.pdb, giving me the total number of 24 (am I correct, ok?)
24 96.0   TOTAL NUMBER OF HYDROGEN BONDS OF TYPE O(I)-->H-N(J)  , SAME NUMBER PER 100 RESIDUES

But when I run this command in R:
> require(biod3d)
> x=dssp(read.pdb("1A11"), full=T)

it doesn't look to have the number of hydrogen bonds. It shows this:
> x$hbonds
     BP1 BP2 NH-O.1   E1 O-HN.1   E2 NH-O.2   E3 O-HN.2   E4 ChainBP1 ChainBP2 Chain1 Chain2 Chain3 Chain4
1-A   NA  NA     NA  0.0      5 -2.1     NA  0.0      4 -0.3     <NA>     <NA>   <NA>      A   <NA>      A
2-A   NA  NA      3 -0.2      6 -1.5      4 -0.2      7 -0.2     <NA>     <NA>      A      A      A      A
3-A   NA  NA      4 -0.2      7 -1.8      5 -0.2      2 -0.2     <NA>     <NA>      A      A      A      A
4-A   NA  NA      1 -0.3      8 -1.5      6 -0.2      7 -0.6     <NA>     <NA>      A      A      A      A
5-A   NA  NA      1 -2.1      9 -1.9      6 -0.2     10 -0.2     <NA>     <NA>      A      A      A      A
6-A   NA  NA      2 -1.5     10 -1.3      1 -0.3      5 -0.2     <NA>     <NA>      A      A      A      A
7-A   NA  NA      3 -1.8     11 -1.3      4 -0.6      5 -0.2     <NA>     <NA>      A      A      A      A
8-A   NA  NA      4 -1.5     12 -1.2      3 -0.2      6 -0.2     <NA>     <NA>      A      A      A      A
9-A   NA  NA      5 -1.9     13 -1.1      4 -0.2      7 -0.2     <NA>     <NA>      A      A      A      A
10-A  NA  NA      6 -1.3     14 -2.3      5 -0.2     13 -0.4     <NA>     <NA>      A      A      A      A
11-A  NA  NA      7 -1.3     15 -1.8     12 -0.2     16 -0.3     <NA>     <NA>      A      A      A      A
12-A  NA  NA      8 -1.2     16 -1.8     13 -0.2     11 -0.2     <NA>     <NA>      A      A      A      A
13-A  NA  NA      9 -1.1     17 -2.4     10 -0.4     18 -0.5     <NA>     <NA>      A      A      A      A
14-A  NA  NA     10 -2.3     18 -1.6     15 -0.2     13 -0.2     <NA>     <NA>      A      A      A      A
15-A  NA  NA     11 -1.8     19 -1.8     17 -0.2     20 -0.5     <NA>     <NA>      A      A      A      A
16-A  NA  NA     12 -1.8     20 -0.8     17 -0.3     14 -0.2     <NA>     <NA>      A      A      A      A
17-A  NA  NA     13 -2.4     21 -1.9     19 -0.2     16 -0.3     <NA>     <NA>      A      A      A      A
18-A  NA  NA     14 -1.6     22 -2.0     13 -0.5     21 -1.0     <NA>     <NA>      A      A      A      A
19-A  NA  NA     15 -1.8     23 -2.0     20 -0.3     24 -0.3     <NA>     <NA>      A      A      A      A
20-A  NA  NA     16 -0.8     24 -1.5     15 -0.5     19 -0.3     <NA>     <NA>      A      A      A      A
21-A  NA  NA     17 -1.9     25 -1.0     18 -1.0     19 -0.2     <NA>     <NA>      A      A      A      A
22-A  NA  NA     18 -2.0     25 -0.3     23 -0.2     20 -0.2     <NA>     <NA>      A      A      A      A
23-A  NA  NA     19 -2.0     22 -0.2     18 -0.3     21 -0.2     <NA>     <NA>      A      A      A      A
24-A  NA  NA     20 -1.5     23 -0.2     19 -0.3     22 -0.2     <NA>     <NA>      A      A      A      A
25-A  NA  NA     21 -1.0     23 -0.2     22 -0.3     24 -0.2     <NA>     <NA>      A      A      A      A

So, my question: Is the total number of hydrogen bonds hidden somewhere in this output or somewhere else (or doesn't exist)?
If I manage to count the number of hydrogen bonds in a single PDB using Bio3D and R, then I can create a loop and iterate over all remainder PDB files.
Thanks for all!

This an initial solution, but can be improved:
out = system2("f:/stride/stride.exe", "f:/stride/1a11.pdb -h", stdout=T)
nh  = strsplit(out[grepl("HBT", out)], "  ")[[1]][2]
print(nh) # Output: 26 (hydrogen bonds)

I compiled an Windows version of Stride and uploaded here:
http://lcrserver.icmc.usp.br/~daniel/bin/stride.exe

I am also interested in this approach. @daniel-bonetti could you make a Linux binary for STRIDE? Thanks.

Apologies, no need, I managed to download and compile it.

The number of hydrogen bonds cannot actually be said from software only inferred. But you could try using STRIDE (http://structure.usc.edu/stride/) which takes the file name with a -h flag to output the number of hydrogen bonds. You could then write a small shell script which would pass in each file and store the data you wanted in whatever format you liked.

It's true! I thought it could exist a direct way to do that :)


text:
Has Staphylococcus aureus ever been used against cancer?
Treating inoperable tumors with bacteria appears to be very effective, albeit being toxic to the patient as well. Has (live attenuated) Staphylococcus aureus ever been used against cancer? If the answer is yes, can you give me a link to some papers on this topic as well?

Amy sources to your claim?  I've never heard of using bacteria against cancer?!

@Christiaan I actually interviewed recently at a company that's doing just that. It's really interesting.

Is OP talking about Coley's toxins? http://www.cancerresearchuk.org/about-cancer/cancers-in-general/cancer-questions/coleys-toxins-cancer-treatment and Streptococcus pyogenes and Serratia marcescens are currently used, not Staph.


text:
Do reptiles hunt?
I encountered the following passage in the book The Art of Interactive Design by Criss Crawford (bold formatting is mine):

[...] From stalking and evasion to the chase, the [interaction between mammalian predator and mammalian prey] is loaded with complex mental twists and turns as each tries to anticipate the opponent’s move and counter it. By contrast, the mammalian hunter’s relationship with reptilian prey is much simpler: the prey’s defense lies in venom, camouflage, inaccessibility, or speed. There’s nothing like the death dance between coyote and jackrabbit. And reptiles themselves don’t hunt in the formal sense; that’s too sequential. They wander around looking for an opportunity, and when they come across one, they strike; that’s all.

How accurate is the claim in bold font?

Welcome to Biology.SE. The answer very much depend on the definition of hunting. I don't think there is any good way to answer this question. I am voting to close. Intuitively I would say that the claim is quite wrong. I suppose that the best you can do to satisfy you intuition of how reptiles forage is to go on youtube and looked at a bunch of videos. Here is one for example showing a caiman who is foraging on snails.

Note also that the term reptiles has two different definitions (see this post). You are probably referring first definition on the post I linked. Knowing what you mean by reptiles will allow you to see how different clades of reptiles are foraging and you can decide if you can call their behaviour hunting or not.

I don't think there is much truth to this statement. It's certainly not true that "They wander around looking for an oppurtunity". Snakes follow trails of scent and heat, crocs wait in ambush at likely crossing points along rivers, and there are surely more examples than that. It's true that having legs underneath the body makes for a more agile/less stable running style and thusly a more interesting race for TV documentaries, but I can't think of any reason why a mammalian brain could cope with that running style better than a reptilian one.

A definition of hunting is required - for example, a crocodile, in my opinion, hunts; food doesn't simply fall in to its mouth. (Voting to close because clarity is needed).

Short answer
I think the author is mostly right, but there are exceptions.
Background
The author is probably referring to hunting as being an "active foraging" strategy, while he ascribes the foraging behavior of reptiles to be a "sit-and-wait" strategy.
Active hunters include the classic, and dramatic high-speed, long-distance pursuit strategies deployed by cheetahs and lions, which are indeed mammals. Lions and dolphins are well-known examples of pack hunters that use consorted team effort to catch prey.

Sources: Dreamstime and OMG facts
Reptiles, on the contrary, indeed often wait silently for passing prey, instead of deploying active hunting strategies. Well-known examples are crocodiles that lurk silently below the water surface to swiftly grab passing prey, and Komodo dragons that patiently wait for hours at a time to take down passing prey.

Source: Deposit Photos
However, there are exceptions. A study performed by Eric McElroy from Ohio State University reports that lizards use two basic foraging techniques. In the first approach which they dubbed sit-and-wait, lizards are basically waiting for their prey to pass. Then, with a quick burst of speed, they run after their prey, snatching it up with their tongues.
In the other form known as wide or active foraging, lizards move constantly but very slowly in their environment, using their chemosensory system to stalk their prey.
Source: Science Daily

Great response. However, there is evidence that Komodo dragons actually do perform a more active form of hunting. See this video of Komodo hunting water buffalo. They 'attack' the buffalo by biting it to inflict infection and then sit and wait! :p

@theforestecologist - the komodo in the video basically uses the active foraging technique mentioned in the last sentence of the answer. The waiting for the infection to kick in is as passive as it gets.

As expressed in the comments, the answer to this question depends on how you define 'hunting'. However, using common definitions in biology, hunting is almost used as a synonym to predation (see quoted definitions below). In that sense, the statement in your question is clearly incorrect, since it is describing the the foraging behaviours of predatory reptiles.
The description of reptile hunting in your quote is also too simplistic, and there is a range from sit-and-wait strategies to active pursuit of prey, see e.g. the section Foraging models in Pianka & Vitt (2006).
A couple of useful definitions can be found below.
From Encyclopaedia Britannica:

Predation, in animal behaviour, the pursuit, capture, and killing of animals for food. Predatory animals may be solitary hunters, like the leopard, or they may be group hunters, like wolves.
The senses of predators are adapted in a variety of ways to facilitate hunting behaviour.

www.thefreedictionary.com:

predation (prɪˈdeɪʃən) n
  1. (Zoology) a relationship between two species of animal in a community, in which one (the predator) hunts, kills, and eats the other (the prey)

Wikipedia: predation:

predation is a biological interaction where a predator (an organism that is hunting) feeds on its prey (the organism that is attacked).[1] Predators may or may not kill their prey prior to feeding on them, but the act of predation often results in the death of its prey and the eventual absorption of the prey's tissue through consumption.

Even if 'hunt' is often defined in terms of active pursuit, it can also include broader and more passive elements, for instance "seek out; search for", see www.thefreedictionary.com:hunt:

hunt  (hŭnt)
  v. hunt·ed, hunt·ing, hunts
  v.tr.
  1. To pursue (game) for food or sport.
  2. To search through (an area) for prey: hunted the ridges.
  3. To make use of (hounds, for example) in pursuing game.
  4. To pursue intensively so as to capture or kill: hunted down the escaped convict.
  5. To seek out; search for.
  6. To drive out forcibly, especially by harassing; chase away: hunted the newcomers out of town.

I can see the point by @AliceD that 'hunting' is often (in every-day language) used in reference to "active foraging". However, in my eyes this is too restrictive. Also note that the main use of 'hunting' is in reference to hunting by humans, and some of these hunting methods mimic the sit-and-wait strategies of reptiles (see e.g. some methods for big game hunting and the use of traps). If sit-and-wait strategies are not considered hunting, then you are also excluding some human hunting practices from 'hunting'.

Nice systematic analysis of the question. +1. The author is indeed not a biologist, but a physicist now active in the gaming industry. I linked some pages to the author and the book in the question.


text:
Do aquatic plants have stomata?
I am wondering if aquatic plants have stomata or not. I know that non-aquatic plants have stomata to release water(transpiration) and oxygen, and to take in carbon dioxide. Do aquatic plants also have stomata, and if so do they take in water through their stomata? If water is taken in through their stomata, wouldn't other substances such as dissolved salts get in the plants vascular system too? Does the aquatic plant use this salt or remove it, and how would they remove it?
Note: I am talking about fully submerged aquatic plants such as kelp.

No
First of all, stomata is of course important for gas exchange and also water conservation. Well, clearly, water conservation isn't needed! Also, gases can diffuse relatively easy in water so gas exchange using stomata isn't needed.
Technical notes
Second of all, technically organisms like kelp are thalloid plants. They are in separate kingdoms. Kelp is a brown algae, placed in kingdom algae in laminariales order of class phaeophyta. They does not contain any kind of vascular or conductive tissue as their plant body is thalloid.

@zack1544 you're welcome. If you have related questions, please ask me in the comments.

They're not in separate kingdoms. Algae and Land plants (embryophytes) are separate Divisions of the Kingdom Plantae.

@naught101 well, I didn't know that green algae were part of plants, as I learnt it as part of Protists. But other aquatic "plants" are not plants, like kelp is in brown algae which is in Protists.

Do you have references for your claims? To say that all aquatic plants lack stomata is quite a strong statement.

@fileunderwater: There are semi aquatic plants that ofter have their leaves above water. Those will have stomata. There are properly aquatic "plants", like kelp, but as Tanmath says, they're not embryophytes, so they don't have stomata.

@naught101 I was referring to fully submerged plants, since that is what the OP is mainly asking about. The answer needs references either way. I'm aware about semiaquatic plants etc (see my answer below).

According to the book Stomatal function (Zeiger et al, 1987), many aquatic angiosperm plants have stomata (since they have evolved from terrestial plants), while some have reduced or complete loss of stomata.
However, the book also states that:

...aquatic plants living underwater are devoid of stomata. Leaves that float in water, which are common in ponds, have stomata on their upper surfaces but lack them on the surfaces in contact with water.

It is true that plants that float on water (hydrophytes) have stomata on one sider, but I think the OP is referring to fully underwater plant-like organisms or plants.

@TanMath I was merely looking at a couple of sources I know of. As it seems, fully submerged plants indeed often/usually lack stomata.

Oops, I was mistaken when I said hydrophytes float on water. Many hydrophytes are submerged underwater.

Are there aquatic angiosperms that never have their leaves out of water? Or at least, where the leaves don't really work out of water?

@naught101 Angiosperms like Ceratophyllum submersum (Hornwort) lives fully submerged. I cannot say to what extent their leaves work out of water, but their supporting structures (branches, stems) aren't adapted do life out of water, and cannot support the weight of the plant.

@naught101 I can, from field expierence, tell you that most if not all submerged plant don't survive outside water (incl. Ceratophyllum). The leaves simply dry out. Sometimes they reach up to the water surface, but they rarely protrude more than a few mm. Many species, like potamogeton, myriophyllum, ranunculus do have flowers that grow a few cm above water level.


text:
Is an egg classified based on the species inside it, or by the species that laid it?
Basically what I'm asking is if an animal of species x were to lay an egg, and the animal inside that egg happened to be the first member of a genetically new species y, would the egg be considered an x egg or y egg?

Parent species is certainly what they'll call it, unless there was some reason to check the genetics.

What you are proposing does not happen in higher Eukaryotic organisms. See UC Berkley site on Speciation for more detail.

Asap Science answer to this question

Species are generally defined in terms of populations (see e.g. the wikipedia page), and it is therefore relatively meaningless to talk about individuals as species. That species is defined in terms of populations is true for many species concepts, e.g. as groups that can produce fertile offspring (biological species concept) or as a evolutionary distinct lineage (phylogenetic species concept). The question is therefore somewhat ill-posed, since it is only framed in terms of individual parents and offspring.
A possible exception could be speciation in apomictic species or speciation events following a change in ploidy level, but this is mostly relevant for certain types of asexual species and probably not what you are after since you are talking about egg-laying animals.

Linguistic
An Ostrich egg. A chicken egg. A quail egg...whether you call an egg based on who laid it or who is inside of it is not a question of science but a question of linguistic.
Non-fertilized chicken eggs do not contain any chicken. We still call these eggs chicken eggs. Following the same logic, I would call an egg based on who laid it. But really this has nothing to do with science.
But, the first question one should ask is whether the scenario you are describing makes any sense. Is it possible for an offspring to be of a different species than its parent?
Can the offspring belong to a different species than the parent?
The concept of species is very poorly defined. The reason is not that we fail to agree on a definition but that the categorization of living things into discrete categories often does not make sense.
Let's think of an individual of species A. Imagine we were to look back at the ancestry of this individual for a relatively high number of generations. You chose one specific ancestor in the lineage and realize that this ancestor looks very different. Maybe we have already named the species that this individual belongs to. Let's say the ancestor belongs to species B. So, at some point there was necessarily an individual from species B who had an offspring who belonged to species A, right? ...not really. The reason is that the concept of species makes little sense. There is no such thing as absolutely clearly defined groups of individuals that you can gather into one single species.
You should read this post on the concept of species and then read this post on species ring and come back here once you finished reading....
We often think of the concept of ring species when thinking about population separated spatially. But the same concept hold true for population separated temporally. If we come back to the two individuals belonging to species A and species B. These two individuals probably cannot reproduce together and are very different. It seems legitimate to classify them in different species. However, all individuals along the way were probably able to reproduce with their own parent and offspring.

This is really convoluted. The simple answer is that unless giving birth to a hybrid, a species will only produce offspring of that species.

Hidden behind your simple answer is hidden the conceptual issue of the species. Saying it is impossible to give birth to an individual belonging to a new species (except hybridization) seems to contradict the existence of speciation events.

What are you talking about?

Well... that is a broad question that you are asking @AMR! Saying a species will only produce offspring of that species is contradictory to a species can evolve to become another one and the reason is that the term species is poorly defined.

In a single generation an organism of a defined species will not give birth to another species, unless the mating is between two individuals of such compatibility as they can produce a hybrid, and more often than not, in those situations the hybrids are sterile. Any single generation will not be that different from the prior one or the next one. It is over time and gene pool separation that different species can be distinguished when making a comparison. So it is not contradictory.

If you move from area A to area B you need to pass by the border at some point. If you evolve from species A to species B you need to make an offspring who is not of the same species. I wanted to make sure the OP understood why this analogy is misleading and the reason is that the concept of species is bad. We are not talking about speciation here, we're only talking about a single lineage that changes through time sufficiently so that we would tend to call the lineage differently at two time step (regardless of whether the lineage actually split in two or more).

This question is interesting. First of all, I recommend you to look a little bit about the most popular definitions of species and, more importantly, how speciation can occur.
I can picture a problem of hybridization when I think of your question. Since speciation takes many (plentiful) generations to happen, and as I can remember, can involve sympatric speciaton and/or extinction of the parent's species since the new one won't be enormously different in matters of food request, habitat and other physiological needs (generally) and so there will be a conquest/fight for resources (you can look out for more details in Charles Darwin's On the Origin of Species). All this to say you won't have a newton coming out of a frog's egg. :)
But hybridization can lead to speciation, and you can have a hybrid coming out of an egg of a well descripted species. This happens with more frequency in fishes, insects and amphibians. For example, you can study individuals that are phenotipically different from their parents, with other types of adaptation (sometimes better) to the environment, and that emerge from different (and phylogenetically proximate) diploid sexually reproducing species... and the resulting individuals can have, of course, di/tri/tetraploid genomes... So, morphological and genetically different from their parents!!
And when referring to these situations, scientists generally call them genus name of the species involved + complex. For ex, the Pelophylax complex, involving 3 types of frogs.
If you really have an urge to search about this, try to go to this paper.
Hope I helped.
PS: You can also research about the Squalius alburnoides complex, which is about a group fishes extant in the Iberian Peninsula, with an amazing (and complex) process of speciation where you have a well characterized hybrid coming out of eggs layed by hybrids or parent species.


text:
What's the determinant of the male-biased birth sex ratio in humans?
Will the baby be male or female? If it was a random biological switch then, with a huge sample number, the sex ratio at birth would be exactly 50-50. But it isn't; the ratio is about 51-49 in favour of males. So how does this inequality arise?
Further to @Remib's comments. I was specifically thinking of the sex ratio in humans. Would it be true to say that the genetic determinant of the sex ratio would be exactly 50:50 M/F? If the disparity is environmental, then how does it work, and wouldn't an environmental effect be more variable than the 51:49% that we see?

Are you talking about humans only? Are you more interested into a mechanistic explanation or rather an evolutionary explanation?

If your interest goes beyond humans, then note that the sex-determination system varies (a lot) from species to species. The post Do males of all sexual species have Y chromosomes? gives an overview of this variation and while the answer does not specifically talk about the sex-ratio, I think you can easily make your way to the understanding of why the sex-ratio isn't always 50:50.

https://www.youtube.com/watch?v=3IaYhG11ckA This is a lovely video explaining it all. There are a ton of references down there in the description

There are a number of ways in which the true sex-ratio at birth (let's assume the 51:49 is well estimated and is the true ratio) could deviate from 50:50. This list is just an brief overview.

Sex, in humans, is determined by the sex chromosome present in the haploid sperm cell which fertilises the egg. If males produced more or less Y-bearing sperm than X-bearing sperm, then the birth sex ratio would be expected to deviate from 50:50. However, studies suggest that sperm production is not biased towards X or Y bearing in humans.
The probability of fertilisation may differ between X- and Y-bearing sperm. If Y-bearing sperm were more likely to succeed in fertilising the egg then there would be a male-bias in the birth sex ratio. I've seen it suggested that the small Y chromosome makes the sperm slightly smaller and therefore faster, but can't find those claims right now. Regardless, it appears that sex ratio at fertilisation is not sex-biased.
Bias in the birth sex ratio can come through sex-biases in the failure rate in fetuses. If female fetuses are more likely to miscarry than male fetuses, over the course of the gestation, then the sex ratio at birth will be male-biased. It appears that there is sex-bias in the failure rate of fetuses which can be male or female-biased throughout gestation, but the tendency is for female-biased failure rate during the second trimester to generate an overall male-bias birth sex ratio.

But would you really consider the 1.5% as a significant deviation? There are of course demographic differences which are in many cases affected by "cultural" practices. In many places the sex ratio is skewed toward male because of female infanticide (preference for a male child).

birth sex ratio won't be affected by infanticide - I've also not said that 1.5% is significant, I'm just operating under the assumption that the quoted statistic of 51:49 at birth in the question is correct and pointing out how it could be


text:
Can formalin fixed tissue stored in absolute ethanol be used for histology?
Can samples which have been stored in buffered formalin and the moved straight to absolute ethanol be used for histology?
I know that the samples normally need to go through a series of ethanol concentrations (70%, 80%, 90%) for dehydration before they reach absolute ethanol, but can you still use samples that have been immediately immersed in absolute ethanol? Or would the rapid dehydration cause too much distortion?

Can they be used? Sure. How much distortion you get will depend on the tissue type and several other factors. How important that distortion is will depend on what you are trying to measure. "Too much distortion" is a relative term. You can't really know how bad it will be without trying it.
Should this ever be done intentionally? No - there is good reason for using the gradual dehydration steps. I would be really hesitant to do any quantitative analysis or draw any solid conclusions from tissue processed incorrectly, though.


text:
Help explain multi alleles in terms of actual genetic code
I understand that someones genetic makeup at an allele is usually denoted as (AA,Aa,aa).
That means that instead of an A-T pair you get a C-G pair on none, 1 or 2 copies.
Now, what exactly happens when you have a tri-allele (as in blood type). Are they looking at two base positions? Or is it instead of an A -> C mutation, you get something weirder like an A->G mutation (and thus you need to account for directionality) etc?
Thanks!

All of these things happen, but triallelic SNPs (single nucleotide polymorphisms) refer to the case where a single specific base in the genome may have one of three bases. e.g.: A/G/C
Cases where more than one base in a sequence that changes.  This doesn't really have a name though: (e.g. AA -> GC ).
These can be called a/b/c alleles I guess.
The reason for this not having a name is probably because two bases don't really change at the same time as a common event.  If two SNPs are next to each other they probably changed at different times, which means that if you look around enough you will find AA, GC, and GA because the A->G happened first and then a few dozen generations the second A->C mutation happened.

Ah, I see, so if the sequence is TCGAT and that the 3 position by default is a G, but can be an A or T that would be tri-allelic. if it can be A,C,G or T, then it's quad-allelic? Can you go higher than a 4 way somehow?

@user1357015 not at a single point, because there are only 4 bases in DNA. However, any one gene may have from a few to hundreds of SNPs, each one creating a separate "allele."

@MattDMo ah, I see. So a single point can be at most tri-allelic but a gene can be multi-allelic. In fact, if a gene is N bases long, it can then be 3N-allelic? Is that correct?

yup - you got it.  additional point is that each new addition to the allele is a separate mutation - it just happened in the same place

There are only 4 bases of DNA, but you can have insertions and deletions as well.  You can also have alleles that differ at multiple points, so no, there are a lot more than 3 x the length of the gene possible alleles.  Of course, you will only see so many possibilities in a real population.

@swbarnes2 Yes, I should of clarified. Assuming only point substitution mutations are allowed on a gene N units long -- that gene can have at most 3N alleles. Does that sound better?

Sound better?  Of course not.  You aren't limited to a single nucleotide change, and at every point, you can have 4 letters, not three.  How does it help to assume things that aren't even close to real?

Many models, for the sake of simplicity only deal with point substitutions. That's what I'm considering at the moment. Now, since each position is only 4 bases (and one is the "canonical"), there are only 3 mutations possible for each position. Since an "allele" is an alternative conformation, and there are only 3 alleles possible for each base (as one is the original one), why is 3N incorrect?

At a given point 4 alternative alleles are possible. its pretty rare is all.

@shigeta: I'm a little confused by the terminology then: Why at a given point 4 alternative alleles are possible. I thought an allele is an "alternative form". So there's the canonical base and then there are 3 possible mutations. Or is it that by "alternative" they mean including the canonical?

ok - well four alleles in any case.  triallelic means 3 possible alleles, bi-allelic 2 possible alleles.  in all these cases one would be most common for a given population. I do tend to think of all the alleles as alternatives to each other.

I understand that someones genetic makeup at an allele is usually
  denoted as (AA,Aa,aa).

No. That's what you learn in high school, because it's easy, and because it's what Mendel worked out for the 7 traits he studied in pea plants.  Real life is a lot more complex.  Most phenotypic differences cannot be explained in terms of exactly two alleles, one of which is classically dominant to the other.

That means that instead of an A-T pair you get a C-G pair on none, 1
  or 2 copies.

Not necessarily.  Two alleles might differ at many many points in their sequence.
And you seem to be a bit confused about how people write out DNA sequence.  Even though DNA is a double helix, when we talk about what the sequence is, we refer only to one strand, like this
GAGCCATGGGGCGCCATGTTGCCACCAGCTGCCACGTGGCCTGGCTTTTGGTGCTGATCT
A mutation might turn that last T into an A, but we don't say "oh, nothing happened, it's still an A-T pair" because it matters which strand has which letter.

Now, what exactly happens when you have a tri-allele (as in blood
  type).

Well, blood type is more complicated that just ABO...but here's a pretty old paper with some helpful details
http://www.ncbi.nlm.nih.gov/pubmed/2333095
"Here we present a molecular basis for the ABO genotypes. The A and B genes differ in a few single-base substitutions, changing four amino-acid residues that may cause differences in A and B transferase specificity.  A critical single-base deletion was found in the O gene, which results in an entirely different, inactive protein incapable of modifying the H antigen."

I'm not sure you've got a really solid understanding of what an allele is, so let me blather a bit and see if it helps.
The gene that codes for the enzyme that puts the "A" type of carbohydrate on a red blood cell is called the "IA" allele of the gene.  This gene is about 1065 base pairs long. If you were to spell it out, it would look like:
CAATGGCCGGGTAATTAAAATTGACGAC...
GTTACCGGCCCATTAATTTTAACTGCTG... (keep going to 1065 letters)
The most common O allele has the same series of base pairs, except one base pair (G_C) is lost at the 261 position. This is a deletion mutation.
The most common B allele is the same gene sequence, except there are seven single base substitutions within the coding sequence at base pairs 297, 526, 657, 703, 796, 803 and 930. These are substitution mutations.
Does that make sense? The basic ABO blood-type gene is almost the same in each allele, but has slight changes that result in different phenotypes.  And this is the simple version. Now that we can easily sequence genes, we can look in lots of people, and see that there are at least TWENTY different gene sequences with small changes in base pairs that still result in type "A" blood. You can see a figure with examples in this paper: http://www.ncbi.nlm.nih.gov/pubmed/12014997 (open-source)
So, since one gene has hundreds of base pairs, there are often many more than two, three or four alleles for that gene. You can add base pairs, delete them, change them, switch them in chunks from other chromosomes -- all kinds of stuff happens.


text:
how do they identify different protein chains?
Can someone please explain how different protein chains occur exactly? I'm not talking about the side chain, but the protein chain which is typically labelled as A,B,C etc in the PDB. I'm curious as to how they are first found and what causes them? As far as I understand, the protein backbone could be in any of several conformations and each conformation has a label? Is that correct?

Chains are individual polypeptides that make up a multimeric protein complex.

I'm curious as to how they are first found and what causes them?

SDS-PAGE will resolve all the different chains (if they are different in molecular weight). Chains are products of translation (and some modifications such as clipping and/or other PTMs etc) and they assemble to form final protein complex.

As far as I understand, the protein backbone could be in any of
  several conformations and each conformation has a label? Is that
  correct?

Yes. The labels are assigned as per the reported conformation.

Is one chain more common than the other? What causes translation to
  produce different chains in this case? And finally, during the x-ray
  crystallography, how do they identify them when they grow the crystal?

There can be different kinds of multimers. There can be homomultimer or a heteromultimer or a multimer of this configuration $(XX)_2$-$(YY)_2$ (a heterodimer of homodimers- just one arbitrary case) etc.
Each chain is a polypeptide and is encoded by a distinct gene. It is possible that in a multimer there are more number of a certain chain than the other for e.g. $X_3$$Y$. This is not because $X$ is produced more then $Y$ but rather because of the way the multimer is assembled.
In X-ray crystallography you basically get the arrangement of atoms. You can also understand which atom is what and similarly the termini can be found out. In any case people don't just proceed to crystallography without understanding the subunits and other biochemical properties.

Is one chain more common than the other? What causes translation to produce different chains in this case? And finally, during the x-ray crystallography, how do they identify them when they grow the crystal? Thank you again for your help!

edited the answer

Awesome, this helps a lot. So to be clear, your heterodimer of homodimers, that would be something like two chain A's bonded to two chain B's? Could it be completely different proteins bonded together? Last question: Also, let's pick a particular structure, say 3GFT in the PDB. There are 6 chains there. Are all 6 in the structure forming an ABCDEF heterodimer? What would be an example of a homodimer (I assume the same chain would be labeled twice?) Thank you again!

Slight addendum, it seems that 3GFT is a monomer, so how do the 6 chains come into play?


text:
simple explanation of a crispr screen vs pooled crispr screen?
I'm familiar with how CRISPR works to make either knockdown or amplification effects for a single gene because you can make precision cuts.
What exactly does a pooled crispr screen do & how does it work?

In the context of pooled CRISPR screen, you first design a library of gRNAs against a certain set of targets (instead of just one target).
The library can have the size you want, most commonly it is either targeting the kinome, or the whole genome (genome-wide).
In this context, you would add the full library on your cell of interest in which you want to make the perturbations.
Depending on how the screen is set-up you try to select the perturbations which either allow you to pass a selection process (toxicity, fluorescent readout, etc). Usually an elegant way is to have either a label also code barcode which helps you to identify the gRNA which generated the surviving/selected phenotype. With the barcode/gRNA you can track back which gene was likely perturbed in the screening process.
Hope that helps and that answers you question, please don't hesitate to further refine it if this is not clear to you.

Hi, i am not a specialist in CRIPSR but should I understand from your answer that the cripsr method is robotic with a computer interface?

@totalMongot: no screen should be interpreted as a biological screen for example in the context of CRISPR, genetic screen: https://en.wikipedia.org/wiki/Genetic_screen

So if I understand well, this works this way: 1/ I analyze my cells to have the genetic screen 2/ I choose from the genetic screen which gene (gene X) I want to alter 3/ the genetic screen tells me for example that gene X is ATCA 4/ I send with crispr vector an enzyme to alter ATCA?


text:
What is an epistasis group?
I have been trying to wrap my head around the concept of epistasis for a couple of days now, and I think I understand it, at least at a basic level, but I still don't understand some of the ways that the term is used.
What does it mean if gene A is epistatic to gene B? Does this simply mean that gene A masks the phenotype of gene B when expressed? or is there more to it?
Also, what does it mean when genes are in the same epistasis group? I am currently studying the transcriptional up-regulation of PSY3 in yeast as a result of UV treatment. PSY3 codes for a protein that forms the Shu complex along with 3 other proteins. One paper I am reading states that PSY3, is in the same epistasis group as the three other genes that code for these other proteins. What does this mean?

What does it mean if gene A is epistatic to gene B? Does this simply mean that gene A masks the phenotype of gene B when expressed?

Yes.  Note that this does not say anything about mechanism. If A converts 1 to 2, and B converts 2 to 3, then A is epistatic to B, but A is also upstream of B.  In a signaling pathway, say B inhibits A and prevents it from signaling. A mutation in B allows A to signal. A mutation in A means there is no signaling. Mutations in both A and B means there is no signaling: A is epistatic to B, but A is downstream of B.
An epistasis group is a group of genes in the same pathway.  Knocking out any combination of these genes will not result in a more severe phenotype than knocking out the most "sensitive" of these genes (the single mutant with the most severe phenotype).


text:
How does myopia develop, exactly?
Recently I was reading about myopia and I understood a few basic facts about it:

Its initial cause is a constant spasm in the ciliary muscle.
To do less work, the eyeball elongates a tiny bit.
During adolescence, because of the growth of the body, the eyeball elongates accordingly even more (i.e. the myopia is progressing).

I don't really understand the exact mechanism responsible for the transition from 1 to 2. Is the ciliary muscle capable of elongating the eyeball on its own, or is there some other relationship to another part of the eye?
It's weird how myopia is so common these days and I wasn't able to find the precise mechanism behind it.

What is myopia?
Myopia, a.k.a. near-sightedness, is a refractory error. Refraction is the process by which the optical system focuses images of objects on the retina, which are then transmitted to the visual cortex of the brain to be interpreted as vision. The major components of refraction are the cornea, lens, and axial eye length (distance from the front to the back of the eye). The problem in myopia is that images are focused anterior to the retina, like this:

Causes of myopia
You ask

I don't really understand the exact mechanism responsible for the transition from 1 [ciliary muscle spasm] to 2 [elongation of the eye].

Swelling or spasm of the ciliary body (the circumferential tissue inside the eye composed of the ciliary muscle and ciliary processes) can be seen after trauma or in inflammatory conditions. Contraction of the ciliary muscles causes decreased tension in the suspensory ligaments that connect the ciliary body to the lens. The results in the lens becoming more rounded and/or moving anteriorly. Both processes also bring the focal point more anterior, i.e. further in front of the retina, resulting in a configuration as in the picture above. You could call this "elongation of the eye" if you wanted. This 25 second video explains the process succinctly with pretty pictures.
Although interesting to think on, this is not the most common cause of myopia. Myopia is an extremely common condition, occurring in ~25% of the US population. Myopia can be classified as axial or refractive.

Axial myopia: The refracting power of the eye is normal but the length of the eye is too long.
Refractive myopia: The length of the eye is normal, but the lens refracts too much for a given axial length.

Both axial and refractive myopia are usually caused by failure of emmetropization, the process by which a normal eye has coordinated growth of its refractive components. This process takes place mostly during the childhood and adolescent years, which is why myopia most commonly develops during that time. There are certain disease conditions that increase lens power (e.g. osmotic effects in diabetes) or axial length (e.g. posterior staphyloma) that may also cause myopia at other points in life, but these are less common.

References:

1. Neil J. Friedman and Peter K. Kaiser. Essentials of Ophthalmology. © 2007, Elsevier Inc.

2. Albert, Daniel M., MD MS.Albert & Jakobiec's Principles & Practice of Ophthalmology, Third Edition. © 2000, 1994 by W.B Saunders Company, © 2008, Elsevier Inc.

Image from:
http://en.wikipedia.org/wiki/Myopia