text:
How do taenia form a species?
I know that there are many hermaphrodite animals and plants. But many of them seem to still exchange genes by mating with another member of their species.
I now happened to read the Wikipedia article on Beef tapeworm, and it turns out that there normally is one worm per host, and it self-fertilizes. Which makes some sense - if I were a large internal parasite, I wouldn't want to wait around for my host to pick up a second member of my species before I can reproduce.
But this means that there is no gene exchange when taenia reproduce. Does it mean that they are all clones of each other, barring spontaneous mutations? How does evolution function in taenia when they don't mate? How comes there are different taenia species if they can't evolutionary adapt to new environments by producing offspring with mixed-up genes?

There's inter-segment fertilization, which should help a little bit with genetic monoculture. If another tapeworm colonizes the same bit of gut, I imagine they reproduce sexually while they can. Curiously few resources on tapeworm sex out there.

You may want to have a look to the various existing definitions of species on the wiki page and eventually this post about ring species

This question has a related issue that should be addressed first: what is a species? To some extent, if you want to understand how speciation can occur, then you have to consider how you are going to define a species. There is no species concept that applies to all species, past or present. The most widely applied concept is the biological species concept (Mayr 1942), which applies (imperfectly) to sexually reproducing species. Of course, Taenia does not always reproduce sexually. I think the discussion of species concepts is beyond this question but I encourage those that are interested to check out references [2-4] as well as a series of papers published in Systematic Zoology in the mid-70s. Here, I'll focus on genetic differentiation with a subtext of reproductive isolation.
Genetic differences can accumulate between populations$^1$ of Taenia in two different ways. The first is non-adaptive evolution via genetic drift. Drift is when allele frequencies change by random processes. For example, just by chance, tapeworms in a particular host may not live very long because the host was killed in a mudslide. Those tapeworms don't produce as many proglottids over their interrupted life so they don't leave as many copies of their alleles. Tapeworms in a host that lives a long time produces lots of proglottids and therefore produce many more copies of their alleles.  The key point here is that the process of genetic drift is random. Allele frequency changes in one population of Taenia will be different from allele frequency changes in another population. Thus, over time, different populations of Taenia can become genetically different solely by chance. It's called non-adaptive evolution because natural selection is not evolved.
Adaptive evolution by natural selection can still occur on individuals that are asexually reproducing. Genetic differences will accumulate in a population over time to due mutations. Some mutations may be beneficial, some may not. Selection can increase the frequency of beneficial mutations and decrease the frequency of very mutations. Note that non-lethal but harmful mutations can accumulate in asexually reproducing species (see Muller's Ratchet) but I am assuming survivorship is decreased by harmful mutations for this example. If we assume that Taenia in different populations are subject to different selective pressures, then genetic differences can accumulate, leading to speciation. Note that drift will also affect the allele frequencies of both beneficial and harmful alleles because drift is random.
That brings us to the "mixed-up genes". I assume you mean the new genetic combinations that occur via sexual reproduction. Even if a host typically has only one individual of Taenia (not always the case), I suspect the opportunities for sexual reproduction in a population of Taenia are frequent, especially over evolutionary time. Consider places where tapeworm infestation of humans is high. Such places often have poor sanitary conditions so the opportunity for mixing of fecal material from different human hosts is high, and therefore the opportunity for mating among different individuals of Taenia is also high. If you have many humans living in squalor over long periods of time, then you have conditions very favorable for sexual reproduction of Taenia. Remember too that Taenia produce lots of proglottids, each with the chance for reproduction. Each reproductive opportunity creates new genetic combinations potentially subject to natural selection.
The final point to consider is population size. If the population size of Taenia is small (relatively few individuals) then genetic differences can accumulate fairly rapidly by genetic drift but the accumulation of beneficial mutations in the population will be low. If the population size is large then new mutations including beneficial ones can occur relatively often, increasing the rate of adaptive evolution among different populations.
Footnote

I'm assuming some sexual reproduction among individuals of the same population and individuals from different populations do not interbreed. Without sexual reproduction, we have to think about the individual as the species and that makes my head hurt.

References

Mayr, E. 1942. Systematics and the origin of speceis from the
viewpoint of a zoologist. Columbia University Press, New York, USA.
Howard, D.J. and S.H. Berlocher (eds.). 1998. Endless forms:
Species and speciation. Oxford University Press, Oxford, England.
Wheeler, Q.D. and Meier, R. (eds.). 2000. Species concepts and
phylogenetic theory: A debate.  Columbia University Press, New
York, USA.
Coyne, J.A. and H.A. Orr. 2004. Speciation. Sinauer Associates,
Inc., Sunderland, Massachusetts, USA.

Extension of Question
Beef tapeworm or Taenia saginata
Beef tapeworm or Taenia saginata shows both asexual and sexual reproduction. As you have mentioned if any other partner is not available then it will carry on asexual reproduction.
Now,

Scolex or the hook attahes to the host.
Scolex reproduce asexually by budding.
One tapeworm segment or proglottid takes around 10-12 weeks to mature.
There can be 1000-2000 Proglottids in the worm body.
Proglottids are Hermaphrodite when mature.
Each of these proglottids will produce around 100s of eggs.

That means,

A full grown tapeworm can produce from 1,000 to 2,000,000 eggs a day. They survive up to 20-25 years
Any mutation can be exponentially magnified in the generations as mostly the reproductions are sexual type(after the initial budding or occasional self sexual)

Update
According to wikipedia:

Because each proglottid contains the male and female reproductive
  structures, they can reproduce independently. Some biologists have
  suggested that each should be considered a single organism, and that
  the tapeworm is actually a colony of proglottids.[3]

Source:
[1] http://en.wikipedia.org/wiki/Beef_tapeworm
[2] http://animaldiversity.ummz.umich.edu/accounts/Taenia_saginata/
[3] http://en.wikipedia.org/wiki/Cestoda

Maybe I got something wrong, but in my understanding, a proglottid is not an animal, but a piece of the animal. The scolex buds asexually, passing its complete gene set to each proglottid. This means all proglottids of the same worm have the same set of genes. Now, a proglottid can fertilize itself or the neighbour proglottid, but it doesn't matter, because the genes of the mother proglottid and the father proglottid are still the same. This doesn't lead to new gene mixes. Or did I misunderstand the budding mechanism?

male and female taenia don't exist. A taenia is a hermaphrodite. So each proglottid can be like the other one, no difference in chromosomes needed.


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Why does the sacrum fuse together?
Everywhere I look describes how the 5 sacral vertebrae start fusing together during adolescence and are totally fused by the time you're 30 or so. But nobody seems to explain why this happens.
It seems like it would be disadvantageous for women, since presumably having a fused sacrum makes giving birth more difficult- apparently post-partum fractures are not uncommon (http://rheumatology.oxfordjournals.org/content/42/2/384.long). So why does it happen?
EDIT: Matthew McTernan gave a great answer, but I am greedy and would like to know more: Why does the sacrum only start fusing together in adolescence, and then finish in your late 20s - early 30s? Most major development ends in your early 20s. Does this have something to do with reproductive concerns? If so, why does it happen on the same timescale in men and women?

It isn't just humans that have fused sacral vertebrae. Animals on the phylogenetic tree ranging from Squamata (lizards), to Aves (birds), to even Monotremata (egg-laying mammals) all have fused sacral vertebrae. The fused vertebrae can serve as a stronger, weight-baring structures for animals that do land locomotion, including humans. Any bones that have evolved to withstand extensive force will also be thick or fused together: and example is the fusion of the radius and ulna in frogs. This fusion of bones allows for the forearms to withstand the force of landing after a large leap.
Photo references:
Bird Sacrum: http://www.discussfossils.com/forum/uploads/842/sacrum_2.jpg
Frog Radioulna: http://classconnection.s3.amazonaws.com/573/flashcards/4420573/png/appendicular_skeleton-frog-142D89D722717E64724.png

source: Stack Exchange

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

sort: votes


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Differentiating Taenia solium and Taenia saginata Infections
I have been told that both are spread by pigs and cattle, respectively. I would like to know the complications caused by Taenia solium and Taenia saginata. Also elaborate how dangerous is one as compared to the other, as well as preventive measure.
I googled , and found no relative comparison between these two.
Thank you.

Taenia solium is more dangerous:

T. saginata is relatively innocuous, since only the intestinal tapeworm phase occurs in man, whereas infection with T. solium has major health effects due to extraintestinal infection by the larval or cyst phase in the CNS [1].

The most feared complication of Taenia solium is cysticercosis. Taenia saginata can lead in extreme cases to intestinal obstruction.
Preventive measures:

improved hygiene
adequate thermal processing of meat [2]
preventing contamination of animals (pigs and cattle) [3]

Differential diagnosis:

PCR [1, 4]
Hematoxylin-Eosin Staining [1]

References:

Mayta H, Talley A, Gilman RH, Jimenez J, Verastegui M, Ruiz M, Garcia HH, Gonzalez AE. Differentiating Taenia solium and Taenia saginata infections by simple hematoxylin-eosin staining and PCR-restriction enzyme analysis. J. Clin. Microbiol. 2000 Jan;38(1):133-7. PubMed PMID: 10618076. Cited text is from full text article available from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC86038/
Wikipedia contributors, "Taenia saginata," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Taenia_saginata&oldid=618599196 (accessed July 28, 2014).
Wikipedia contributors, "Taenia solium," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Taenia_solium&oldid=618599210 (accessed July 28, 2014).
Luis Miguel González, Estrella Montero, Leslie J. S. Harrison, R. Michael E. Parkhouse, and Teresa Garate. Differential Diagnosis of Taenia saginata and Taenia solium Infection by PCR. J. Clin. Microbiol. February 2000 vol. 38 no. 2 737-744

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


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Do women experience more bonding hormones than men after sex?
Does Oxytocin (or any other bonding hormone) increase more so for women than for men after sex?
Someone told me that it increases 4-fold for men and 12-fold for women (unconfirmed).
Is there any observable or scientific relationship between sex, Oxytocin and the desire for a monogamous relationship with a sexual partner?

Why did you delete (vandalize) your own post?

You've been told to stop vandalising your own posts already; you've been suspended on [so] for it. Stop, before a staff member has to suspend you everywhere.

Does Oxytocin increase more so for women than for men after sex?

Answer: Yes, Oxytocin level shoot up for female after sexual. It is highest at orgasm, which is the main cause women could have multiple orgasm.

Someone told me that it increases 4-fold for men and 12-fold for women
  (unconfirmed).

Answer: The level of oxytocin actually increase 5 times during sexual intercourse. Though some online article claim the male and female level as much you said, but it is not confirmed in humans.

Is there any observable or scientific relationship between sex, Oxytocin and the desire for a monogomous relationship with a sexual partner?

Answer:
Take a look at this experiment done on people to test Bonding:

Bonding is an important part of human romantic relationships, and
  research has suggested OT as a possible mediator of this effect. A
  2005 study by $Grewen\ et\ al^{4}$. found that couples who reported a greater
  amount of partner support showed higher baseline OT plasma levels.
  These couples also showed higher levels at 4, 7, and 10 min following
  warm partner contact. For women, OT levels increased sharply 7 min
  following warm partner contact, regardless of partner support, while
  male levels remained unchanged. This study demonstrates a
  relationship between supportive romantic bonding and OT, and shows
  that warm contact has a greater physiological effect on women than on
  men.[1]

A very famous study done on rats confirm that Vassopressin and Oxytocin is actually the reason behind monogamous relationship.

Almost a decade ago, Thomas Insel, Director of the Center for
  Behavioral Neuroscience at Emory University, and colleagues at the
  National Institute of Mental Health and the University of Maryland
  implicated vasopressin and oxytocin in controlling the preference for
  particular partners in both male and female prairie voles. These
  investigators found that giving a male vasopressin causes it to stay
  with its mate, whereas blocking this hormone prevents a pair-bond from
  forming. The scientists saw similar effects in female prairie voles,
  with oxytocin determining the extent of pair-bonding. In contrast, the
  administration of these substances had no influence on social
  interactions in the promiscuous montane voles. Surprisingly,
  vasopressin and oxytocin are naturally found at similar levels in both
  prairie and montane voles.[5]

Source:
[1]. The role of oxytocin in mating and pregnancy
[2]. http://en.wikibooks.org/wiki/Relationships/Hormones#Oxytocin
[3]. The role of oxytocin in relation to female sexual arousal.
[4] Grewen, K.M., Girdler, S.S., Amico, J., Light, K.C., 2005. [Effects of partner support on resting oxytocin, cortisol, norepinephrine, and blood pressure before and after warm partner contact](Effects of partner support on resting oxytocin, cortisol, norepinephrine, and blood pressure before and after warm partner contact.). Psychosom. Med. 67, 531–538.
[5] http://www.smart-publications.com/articles/oxytocin-the-real-love-hormone

I want to clear up something the other answer omit. It doesn't matter how much the comparative differences are between the oxy levels of men and women. This is because we are basically two entirely different subspecies concerning our neurology. The effects of biochemistry on each system are going to be significantly different.


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Why are there so many sex determining systems in animals
There are several sex determining systems in animals.
In mammals XY = male(except in rare cases where SRY crosses with genes on the X so that it is the reverse) and XX = female.
In  some birds it is just the opposite. That is XY(actually ZW) = fertile female and XX(actually ZZ) = fertile male.
In  some reptiles it is determined by temperature and has no genetic determination.
In lots of insects there is XX = female and X0 = male. This is usually accompanied by males being haploid and females being diploid like it is in bees.
In some insects and reptiles there is also the ZW/ZZ system but they are not dependent on it. In other words ZZW in some insects and reptiles can give rise to either sex but there is no temperature determination either.
Why are there so many sex determining systems? Why did animals evolve to not all have the familiar XY system? It must be so confusing as to which species has which sex determining system when biologists are trying to determine the gender of an animal.

Could not fit in a comment…
I don't quite know how to answer. I think that the only answer one could give is why not?. Various mechanisms may evolve under different life-history, different environment, different ecological strategy, different mutations occuring,..
In some species (including some amphibians) the evolution of sex determination system is highly dynamic and switch back and forth between one system and another.
I highly recommend the book: The Evolution of sex determination system (2014) that will give you a very good theoretical understanding of how sexual determination system evolve and make a complete review of empirical studies on the evolution and mechanisms of sex determination system. I think it is the only book existing on the subject.

I felt the same way ,thought of writing a comment but this will do.

Here's just the paper for you: Sex Determination: Why So Many Ways of Doing It? (Bachtrog et al, 2014.)
(And, it's open access!)
One important point is that although the initial "triggers" are diverse, the downstream pathways can be highly evolutionarily conserved.
Some tidbits from the paper:

ESD [Environmental Sex Determination] is favored over GSD [Genotypic Sex Determination] when specific environments are more beneficial to one sex, selecting for sex-determining mechanisms that match each sex to its best environment...
The reverse transition, from ESD to GSD, is thought to be favored when the environment is unpredictable or not variable enough, in which case ESD could produce strongly skewed sex ratios or intersex individuals.
In species with genotypic sex determination, the chromosome pair that determines sex can change rapidly over time... Sexually antagonistic selection, which occurs when a mutation is beneficial to one sex but detrimental to the other, can... drive transitions between sex determination by different pairs of chromosomes. For example, if an allele of an autosomal gene is beneficial to males but harmful to females and becomes linked to a dominant masculinizing mutation, then chromosomes that carry both the male-beneficial and male-dominant alleles create a novel Y that can replace the ancestral mechanisms. Conversely, alleles that benefit females and harm males can create novel W chromosomes when linked to feminizing mutations...

And more. Check it out!


text:
How common is it to be pregnant with periods?
As you may know, some women claim that they have their period while they are pregnant. In the arab world they call it "Deer pregnancy", since when the deer gets pregnant, it still gets its' monthly cycle.
Their doctors do confirm that. The appearance of such: The bleeding comes at the times when the period is expected, but is usually without pain, or smell, and lasts for less days. It is also of different color. But many women (and doctors) still call it a period.
(Although we all know, a real period is impossible biologically).
How common is that?
This is, I think, different from implantation bleeding, since it mostly continues to three months and after that.

But many women (and doctors) still call it a period.

It is not a period:

Pregnant women can have some light irregular bleeding during pregnancy, but it should not be like a “normal” period. Some women can confuse this for their period because often it can come right around the time she was expecting her normal period. [...] It should not be enough bleeding to fill pads or tampons over a few days [1].

It is quite common in the first trimester:

Vaginal bleeding during pregnancy can occur frequently in the first trimester of pregnancy and may not be a sign of problems. But bleeding that occurs in the second and third trimester of pregnancy can often be a sign of a possible complication [2].

It happens to about 25 % of pregnant women:

Up to 1 in 4 women have vaginal bleeding at some time during their pregnancy. Bleeding is more commonin the first 3 months (first trimester), especially with twins [3].

Repetitive bleeding is associated with preterm birth:

Bleeding of multiple episodes, on multiple days, and with more total blood loss was associated with an approximate twofold increased risk of earlier preterm birth, PPROM (preterm premature rupture of the membranes), and preterm labor. In contrast, bleeding in the second trimester only, of a single episode, on a single day, and with less total blood loss was not associated with any category of preterm birth [4].

References:

American Pregnancy Association. Am I Pregnant: FAQs On Early Pregnancy. Available from http://americanpregnancy.org/gettingpregnant/pregnancyfaq.htm (accessed 29.07.2014)
American Pregnancy Association. Bleeding During Pregnancy. Available from http://americanpregnancy.org/pregnancycomplications/bleedingduringpreg.html (accessed 29.07.2014)
U.S. National Library of Medicine. A.D.A.M. Medical Encyclopedia. Vaginal bleeding in pregnancy. Available from http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0003748/ (accessed 29.07.2014)
Yang J, Hartmann KE, Savitz DA, Herring AH, Dole N, Olshan AF, Thorp JM. Vaginal bleeding during pregnancy and preterm birth. Am. J. Epidemiol. 2004 Jul 15;160(2):118-25. doi: 10.1093/aje/kwh180. PubMed PMID: 15234932.

I've read all the references you attached before (except #4). Great information.
One now would come and ask: How come that there are women who get this about 6-8 months long, and still produce a healthy baby?
I believe there is a factor we still do not understand regarding this subject.

@TheNotMe there is association (correlation) but not causation between pregnancy bleeding and preterm birth.


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Teens concerned about impregnation through clothes
Dry Humping, is:

dry humping is the process of two people repeatedly moving up and down and back and forth on top of each other fully clothed( or missing various pieces, but the penis must not come in contact with the vagina with out some sort of fabric separating them ex: boxers,panties, or even sheets!!)

We all know that the basic rule for impregnation is that the sperm must come in contact with the egg, and even be able to fertilize it. While sperm can get through clothes, semen (but this is yet been proven or disproved) gets stuck, thus the sperm dies.
What is your opinion about this? If two people are on top of each other, fully clothed, and the male comes to ejaculation, is there any chance that pregnancy can happen, in the realistic and biological look at it (and not some probability or statistical way)? What advice should be given to teens on the matter?
I am a computer scientist with no biology knowledge, and am very interested in getting the opinion of biologists.
But since I know that the stackexchange community likes to see work done before asking questions, I did my own research (I am used to googling code and algorithms):
Very few research has been done on the subject. There is one shining research that  concluded, as I recall, that:

If the underwear is completely saturated with semen, and is in direct contact with the woman's vagina, pregnancy is possible statistically, but highly unlikely.

If there has been an ejaculation by the male, and semen is present, there is a chance of getting pregnant. Period. Teens really need to know that.
I think you may have your terms confused - semen is the overall fluid released during an ejaculation, sperm are the cells with tails that are produced in the testes and fertilize the egg. At any rate, according to the WHO, a normal sperm count is over 15 million per milliliter, with some counts much higher (>50e6/ml ), and an average between 20 and 40 million. The volume of the ejeculate tends to be anywhere from 1-6 ml. If you take a healthy young male at the peak of his reproductive capabilities, this equates to a very large number of sperm being released during a sexual encounter. All it takes is for one to reach an egg and fertilize it. Sperm are very very small, much smaller than the pore size of average fabric, so clothing will do very little to stop them. The female is likely sexually aroused during this activity as well, and produces additional fluids and lubricants that promote the survival and motility of sperm, among other things.
So, it depends on many factors. If both parties are fully clothed (at least 4 layers of clothing between their respective reproductive organs) and there is a minumum of soaking through, the chances of pregnancy are correspondingly quite low. On the other hand, if only one partner is wearing just their underwear, it's essentially like there is no clothing present at all, and the relative chances go up significantly.
Safe sex practices can't be emphasized enough to young people, as education and awareness is so much better than ignorance and myths. Even aside from pregnancy, if condoms are not utilized properly to contain all the semen there is the chance of sexually-transmitted diseases, ranging from herpes and gonorrhea to AIDS. None of these require penetration to be passed along, and one might argue that the additional presence of potentially irritating fabrics could open up raw areas or cuts and enhance their transmittal.

Take home message
Now, all this being said, the chances of impregnation through clothing without direct penetration of the penis into the vagina is quite low compared to "typical" unprotected fully-penetrating intercourse, especially depending on where the female is in her fertility cycle. According to this study, a woman's most fertile day is two days before ovulation (as had been postulated before), and the chances of pregnancy on that day are about 25% (assuming penetrating intercourse). Overall, the chance of pregnancy throughout the month is about 5%.
I don't have any hard numbers on the pregnancy chances when one or both partners have at least some clothing on, as obviously it will vary greatly depending on who is wearing what, the volume of ejaculate, contact time after ejaculation, etc. Just for fun, let's assume it's 100 times lower. That means the chances of impregnation two days pre-ovulation would be 0.25%, or 1 in 400. While rather low, this is still a non-zero chance.
Condoms are about 98% effective if used properly during penetrative vaginal intercourse. Various other birth control methods such as contraceptive pills, intrauterine devices, implants and injections are quoted as being 99% effective on their own, although they do not protect against sexually transmitted diseases. I'm certainly not one for preaching abstinence, but done properly it should be 100% effective. Ultimately, it is up to both partners to decide what their risk tolerances are, together. It is much better to seriously talk about it beforehand than to be panicked and unsure afterwards.

Hopefully this addresses your concerns, please leave comments if you have additional questions.

P.S.: I am gathering all this information in order to write a few articles, to make more teens aware of the risks. Now we know that it is certainly possible by statistics and probabilities. But realistically, considering you know all the technical information about semen and sperm. Is it realistically possible? What kind of advice would you give teens whom this way of sexual interaction is their only option?

Matt this is a bad answer

House did a much better job www.imdb.com/title/tt1273714/synopsis

@TheNotMe after washing clothes with detergent they are generally rinsed in clean water, so the amount of "chemicals" left over should be relatively minimal. Some sperm may die, but how much of a chance do you want to take? Your best option is to wear a condom, which, when worn properly, retains the semen in the tip. It'll prevent your pants from getting soaked, make clean-up a lot easier, and give you much greater peace of mind.

@TheNotMe in regards to your second comment, yes, I think getting pregnant via "dry humping" is realistically possible. It's not very likely, as compared to unprotected vaginal intercourse, but it is definitely possible. However, like I said in my previous comment, condom use will significantly reduce the risk.

@caseyr547 could you at least explain why this is a bad answer? Comparing an answer based on scientific and medical facts to a TV show is not an answer.

There is only a real chance of getting pregnant if you have sex secondary transfer isn't realistic

@caseyr547 The point of my answer is that it is realistic. The overall likelihood is low, just as the chances of getting pregnant during any one typical vaginal sex session are, but there is a nonzero chance that it could happen, and there are several factors that affect that, as I described. I'm trying to stress that if you are going to engage in this behavior, then you need to protect yourself as much as possible. I'm also trying to dispel myths. The fewer unwanted teen pregnancies in this world, the better, and the fewer STDs the better. Calling this a bad answer is counterproductive.

Meh it's bad science wrapped in a lot of excuses...winning the lottery is also realistic by your math

the my answers are so good it's counterproductive to question me is also silly

It seems like it would be simple experiment to put sperm one side of a cloth barrier of a petri dish and count sperm that appeared on the other side. I'm not familiar enough with the spermology literature to know if it's been done.

Matt, It likely is a bad answer. Take a look at this WebMD blog post. http://blogs.webmd.com/womens-health/2010/01/urban-or-suburban-legends-about-sex.html from a factual perspective about pregnancy risk.

I do not think it is a bad answer from the perspective of always practicing safer sex and for people to use barrier protection at all times, to know their STD status, and only to not use protection when he purpose is to conceive and both partners have been cleared by their doctors as health, or are informed of the risks they are taking.

I've edited the answer to add some more information as well as some verified and off-the-cuff numbers, as well as discussed family planning in greater detail.

It is effectively impossible to get pregnant by dry-humping because the conditions that would have to be met for sperm to pass through multiple layers of clothes, survive on skin, find the vaginal opening, survive in the vaginal environment and finally impregnate an egg are simply unrealistic.
The barrier of clothing that we can assume present during 'dry humping' is significant. Semen begins to die as soon as it begins to dry out and any clothes you're wearing are likely to draw water away from the sperm cells through adhesion of water to the fabric. One layer is absolutely not "like there is no clothing present at all".
Assuming some sperm cells made it through all that and onto skin, their motion isn't directed towards the vaginal opening, so a sizable fraction will be literally lost at that step. Skin is also a toxic environment on its own, so these improbable sperm have a very limited time to find their way.
That last battle buddy team of sperm has very little chance of surviving the vaginal environment. A lot of sperm need to enter the vaginal environment together to ensure that just a few survive.
As far as dry humping is concerned, there's no realistic reason to worry about pregnancy.


text:
"Same" DNA vs genes
It is often cited that humans share 99% (or 98%) of their DNA with chimpanzees.
On the other hand it is stated that siblings share only half of their genes.
What (if any) is the difference between DNA and genes; or, how can the above two claims be reconciled? (I am assuming of course that chimps and humans are more different from each other than two siblings are from each other.)
(I am asking this question as a layperson, who had a little biology in school but not much more.)
June 2015 Addendum: Here is a nice YouTube video just released by MinuteEarth; I do not know how accurate this video is, but as a layperson I found it insightful.

Repeat of http://biology.stackexchange.com/questions/9172/do-apes-and-humans-share-99-of-dna-or-99-of-genes-what-is-the-difference?rq=1

Note that siblings sharing half their genes only reflects the approximation that they get one of each pair from their father and one from their mother.  If the father and mother have the same genes at that location, the siblings will match 100%

Human DNA and chimp DNA is very similar(depending on how you measure, 98% or more). Siblings are even more similar, and they are guaranteed to share at least 50% of their DNA.  People say siblings 'share' 50% of their genes because that is the fraction that is always identical, even though in practice way more than that is identical. The two statements are contradictory because they use two different meanings of 'share': 'Happens to be the same' and 'Is enforced by genetic machinery to be identical'.

It is not a duplicate of the marked question; that question only considers genes vs. DNA - this question asks about the conflict between 50% of genes being shared with siblings and 99% of DNA with chimps.

The human genome is composed of roughly 3 billion DNA bases called "nucleotides", typically represented as A, T, C, G.
Genes are sequences of nucleotides that encode a protein; but they only comprise about 2% of the full genome. (http://en.wikipedia.org/wiki/Human_genome). Most components of cells are made of proteins.
The rest of the genome is made up of nucleotide sequences that:

have regulatory functions in controlling when and to what degree genes are expressed to create the proteins they encode
do not have any known function
are likely remnants from certain viral infections we or our ancestors contracted

The DNA that makes it into our genome is not necessarily there because we need it or because it confers some kind of reproductive advantage. A lot of our DNA is in our genome just because our ancestors had it and they happened to be reproductively successful.
So basically: humans and chimpanzees can share 99% of their DNA and have quite different genes because genes make up only a very small part of our genome.
That said, having similar nucleotide sequences in our genes does not guarantee that we will be similar because we still need to consider things like:

how similar are the genes really?
  Some differences in a gene's sequence mean more than others
how similar are regulatory sequences affecting the gene?
  Having the same gene as another species is not the same as expressing it the same
how many copies of the gene are present?
  There's more than one way to take this into consideration

For more information about comparing genes, refer to the other answers offered which go into greater detail.
Here's a genetics learning resource that is pretty accessible to laypeople: http://learn.genetics.utah.edu/content/basics/

Also, different alleles are often very similar when comparing nucleotide sequence. The difference may be as small as a single nucleotide polymorphism.

The proportion of the genome that is coding has absolutely nothing to do with the answer to this question. The same conditions would hold for, say, yeast which has a much higher C-value.

The question asks about the difference between DNA and genes; pointing out that genes make up only a small fraction of the genome is an important distinction for lay people.

Sorry, I should have specified: the bolded bit of the answer is completely and utterly wrong. In fact the sequence similarity between chimps and humans is higher for genes than for non-coding DNA as you should expect. The rest of the answer is fine.

I see what you mean; you're right - that is wrong. The proportion of coding/non-coding DNA has nothing to do with the similarity of either between individuals.

When people say that siblings share half of their genes, they're talking about alleles, which are different versions of the same gene and generally differ slightly in nucleotide sequence. In essence, all humans share 100% of their genes (almost), but the number of shared alleles varies.
Example:
geneA, allele1: atgccc
geneA, allele2: atgccg
geneA, allele3: atgcac
Indeed, we share about 99% of our DNA and consequently genes with chimps and bonobos. There are alleles of these genes that are unique to humans, unique to chimps and unique to bonobos. Of course, there are also many alleles that are shared between all three species. There are more shared alleles still between chimps and bonobos, since their most recent common ancestor lived after the most recent common ancestor of humans, chimps and bonobos. However, looking at the above example, you can nonetheless have a situation where Joe Sixpack and Charlie Chimp both have allele1 of geneA, whereas Joel Sixpack has allele2 of geneA.
Also, the conclusion of Slavatron's answer is complete nonsense.
Somebody made the same question here.

Curious as to what you think about @Slavatron's answer is nonsensical. You both look to have given correct answers to me, approaching this complex question from different angles.

The fact that humans and chimps share about 99% of their DNA means that they also share about 99% of their genes. Humans on the other hand share practically 100% of their genes with one another. There might be a tiny difference due to "horizontal gene transfer" from Neanderthals, Denisovans and other possible archaic humans to just certain populations, and I guess that it's also possible that some bottle-necked populations have lost something, but in practice, humans share all their genes with each other. It's the alleles that vary within families, populations and such.

@5hekki Ah, I see. It's confusion over genes/alleles that's caused that, I suspect. Thanks for clearing it up.

This has nothing to do with the proportion of the genome that is coding as suggested in another answers.
The reason the figures are so different is because they are measuring different things. The chimp-human figure is measuring sequence similarity whilst the figure for kin are measuring gene similarity by descent.
This gives two sources of difference in the two numbers: firstly, there is the distinction between sequence similarity and gene similarity. Let us suppose you have a 1000bp gene, which contains or does not contain a single nucleotide polymorphism. These two variants are different alleles so if you're considering gene similarity then you would say these are 100% different but if you're comparing sequence similarity then you would say that there is just a 1bp difference so these are 99.9% similar. This is how chimps can be both so similar to humans and so different - it is not a matter of how many base pairs are different but where those differences are. A single base pair change in a 1000 bp gene can have a dramatic effect.
Secondly, the figure for relatedness to your parents/siblings is talking about similarity by descent. In fact, your actual gene similarity to your parents is likely to be substantially higher than 50% because your parents are likely to have the same version of many genes so which parent you inherit the gene from makes no difference. Additionally, they will also be homozygous for a number of alleles so that you always inherit the same version of this gene from that parent and are thus more related to your siblings than a crude calculation of relatedness would suggest. The 50% figure comes from only considering two genes the same if they come from the same source, i.e. similarity by descent.
Another, perhaps, better way of thinking of this would be: among those genes that exist in different forms in your parents you will share 50% of them with your parents and 50% of them with each of your siblings on average.
As a bit of an aside: the figure for similarity between human and chimp DNA you've given is based on crude annealing. So if a highly similar piece of DNA occurs in both human and chimp DNA they will match up but this does not consider how the DNA is arranged within the genome so it actually misses a considerable amount of the variation between organisms.

Here's a language metaphor. In a single language, words may be said or written across a spectrum of accents or spellings but have the same meaning. Likewise in a single species, genes (words) may exist in a spectrum of diversity (DNA sequence) but maintain the same meaning. So, when 2 species share "most of their DNA" they share most of the same genetic meaning (like 2 languages which share word origins). While siblings who share "half their DNA" share half sequence identity (same accent or spelling).


text:
what would be the scientific name of this variety of dove
recently i came across a small dove who had its feathers tied by a rubber band so that it $would'nt$ fly. it looks some what like this

i was stunned by seeing it as i have never seen a dove in brown colour. and after staring it for some time i noticed that it's feathers or hairs near the neck region were made into a cluster that makes it look like $spike$ $hair$ $style$
so in short what would be the scientific name of this dove ??

This look like a Indian Pigeon(Rock Dove).

@DevashishDas i know you live in bangalore so have you seen these birds around your locality as these birds are'nt seen very often in hyderabad

It's a rock pigeons (Columba livia).

The Color coding of Pigeon
There are three genes responsible for pigmentation in pigeons.

– Tyrp1 gene produces a protein that helps make the pigment eumelanin.
  Pigeons with blue-black feathers have normal Tyrp1. Ash-red and brown
  birds pigeons contain different mutations in the Tyrp1 gene, which
  leads to less or different pigmentation.
– Mutations that affect the Sox10 gene override colors determined by
  various versions of the Tyrp1 gene. Regardless of whether the Tyrp1
  version makes pigeons blue-black, ash-red or brown, mutations that
  regulate the Sox10 gene result in red pigeons.
– Mutation of the Slc45a2 gene decreases the intensity of colors
  determined by Tyrp1, Sox10 and their mutants. Depending on the version
  of the Tyrp1 gene – blue-black, ash-red, and brown − pigeons harboring
  the mutant Slc45a2 gene still display the same colors, but in
  watered-down or diluted versions, less intense than those with normal
  Slc45a2. For example, a pigeon with both the ash-red version of Tyrp1
  and the mutant Slc45a2 gene has ash-yellow feathers. Pigeons with
  Sox10 and Slc45a2 mutations are yellow, which is the dilute form of
  red.

Source: http://unews.utah.edu/news_releases/birds-of-a-different-color/
Source: University of Utah

but what about the arrangement of birds hairs on its neck ???

@agharehanabbas: I pretty sure this a pigeon because of the beak. PS: can you post the picture of the neck if you are in doubt?

surely i will edit my question with that pic

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


text:
What is the core mechanism behind neuroplasticity?
Specifically I am looking at reopening of the critical period of plasticity.
Modern neuroscience has started to unlock the secret of neuroplasticity.
A common experimental setup is with mice. They have a critical period between days 20 and 32 when they learn binocular vision. And if you cover one eye during this period, they never learn to use it properly. Covering the eye even for extended periods outside of this window has no long term effect.
Scientists can then test out various plasticity hypotheses. And they had indeed found several mechanisms that can restore binocular vision to adult mice.
You can find a list towards the bottom of this paper: Autism -- A 'Critical Period' disorder?

enzymatic degradation of PNNs
SSRI
HDAC inhibitors (which are suggested to knock out Nogo-66 receptor)
AcetylCholineSterase inhibitors

It is suggested that there is an underlying pattern of excitation/inhibition (E/I) balance that all of these 4 techniques perturb.
Where can I read about this E/I balance in detail? The Wikipedia page on NeuroPlasticity (here) appears to be a dead-end.
I am looking for an overview, rather than technical scientific papers that explore a particular aspect, already assuming familiarity with the big picture.
How to get the big picture?
EDIT: T K Hensch seems to be a world leader in this research, and his papers answering my questions, for example http://www.ncbi.nlm.nih.gov/pubmed/24439367

a bit strange you call the long wikipedia article with many related links a "dead end". there are probably many different biological mechanisms for neuroplasticity. note that new synaptic changes/ growth are a part of the puzzle. see also growth cone

This is a good first source which suggests further references:
http://www.scholarpedia.org/article/Balance_of_excitation_and_inhibition


text:
Why do pigeons kill their chicks when touched by a human?
I used to have many pigeons around the house. If by chance one of the chicks fell out of the nest, we used to put it back using gloves.
Usually, if we would touch the chicks with our bare hands, however, the other pigeons would usually kill the chick. I want to know why they do that?

This is covered at Skeptics.SE: http://skeptics.stackexchange.com/q/3132/43

This is a story I have been told as well when I was a kid. Usually this is related to the foreign smell that the humans leave on the chick. However, this seems to be an urban legend, as birds have not a great sense of smell.
Snopes says about this:

However, Mother birds will not reject their babies because they smell
  human scent on them, nor will they refuse to set on eggs that have
  been handled by a person. Many birds have a limited sense of smell and
  cannot detect human scent, or if they can detect it, do not react to
  it.

What can happen is that the birds returning to their nest which find the nest disturbed compared to the situation when they left might cause them to temporarily or permanently abondon their nest.
You can find this and more urban legends about birds here and here.


text:
How to remove bad lanes in ImageJ Westernblot analysis
I use ImageJ to do an analysis of a Westernblot Image.
If everything goes as wanted the workflow is fine. But if I do something wrong creating a lane there is no undo for a lane and also no way to remove all lanes that I can find.
How do I get back to my original image or undo a lane creation?
I'm using 1.49e on Mac OS

You question is slightly unclear! do you mean how to crop out a WB lane in an image or how to remove a lane from the middle of an image if it did not produce the results you were looking for?

So you chose a lane by accident which you don't want to include in your analysis?

Yeah I created a lane with the wrong size and I can't find a way to undo the creation to recreate the lane correctly.

ImageJ doesn't have a feature to remove individual lanes. But that shouldn't be a problem. All you have to do is draw the first lane correctly (I'm referring to size). Then press 1. Now, while the selection is still... selected, click inside it, but not on the number (where the cursor becomes hand), and drag it where you want the next lane. And press 2. And so on. Draw all your lanes.
Now, if you misplaced a lane, click the rectangle selection tool, then click on the lane number while the cursor is a hand. It will be selected. If you're having troubles with this, use the shortcuts Ctrl+1 and Ctrl+2 or the menu Analyze - Gels - Select Previous/Next Lane to select between lanes. The cursor turns to normal. Click anywhere inside the lane and drag it on the right place.
If the first lane was bad and you want to remove all lanes, just go to Analyze, Gels and click on Reset.

Hi Cornelius the menu contains only select first and next lane. There is no way to move between lanes. And for me it is also not possible to select lanes with the mouse. But pressing [ctrl/command] [1] removes all lanes but the first and lets me recreate the lanes. That helps a lot.


text:
Recommended sequence clustering algorithm for transcriptome data
I'm working on a project where I'm going to analyze a large amount of transcriptome data. After assembling our RNA-Seq reads into contigs using Trinity, it looks like I'm going to have about 10GB of sequences in fasta format. Since these sequences are from several hundred tissue libraries but from a single species (chicken), I'm expecting there to be a lot of redundancy, so I'd like to cluster these sequences and just use a representative sequence from each cluster as I go forward with my analysis. I see there are quite a few tools that exist to do things like this, and I'm wondering which you all would recommend. I'll be running this on a Linux machine with 64 CPU cores and ~500GB of RAM.
I started looking at USEARCH, but it seems I'm going to run into some memory issues with the free 32-bit version and as much as I clicked around on their site I couldn't figure out how much the 64-bit version costs or how to buy it.

I guess clustalw should be able to do this.. but I am not sure how to get the clusters.. May be in one of the output files.. Just check it... If you want to use multicores then you need a parallelizable tool.. i'll look up

It does sound like you have a lot of data.
I would first try Robert Edgar's other newer tool UPARSE which is faster and can handle more data using the free 32-bit version.  I think you'll mainly be limited by machine memory though, right?
Did you try CD-Hit?

Yeah, memory is going to be the limiting factor. I did just set up CD-Hit on my machine, so I'll give that a try.

cd-hit-est is probably a good option

Colin the only way to go is Edgar's software write him robert@drive5.com it's a thousand for a copy (in 2012) worth every penny.


text:
Is there evolution in humans since the first homo sapiens sapiens
Has the human species changed since first defined as homo sapiens sapiens?
I'm asking this question partly because I'm wondering how we might evolve next.

Do you mean in genetic sense or physiological sense or both? and what do you consider as change i.e. to what extent does evolution have to occur before it amounts to a change in your definition. Evolution depends on genetic and environmental factors so it is highly dependent on many factors and this question can have a highly speculative and subjective responses!

Highly Related: 1) How is evolution possible in contemporary humans? 2) Human Evolution in Modern Times 3) Are humans done changing?

We continue to evolve all the time: http://www.npr.org/2013/09/27/226837803/modern-humans-still-evolving-and-faster-than-ever

For those who think the forces of natural selection no longer apply to modern humans, paleoanthropologist John Hawks would urge you to reconsider. In recent times — that's 10 to 20 thousand years, for a paleoanthropologist — Hawks says we've picked up genetic variations in skin color, and other traits that allow us to break down starch and digest cheese.

Homo sapiens sapiens is over 100,000 years old and we have changed in many ways since then, as noted in the above NPR article!
I'm not sure we can say there is a "first" homo sapiens sapiens -- the change from one species to another is gradual.  You may know that mixing red and blue gives purple, but at what points do we officially have red, purple, or blue when mixing different levels of red and blue?

An additional question is, are we evolving in a positive or negative way stronger vs weaker.

Well, it doesn't matter to evolution as long as we reproduce more. Hence Idiocracy. As to whether there's a "first" homo sapiens sapiens -- it depends on your view of our evolutionary history. If you agree with Out of Africa, probably a group of them. If not, then you likely think Homo erectus slowly changed into Homo sapiens through propagation of traits.

Oh my god that movie. It's really shocking how just having more children can change the allelic frequencies in a population

There is certainly some evolution.
Take, for example, lactose tolerance. It's a relatively new mutation that happened less than 8000 years ago. Yes, basically all humans in the stone age were lactose intolerant. The change started to be common after humans defeloped argriculture on a big scale and is still less common in some groups than in others even today.
As another example, our jaws have become smaller and now we get trouble with the amount of teeth that hasn't changed since the first modern humans developed. Some people don't have wisdom teeth, that is part of the evolutionary answer to that.
Also people have become bigger since the early days.
I can't assure how humans will develop in the future, but even smaller jaws, weaker limbs (due to more dependence on technology and less use of personal strength) and longer fingers (because presicion is more important nowadays than raw power) might be some factors. Also with the increase of modern globalization, humans might become less diverse in appearance.

Hi Welcome to Bio.SE. We ask that answers on this site include citations or references. Please update your answer with reputable sources that substantiate your claims. Even though something might seem trivial and obvious, other users will benefit from having legitimate sources to continue researching. Thanks!

I second that - With references and sources you would get the upvotes you deserve +1

An additional question is, are we evolving in a positive or negative
  way stronger vs weaker.

That would depend on what you consider week or strong. All evolution really cares about is how many babies do you successful raise to adulthood.
You may be the strongest, smartest and most handsome man in the world. But at the end of the day, if you do not have children you are a failure.
So are we evolving better... here is something to think about. The BRCA mutation that causes breast cancer in women... also causes increase fertility in women. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4457526/  So is that good or bad? Bad for the individual.... but good for evolution. More children.
Or how about muscle strength... humans muscle strength per body weight is terrible compared to every other ape. The average chimp is half the weight of a man and 6 times stronger. So humans are weak.... well we can pick up and sewing needle and tread that needle but a chimp can't. In human evolution we have sacrificed strength for dexterity. So is this good or bad. Strong or week?
Answering the first question. Yes we have. Human evolved in africa. The most ancient population are in africa. All those strange looking non-africans are the produces of evolution in the past 60,000 years. Those moving northwards became paler. And developed longer hair. Mutations resulted in lost of eye pigments 5000yr ago resulting in green then later blue eyes. (Terrible in the savannah of africa but meh in Europe)
Also some evolution occurred in receptors targeted by viruses. So better immunity. Think the black plague 60% death in Europe and Smallpox in Americas, 90-95% death rate.


text:
Is there a realistic "family tree" model for the human population?
I would like to do some gene inheritance simulations, and I was wondering if there is an accepted model for what mating looks like in the general human population? I am not necessarily looking for the exact graph of any population.
For example, my current model has generations 1, 2, ..., n, n+1, ... where each individual in generation i is the product of a mating between two individuals in generation i-1. This is obviously over simplistic, and I was wondering if there are better models out there?

Well, there are some questions regarding what population. I don't have 50 rep, so I can't really ask for clarifications; populations range a lot, from your typical avoidance of inbreeding (laws against cousin marriage) to Tamils with their high rates of first cousin marriage (so high that they don't have any pedigree inbreeding depression due to selection, so it's not unhealthy).
Mating in humans is often assortative for many traits including education, vocation, etc. When the Americas were settled (after aboriginal Americans were devastated by disease), skin color was a source of assortative mating. Arguably it still is. On the other hand, people tend to mate disassortatively for traits such as Major Histocompatibility Complex.
Furthermore, isolation in human populations tends to be by distance (though this is of course changing, leading to a lot of admixture in recent population history).
As a result, what your population is will have a huge impact on your results; you'll need to calculate f for any particular locus, and take a look at admixture. If f is 0, then you have a random mating scenario (neither preference nor avoidance of inbreeding, and neither assortative nor disassortative mating).
TL;DR if you're doing a very simple analysis on dummy data, you can probably get away with assuming that mating is totally random. But if we're talking about actual populations, you'll need to run the models/calculations of f and other population measures.

My analysis applies first to the United States. Perhaps I can generalize after that. It is okay if subpopulations are neglected as long as I can make get good results for the vast majority.  I might just start with a random mating model as you suggest.

On the one hand, there's papers such as this that discuss assortative mating. On the other hand, you have things like this that indicate some level of disassortative mating as well -- but note that that only applies to some of the populations. If you can't do any analysis of f values, then you could also try doing a statistical test of f; for instance, run a simulation using f=0 and compare to your data.

An unbounded model with no carrying capacity(unregulated reproduction) will be easier to model, but it would have no long term resemblance to actual population change. It is easier to model by virtue of one not being required to know the carrying capacity. That being said, the carrying capacity is important in a realistic model since the population is naturally regulated by external factors. You might do well to look at Discrete time logistical model. The reason I suggest this model is that it is discrete and recursively defined, thereby lending itself to represent each iteration as a likely branch in the graph.


text:
What does salt do to styes?
Styes formed in the eyes are cured by dabbing at them with lukewarm water(I saw this being done many a times as a home remedy.) At times, common salt is added to the water before dabbing. My mother says, NaCl hastens the healing process; why is it so? What does salt do to cure the styes faster? Can salt be used for treating other eruptions anywhere else?

Same reason as this http://biology.stackexchange.com/questions/189/why-does-salt-water-help-sore-throats

Is there no difference between the cause for sore throat and that for sty formation? I guess there is. So, I wonder how the reasons for salt healing both can exactly be the same. Anyways, thanks a lot.

Stye is caused due to infection by micro-organisms. So the same theory applies. Salt water does not discriminate between organisms

authors: วันชัย แสนหวู่


text:
Mammal body density
Human body density is approximately 1 kg/l (same as fresh water) - which is not surprising (at first) given that we are 70% water, and is surprising (on a second thought), given that the other 30% can be just about anything (from the air in the lungs to the relatively heavy bones).
How remarkable is that?
Consider other mammalian species.
For each species, compute the average body density of an adult.
Thus, for each species we have the number - the mean body density.
How are these numbers distributed?
Mostly heavier than water? Lighter?
It is unlikely that this kind of research has been done, so I would settle for something simpler: what are the densest/lightest mammals? (or, in general, vertebrae)
PS. As you can guess, I am a mathematician, not a biologist :-)
PPS. Given abundance of water of Earth's surface (70%, same as above!), it makes a lot of sense to be as dense as water: not heavier (to avoid drowning), not lighter (to be able to dive for food), so natural selection should favor the density of 1.  Are there exceptions?

Great question! Never gave much thought to it. Human body have nearly 985$kg/m^3$ nearly equal to sea water(1020 $kg/m^3$)

Lightest have got to be bats, right?

@Oreotrephes: it would make sense that flying requires lower body density, but what it the actual number? how light are the bats?

This might help you or another answerer: http://epub.ub.uni-muenchen.de/12010/1/zitteliana_2008_b28_08.pdf and works it cites; although as far as I can tell they only give figures for birds, not bats / other mammals.

I would be careful how you measure this. Do lung insides count? Do the air sacs in bird bones count? Maybe those frogs that inflate their throat sacs would win, but only for like half a second at a time? (most importantly, do bats float?)

@JeremyKemball: mean body volume over, say, 24 hours: lungs average out; bone air sacs count; throat sacs do not.

Why do throat sacs not count?  I'm actually thinking of aquatic mammals that can purposefully adjust buoyancy with gas exchange/ retia mirabilia / etc.

@AtlLED: air sacs average out over 24 hours. E.g., what is the density of a human during inhale vs exhale?

Until someone has a better method to determine this, and I'm willing to go with idea of that this question is not answerable, I put forward the two likely forms of selection criteria:
Which mammal has the highest percentage of keratin in it's body for the highest density, and which has the highest percentage of gas (over the day) for the lowest.
I also want point that measuring the density of mammals is tricky because we can change our "volume."  Perhaps this doesn't seem like much for humans, but a small mammal with a large tongue stuck out could have an appreciable different density than one with the tongue in.  Same for retractable limbs (which are generically cool).
This article gives us an estimate for the density of keratin at "1.283 g/c.c. for cow horn to 1.335 g/c.c. for echidna quill tip" which putts it solidly more dense than water.  This means we're looking for a small heavily armored mammal, which leads me to suspect the pangolin.  I don't readily know it's density, and I would be fine with others taking the time to calculate it (I'm not interested in getting that specific).
I have fewer ideas on which mammals are least dense.  Going by this article I would guess rodents have the least dense skeletons. In particular I was surprised by this graph:

But also don't know that means we should exclude something like a sperm whale which has a lot of fat (lower density than water) and has enough lung capacity to dive for hours in deep water.  But on the off chance that the skeletal density is the best bet, I'm going to guess the least dense animal is a rodent, and if I have to pick one species I'm going with the least massive, the shrew.
Doubt any one has really researched the displacement of many of the animals that should be in the running for this, so I'm not convinced a more exact answer could be reached.

Rodents don't have air-filled bones. Birds do however.

@kmm that has been my experience as well (no air) when harvesting bone marrow in mice.  I'm going to remove that because I'm now looking at what I think is conflicting statements.


text:
What is the state-of-the-art algorithm for multiple sequence alignment?
Which algorithm or algorithms are considered the standard or state-of-the-art for multiple sequence alignment?
How big is the need for better algorithms? How many sequences need to be alignment in a typical test? I am trying to understand how important problem this is in bioinformatics.

This would be better asked on https://www.biostars.org, the bioinformatics stack exchange. For the typical number of sequences aligned: you cannot say that. There are so many different uses of MSAs and too many different datasets one could have to be able to give one typical example.

@skymninge Bioinformatics are on-topic here, and Biostars is not affiliated with SE in any way now (it was a SE 1.0 site, which means they used the SE software but SE wasn't involved otherwise in running the site)

@Mad Scientist Still, the chances that this type of theoretical question will be answered on Biostars are higher. The answered bioinformatics questions on this site are usually more practical approaches/use cases/... I did not imply the question is off-topic otherwise I would have flagged it as such. I just wanted to be helpful.

All bioinformatics questions are on-topic. Just that if someone requires technical help then biostars has more people who can help.

having said that, this question seems quite broad to me. More details need to be provided.

btw if you want a good bioinformatics problem, come up with an assembler that assembles any paired end illumina run optimally de novo without any input parameters.

My Vote goes to Mafft(insi) as it have ~86% accuracy and results in ~1.2 hour. Though fastest will be kalign takes only ~3 minutes to finish with an accuracy of 74.3%.
For testing:

For each of the 218 reference alignments in the benchmark, we applied
eight alignment programs, resulting in a total of 1744 automatically
constructed MSAs. The overall quality of these automatic alignments
was measured using the Column Score (CS) described in Methods.

FIGURE 1: Overall alignment performance for each of the MSA programs tested.
(A) Overall Accuracy
(B) Total run time for constructing all alignments (a log10 scale is used for display purposes).
doi:10.1371/journal.pone.0018093.g003
Compared Tools

(source: plosone.org)
Source and Photo Credits:
A Comprehensive Benchmark Study of Multiple Sequence Alignment Methods: Current Challenges and Future Perspectives
PS: This is from an old paper of 2011. If you want the new statistics you can always test on your own, by the process described in the source paper.

Personally, I always use muscle + gblocks for proteins. Does the job well enough, IMO.

@5heikki: I agree. Muscle is actually good.

Always Clustalx FTW!

I dont think any of them has a parallelization option. I think parallelization is possible for pairwise distance calculation step atleast.

Bare in mind that the results from this benchmark are already very out of date.

The PRANK and PAGAN algorithms have both come out of the Loytynoja lab in Finnland, and are stirring up the pot a bit. They use inferred phylogenetic relationships as a parameter, and tend to yield a much more 'gappy' alignment, supposedly due to more accurate handling of indels. For easy alignments the method doesn't matter so much, but if the sequences are highly divergent it might be worth while checking out PAGAN and PRANK.

Clustal has reinvented itself as Clustal Omega using Hidden Markov Models, and is particularly suited to the alignment of very many sequences.


text:
Standard datasets for testing new multiple sequence alignment algorithms?
Are there any open and freely distributed standard datasets for testing new algorithms for multiple sequence alignment?

possible duplicate of What is the state-of-the-art algorithm for multiple sequence alignment?

Welcome to Biology Beta @msa!!! Thanks for asking the wonderful question but I suggest you close any on one of ones you asked as they are duplicate of each other.

I have always myself wondered about this so it would be great to get a detailed response! but for the moment, could you not look at a known protein or DNA sequence like Ras within a organism or different species and align them? The best way to do it is to go to UniProt (http://www.uniprot.org/) and type in a protein such as Ras. Once you select a particular Ras, then under the phylogenomic databases you can select OrthoDB and once you enter the page you can select get FASTA or Tab delimited on the top of the page!

@DevashishDas This question is not a duplicate of the linked question as it is asking for a standard dataset for msa to test a new algorithm on and the previous question is not answered as far as I can tell so it is not of much help!

@Bez: Ok. But they seems awfully linked they could be asked in single question. Anyway, I will try to answer both.

I would suggest you PAcAlCI or Prediction of Accuracy in Alignments based on Computational Intelligence, though the acronym in wierd the tool is good for testing new Sequence Alignments. They
But before you start testing your algorithm, I suggest take a look at these papers:
[1] Who Watches the Watchmen? An Appraisal of Benchmarks for Multiple Sequence
Alignment
[2] Issues in bioinformatics benchmarking: the case study of multiple sequence alignment
PS: I haven't tested or used the tool myself.


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Is the human collarbone supposed to break?
I've read it in a book and have heard people mention it, but I can't find any documentation about it. But the point being made is this:

The human collarbone acts as a shock absorber for impact on the shoulder or stretched arm. If too much force is put on the shoulder (EG: during a fall), the collarbone is designed to break to prevent injury to the neck and/or head.

Is this actually true and if so, can anybody point me to some documentation about it?

This looks like a misinterpretation. Because collarbone is the only horizontal long bone of the human body [1], it is the first to fracture when falling on the shoulder.
Its fracture can affect many structures:

The muscles involved in clavicle fractures include the deltoid, trapezius, subclavius, sternocleidomastoid, sternohyoid and pectoralis major muscles. The ligaments involved include the Conoid ligament and Trapezoid ligament [1].

It is indeed a shock absorber, but for the upper torso (some way or another any bone can be considered a shock absorber):

The clavicle also serves as something of a "shock-absorber" for the upper torso. Physical contact from the side will be partially absorbed by the clavicle. Because of this function, the clavicle is a very commonly broken bone [2].

The fracture can lead to severe injuries:

Displaced or comminuted clavicle fractures are associated with complications such as subclavian vessels injury, hemopneumothorax, brachial plexus paresis [...] [3]

References:

Wikipedia contributors, "Clavicle fracture," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Clavicle_fracture&oldid=615723256 (accessed July 30, 2014).
Erich Rosenberger M.D. Anatomy And Physiology (2009). Available from http://www.sciences360.com/index.php/anatomy-physiology-299-12859/ (accessed 30.07.2014)
George Mouzopoulos, Emmanuil Morakis, Michalis Stamatakos, Mathaios Tzurbakis. Complications Associated With Clavicular Fracture. Orthopaedic Nursing, October 2009, Volume 28, Number 5, Pages 217 - 224 - See more at: http://www.nursingcenter.com/lnc/cearticle?tid=938803#sthash.F09wonvJ.dpuf

It's hard to accept a "nevagtive answer" as the accepted one. I had found all the links you have and read them. So maybe it is a "Misinterpretation", but it sure seems like a plausible one. Even doctors/physicians seems to mention it. And googling for Crumple zone collarbone gives a ton of people mentioning it. So I'll upvote for the effort, but i'm not ready to accept it yet.

Forgot to come back and accept. Sorry for the long wait.


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What exactly does adaptive mean?
This is a quote from Dey et al 2014:

Hatching asynchrony is thought to be adaptive because...

What exactly does adaptive mean here? Does it mean hatching asynchrony has fitness benefits? Or does it mean hatching asynchrony is likely to be selected for?

A trait is said to be adaptive when it causes fitness to increase. Fitness is generally understood as the (relative) contribution to future generations in terms of offspring or genes. The trait is selected for by the environment and hence increases fitness.
In the paper of Dey et al. this is the fitness of the parent birds. Hatching asynchrony causes size differences between chicks which may (1) "facilitate brood reduction in unfavourable environmental conditions", (2) "provide insurance against the failure of core offspring" and (3) "reduce competition among nestlings". Dey et al. also cite a reason why hatching asynchrony may be sustained in a population despite being maladaptive: initiating incubation before the clutch is completely laid is selected for and causes asynchronous hatching as a by-product. In this case, hatching asynchrony merely correlates with fitness, but does not cause fitness to increase and is thus not adaptive.

Can you add a link to the paper you cite?

@Chris, the link to the journal's webpage in luciano's question has links to the full text of the paper, however, you need a subscription to access them.

Thanks. The subscription is not so much a problem for me :-)

The question is probably more complicated than it seems because, if I am not wrong, the word adaptation here is understood at the group level.
Definitions of adaptation
Unfortunately, there is not such thing as a single, standard definition of adaptation. But for most cases the accurate definition the author is using is not of much importance as all of the usual definitions totally fit in the sentence without changing the meaning of the concept they want to express. In you case however, the concept of adaptation seems to be a bit more complicated (and interesting) because it refers to a group-level adaptation.
Note that most people does not really care about the exact definition they're using and this might yield to some confusion. It will probably be a bit hard to know exactly what the authors  (Dey et al.) of your article had in mind.
Definition of Group-level adaptation
I am here going to talk about how the term adaptation can be understood for a (social) group. This is important as I suspect the authors to use the term adaptation on a group phenotypic trait (emergent trait if you want).
Pareto optimality
To my experience, the concept of group-level adaptation is defined in relation to the concept of Pareto optimality which is a concept used in evolutionary game theory. Shortly speaking, in a system that is at Pareto optimality no individual can by any change of the trait under consideration increase its fitness without decreasing the fitness of another individual. In other words, a population that is at Pareto optimality has the greatest achievable population mean fitness. Therefore, it makes sense to consider a group to be (perfectly) adapted when it is at Pareto optimality.
Nash equilibrium
Depending on the underlying evolutionary game, the Pareto optimality may or may not be a Nash equilibrium. Shortly speaking, a population is at Nash equilibrium if no individual can increase its fitness by changing the trait under consideration. Therefore, group-level adaptation can only be stable if the Nash equilibrium is Pareto optimal. An example of game where the Nash equilibrium is the free-market game.
In your case
At first sight, because asynchrony is a group level trait, it seems to me that the sentence "Hatching asynchrony is thought to be adaptive [..]" means that hatching asynchrony is thought to be at Pareto optimality. In other words, it means that hatching asynchrony is thought to be the state of the system where the mean fitness of the group is maximized, that is no individual can increase its fitness without decreasing the fitness of another individual by being synchronous.

Your questions mean basically the same. Birdcare.com says:

The situation in which all the eggs in a clutch do not hatch at (more or less) the same time, as is more usual among birds, but have their hatching spread over several days. It is well seen in the various types of raptor, and is an adaptation to a type of food supply which may fluctuate. During seasons when food is short the later hatched young will probably starve as the earlier hatched young, being larger and stronger, deprive them of food, and so the size of the brood is reduced to a level in balance with the available food supply. In years of plenty all the young may be able to survive. In 'synchronous hatching' all the eggs hatch at more or less the same time.

The fitness benefit of hatching asynchrony on the species level is due to increased range of individual fitness among the young birds. The available resources do not need to be distributed equally among the offspring during unfavorable seasons such that fewer, but at least some of the hatchlings (the 'strongest') can survive. You see that this is the same as beeing selected for because on average the number of agents passing their genes to the next generation is higher with asynchronous hatching than with synchronous hatching. Of course, the success of this strategy is strongly dependent on environmental factors. In very stable habitats it might turn out to be disadvantageous on the long run.


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No digested product bands, but markers are visible. What could be the reasons?
I had to digest my insert containing plasmid and another vector into which my insert has to be ligated, each with BamHI and NotI.
Upon digestion, I ran the gel to check for results. The digestion seemed to be ok the first time with reasonably good bands. Since I needed more concentration I ran the gel with the same reaction setup (30microL) for the second time.
Well 1 - 100bp marker
Well 2 - Insert in a vector (820 ng/microL, 3microL)
Well 3- Plasmid vector into which the insert has to be ligated (1000 ng/microL, 2microL)
The marker bands were faint while there were absolutely no bands in the other wells. What could be the reason for failure during the second run? I've performed the second time digestion in a span of 40 min after the first one.

Usually there is no issue of mixing. One possible reason is degradation. But you say marker is faint (marker wont get degraded). Stain the gel with extra EtBr and see again.
Was it the same gel?? (If so then definitely stain it again beccause EtBr migrates towards the cathode)

Can you show the gel image? Otherwise I support WYSIWIGs idea. There might not be enough EtBr left in the gel. What bands of the marker are visible? All, or only the highest? Additionally: Are there marker bands visible in the same size region as you digested DNA? If so, your problem is on the digest side. You are loading a ton of DNA on the gel, this should be visible.

Chris and WYSIWYG are right sounds like it degraded or was a bad batch of gel. I feel for you such are the things of nightmares.

Ethidium will also break down slowly under fluorescent lights. It's usually not a problem, but I did an internship at a startup so poor that they reused the same gel over and over, so we kept it covered in aluminum foil and had to restain it all the time. But it looks like you're using enough DNA to see. Make sure the EtBr and gel and buffers are fresh.

@user137..EtBr doesn't get degraded soon.. It diffuses/moves out of the gel.

Yup, it looks like the DNA degraded. Because my first gel run gave expected results. What is surprising is, this never happened to me. I used the same reagents and protocol. I am unable to understand what caused the degradation. If any of the samples or reagents is contaminated with DNase, I'll have to dispose all the stock and prepare fresh one now. But, how do I know what caused this? Could one of the causes be voltage too?

@WYSIWYG yes, it was the same gel. I've disposed the gel already. I want to try it again, I've got enough samples left with me. But, if the problem is degradation, I should be able to identify what is causing this.
I've gel image, with nothing but marker bands. All the bands of the marker well are visible.

Usually there is no issue of mixing. One possible reason is degradation. But you say marker is faint (marker wont get degraded). Stain the gel with extra EtBr and see again. If you reused the gel then definitely stain it again because EtBr migrates towards the cathode.
It doesn't seem like degradation to me but to be cautious for the next time:

Use freshly autoclaved water. If you are not sure then filter using syringe and keep some 10ml for yourself
Ensure that the plasticware are also autoclaved properly.
Use endo - plasmid extraction kits, if available
Dissolve the plasmid in TE (only if conc is high and you need not put much in the reaction mix else EDTA interferes in the reactions. In that case use Tris-Cl pH-7.6 ).
If you have to digest a lot of DNA then set up small reactions in many tubes.
Do not incubate the reaction for a very long time (>6h).
Inactivate the enzyme by heating if you are not running the gel immediately.
Ensure that the gel running buffers are not too old.

Agreed, seems like overall signal is week, so a stain/destain seems in order


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Conservation Genetics - Book recommendations
Can you please give me some advice for a book in (evolutionary) conservation genetics that offers an in-depth review of the mathematical formulations used in this field.
I read the book Evolutionary Conservation Biology (Ferrière and Dieckmann, 2009) and I really liked it. I'm seeking for another book of the same kind that goes further on the part A (Theory of Extinction) and especially on the concern of the importance of population structure and the genetic load. I am also interested in landscape genetics.

It would be more informative to use google scholar and read papers instead of a single book

A comprehensive book on ecology????

@caseyrs547 as the subject remains fairly broad I hoped I could find a book rather than articles. Books are often more entertaining than articles. But you might be right. I'll wait to see if anyone suggest me something.

@WYSIWYG No, I am not looking at a book on ecology. I am interested in genetics extinction (population genetics based explanation for population extinction) and about how the environment shape the genome of populations. Not a book on this extremely broad field which is ecology.

This book "A primer of conservation genetics" would suit quite well I think. In particular chapter five deals with "Genetics and Extinction" and is preceded by a lot of population genetics based theory. A beginner might also combine it with "A primer of ecological genetics" (Hartl & Conner) but you seem to have enough Pop gen knowledge to not need it!
The landscape genetics is perhaps a bit lacking from this book though. Maybe a better and more comprehensive solution, but slightly more advanced, is this book which does feature some aspects of landscape genetics in chapter 15 along with good population genetics type coverage of extinction.

If you're interested in learning about the mathematics of population genetics, Population Genetics and Microevolutionary Theory by Alan Templeton is an absolutely amazing resource.
If you check out the index, here are entries under population structure:
assortative mating, admixture, linkage disequilibrium, coarse-grained spatial heterogeneity, gene flow, gene flow and population history, gene flow vs admixture, microevolution modeling, multiple inheritance modes, natural selection, adaptation, and fitness.
Heterozygosity and other mathematical descriptors are particularly relevant to conservation (the author has been involved in various conservation projects). Furthermore, there are various entries on viability.
Plus there's plenty of information in it about the effects of landscape on gene flow and other population structural features.


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What kind of skull is this?

We found this skull on a beach in southwestern Sweden, and are curious as to what kind of animal it was.

It's definitely a bird pelvis (synsacrum). Based on the size (~30 cm), it came from a very large bird. Unfortunately, comparative images of bird pelves are rare on the internet. Some possibilities (large birds of Sweden possibly found on the coast):

Great northern loon
Golden eagle
Common crane

A loon skeleton (from http://paolov.wordpress.com/2011/08/05/friday-mystery-object-107/) shown below.

kmm FTW good job

Thanks for your prompt response - you must be right. We have looked at some alternatives - a cormorant, perhaps, or a goose?

The top of the synsacrum in the loon isn't flat enough to be a good match. I know that loons have strange pelves, so that was my best guess. Whatever it is, it was a very large bird.

Crane looks like a decent match, see link, in geese and gulls it is mush shorter and squarer, https://www.researchgate.net/figure/Ventral-view-of-the-synsacrum-fused-with-the-pelvis-A-and-their-scheme-B-in_fig4_259319680


text:
What organism most efficiently converts a given quantity of mass into heat?
Question I am trying to answer:
In the popular film The Matrix, heat given off by humans is harvested as an energy source. I wondered, if this were possible, would humans be a good organism to choose? Would any other organism be better?
Question I want to ask:
Many warm-blooded organisms produce heat by metabolism. Do different organisms produce different levels of heat for the same mass of input (food)? Is there any organism that directs energy flux into heat production more than any other organism?

This question appears to be off-topic because it not focusing on a biological aspect. SciFi-SE may be a better site for this question.

I've made some changes and think it's both interesting and (now) on-topic!

Although, one extant issue would be heat varies enormously depending on what the organism is doing: hibernation, vigorous activity, using its body heat to melt snow (skunk cabbage), etc.

Matrix doesn't work either way because even rats need to be fed. If there's no sunlight, there's no autotrophic assimilation and thus no food for any warm-blooded organism. Still a nice movie.

A small hardy warm blooded omnivore that is easily tamed.  I suggest rats.
Small:  You don't want a lot of metabolic effort going into building bone and structure to support structure.
Hardy:  it needs to be survivable with little care.
Warm blooded:  You want to harvest energy from it.
Easily tamed:  The animal shouldn't try to escape its captivity.

Warm blooded, good point. I was thinking it'd be some kind of bacteria.


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Why is assembling paired end illumina without any input parameters an important problem?
In one of the comments in this question about multiple sequence alignment, it was stated

@5heikki: btw if you want a good bioinformatics problem, come up with an assembler that assembles any paired end illumina run optimally de novo without any input parameters.

What is a paired end illumina? How is optimally defined in this context? What are the usual input parameters?

The Next-Gen sequencers cannot sequence a very long stretch of DNA with good reliability (~150 for the recent model- HiSeq2000; even less for older models such as GA (40), GA-II (70), GA-IIx (90)). For increasing the confidence in a certain hit, it was sequenced from both the ends.
For example, if you have selected 500bp DNA fragment, then after ligating adapters to both the ends, it is sequenced from both the direction up to 150bp. This would leave an unsequenced "insert" region of 200bp. (In the example image below, they have sequenced up to 40bp [case of old GA] )

During assembly you stitch together the fragments of DNA to find out the larger DNA from where the fragments arise. In case of RNAseq, these arise from a transcript, and your assembly should give you the complete transcript (mRNA or ncRNA etc). There are two basic types of assembly: reference guided assembly and de-novo assembly. In the former you use a sequence such as the genome as a reference to assemble the transcripts. If such a reference is not available then you have to go for de-novo assembly.
The assembly algorithms use several parameters and since these are computer algorithms and not some kind of magic, their output depends to an extent on the different parameters.
In case of paired end data there are some parameters that are important. Most important is the size of the insert. In case of a 500bp fragment, you'll end up with an unsequenced region of 200bp. This is not much of a problem with reference guided assembly because you can figure out the sequence of the insert based on where the sequenced region align to the reference. The average insert length is important to remove discordant reads (aligning too far apart in the reference). In case of de-novo assembly, the insert will remain unsequenced even if you know that the final transcript looks something like:
frag1-frag6-frag3-frag9-frag4
So, to get the sequence of the assembly, you need to sequence the insert regions. This is not a problem if you at least know the order of fragments in the assembly. However you should know the insert size to get the assembly size correct and as skyminge said, in scaffolding. Obtaining this insert length is not that difficult (You need not provide it as a parameter. Most algorithms can calculate it automatically).
Another parameter in de-novo assembly is k-mer length (the sequence reads are broken down into k-mers for better assembly). I cannot explain the algorithm of assembly here in detail. You can check the manuals/papers of common assembly algorithms like Velvet, SOAPdenovo, Euler [de novo]; cufflinks [reference based]
I have mentioned transcriptome sequencing here but the principles are same for genome sequencing too.
Back to your main question:
Why is assembling paired end illumina without any input parameters an important problem?
Because it is less effort; but tweaking may be difficult. I won't consider it as an important problem. There are other important algorithmic optimizations that are required with de-novo assembly.

Another important wrinkle in this kind of data, it's relatively error prone.

@swbarnes2.. There is some level of error but when you say "relatively error prone", what are you comparing it with?

@WYSIWYG You wrote: "if you have selected 500bp DNA fragment". Does this guarantee that the fragments would be 500bp each? If yes, then how does the NG sequencer do that? (If I understand correctly, https://emea.illumina.com/content/dam/illumina-marketing/documents/products/illumina_sequencing_introduction.pdf says that the DNA is fragmented randomly)

@OrenMilman I was just giving an example; not saying that DNA would be of this precise length. The DNA is sheared randomly but the library is constructed from DNA pieces in a selected size range.

In Illumina sequencing, the DNA is (usually randomly) sheared into fragments. For paired end sequencing, fragments of a specific size range are selected and then sequenced from both sides.
This results in two reads for each fragment. As read length is fixed, also the remaining "middle part" of the fragment is in a specific size range. In some cases there is no middle part, because the fragments have been chosen so small, that the reads overlap.
The information about the size of the fragment and/or the "middle part" as well as read length are some of the most important parameters you need for de novo assembly. Your could get away with not taking read size as a parameter, if you need it you can still run over all reads and check. But fragment size or insert size is important to place the reads, especially in scaffolding.
This blog entry also has some nice information about the often upcoming discussion what is meant by insert size (fragment size, the size of the middle part) and what can happen with overlapping reads and read-through.
There is lots more to say about this. Illumina also provides some nice videos available on youtube.


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What makes certain obligate anaerobes viable in fermentation starter cultures?
If Propionibacterium are obligate anaerobes (to wit, poisoned by oxygen), what makes 'Dairy' or classical propionibacteria (e.g. P. shermanii, P. jensenii, P. acidicpropionici, et al) viable in Fermentation starter cultures?

Do you have a reference for the fact that they are obligate anaerobes?

they are not obligate anaerobes..

@AlanBoyd Obligate anaerobe on wikipedia

@WYSIWYG What are they?

@WYSIWYG Here's a quote from this source: "Their [Propionibacteria] exact atmospheric requirements remain a matter of controversy, and they are often described as obligate anaerobes."

http://mic.sgmjournals.org/content/127/1/121.full.pdf

link to a paper in which P. shermanii is grown in flask culture. Although the conditions are clearly designed to achieve low oxygen concentrations in the culture, they also indicate that oxygen is not toxic for this organism. This is from the WP page you linked to: "Obligate anaerobes are microorganisms that are killed by normal atmospheric concentrations of oxygen (21% O2). Oxygen tolerance varies between species, some capable of surviving in up to 8% oxygen, others losing viability unless the oxygen concentration is less than 0.5%."

Here (mic.sgmjournals.org/content/127/1/121.full.pdf) is a link to a paper in which P. shermanii is grown in flask culture. Although the conditions are clearly designed to achieve low oxygen concentrations in the culture (the flask is almost full and is only shaken occasionally), they also indicate that oxygen is not toxic for this organism.
Also, this is from the WP page you linked to:

Obligate anaerobes are microorganisms that are killed by normal atmospheric concentrations of oxygen (21% O2). Oxygen tolerance varies between species, some capable of surviving in up to 8% oxygen, others losing viability unless the oxygen concentration is less than 0.5%.


text:
How do I read a sequence logo?
I'm looking at a paper that uses several sequence logos to illustrate the consensus sequence of certain sites.
Here is the most important of the sequence logos I'm interested in:

The explanations I found about the exact meaning of this visualization were rather abstract and mathematical. I understand that the height of the letter stack is indicating in some way how strongly conserved that position is, but I have some difficulty judging the absolute values.
When are the positions considered to be significantly conserved? The paper where this data is from mentions the positions 5 and 6 as characteristic for the consensus sequence, which is not really obvious to me from this graph.
How do I interpret the absolute value on the y-axis? What does it actually mean if position 16 has around 0.6 bits of information?
I'm not so much interested in an exact mathematical treatment, but a general guide on how to read these graphs and how to interpret them in practice.

For this kind of logo you compare a number of sequences. The height on the y-axis is indeed an indicator for the frequency of a certain base. The sequence logos I know use a height to 1 for  positions where only one base occurs and go lower for less conserved bases. I might have some papers about the generation of these logos in my database, I can look this up later today if you are interested.

Finally, Bioinformatics questions are coming in this site. Anyway, everything is in the main paper. I will be explaining in the answer soon!

DNA/RNA only has 4 nucleotides, and information content is often represented in log2 form. So a fully conserved site of, say, 10 sequences contains log(10/10/.25) = log(4) = 2 bits of information. The .25 is the probability of a given nucleotide, and the overall probability is represented by the height of the letter.

A very clear description is given in Wikipedia.
The starting point is an alignment for the region under investigation.
A. Basically, to get the height of the stack of letters for every position one has to calculate the degree of certainty about the residue (= degree of conservation) at this position in the sequences belonging to this class. I'll explain what it means:
The key parameter in this context is information. 1 bit of information can be understood as the amount "knowledge" you get when receiving an answer to one yes/no question.
Let's say we have equal proportions of all four bases at a certain position in a set of DNA sequences. To "guess" a base at this position in some sequence we have to ask two binary questions. For example: "is it Pyrimidine?" If 'yes' we'd ask "is it 'T'?" Otherwise: "is it G?". So, when the frequencies are equal we can get 2 bits of information from one observation of a base at this position in a sequence.
If the frequencies are distorted, we already have some ideas about the bases when coming to an individual observation. If we already know, say, that we have just G and A at this position with ratio of 1:1, we can just ask "is it G?", so we get clearly 1 bit. When the ratios are not even (or when the number of alternative states is not 2n), the analogy with the questions becomes much less clear and we have to resort to the very simple formula for Shannon entropy. Intuition and brief inspection of this formula would bring you the idea, that when the ratios of the residues are biased, we always have less information than for the case of equal frequencies (2 in the case of DNA).
Now to estimate the "the degree of certainty" we simply calculate the information based on the observed frequencies of different residues at this position and subtract it from the theoretical maximum (again: 2 in the case of DNA):
certainty = maximal information possible - actual information
This value defines the height of a stack of letters at each position.
The maximum value (2 bits) would be observed when we always have the same base, because "actual information" would be zero (there is no need to ask questions - we "know" the answer anycase). The minimum (0 bits) is when we have no idea about the base. One bit would be obtained if we had, say, just two equally frequent bases. And, for example, the value of 0.6 would be observed if you had, e.g. 68.5% of the time the same base A and in all other case C, G or T with equal frequencies of 10.5%.
B. As you probably already know: the proportions of all alternative bases are shown as relative heights of individual letters.