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Macromolecule levels in daughter cells after fission
When a prokaryote undergoes binary fission, how are the non-DNA macromolecules distributed between the two daughter cells? This is motivated by comments on a previous question and a G+ discussion. I am primarily interested in explicit mathematical models.

Naive model
For DNA, each copy is attached to a different part of the cell membrane, to ensure each of the daughters receives a copy. As far as I understand, there isn't such specific mechanism in place for other macromolecules. If we are allowed to assume that non-DNA macromolecules are distributed uniformly through the parent cell than this would mean the two daughter cells would receive half the proteins within statistical fluctuation. This has a specific meaning: if there are $N$ molecules of type A in the parent, then the difference in number of type A molecules in the two daughters after fission will be on the order of $\sqrt{N}$.
However, this model might be wrong. For instance, as the new cell-wall is being formed it could have in it specific pumps that either balance the protein levels below chance (producing an average difference lower than $\sqrt{N}$) or to create asymmetries higher than chance. Altenrnatively, the initial distribution of macromolecules in the parent could be far from symmetric for some other reasons. Which is the case?
If the naive model is correct, is there experimental evidence explicitly showing this?

blog post discussion of how the cytoplasm can't just be modeled as a homogeneous mixture.

Many years ago I worked in the field of bacterial chemotaxis, and your question brought this paper to mind:

JL Spudich & DE Koshland Jr. (1976) Non-genetic individuality: chance in the single cell. Nature 262:467-471.

The authors report an analysis of the chemotactic behaviour of individual bacterial cells from a single homogeneous culture. They find marked differences between individuals, and their favoured model is what they refer to as a Poissonian variation in the inheritance of key proteins that are present in small numbers.
According to ISI Web of Science this paper has been cited 241 times - presumably at least some of those papers might be about other more recent examples of this type of phenomenon.

This is a great starting point, thank you! I will search forward from here.

Incidentally, as a counter example, there is a lot of good work showing that mRNAs are actively moved around during bud formation in yeast. This paper is probably a good place to start (in the middle of the story!).
K. A. Shepard et al. (2003) Widespread cytoplasmic mRNA transport in yeast: Identification of 22 bud-localized transcripts using DNA microarray analysis. Proc Natl Acad Sci U S A. 100:11429–11434.
doi:  10.1073/pnas.2033246100


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Structure of fitness landscapes in the NK model
The NK model of rugged fitness landscapes consists of $N$ sites where fitness contribution of each site depends on its state $\{0,1\}$ and is epistatically affected by $K$ other sites. When defining the model, Kauffman & Weinberger (1989) stressed that:

The actual structure of [fitness] landscapes, although knowable is currently unknown

They then go on to assume either epistatic interactions are with adjacent sites in a linear ordering or at random, and that fitnesses are assigned to each of the $2^{K + 1}$ epistatic combinations at each site uniformly at random in $[0,1]$. Although it is definitely possible to justify this random generation, it tends to produce a very structured fitness landscapes, that although rugged (for high $K$), has a very regular distribution of local fitness optima. As a computer scientist, this assumption of an arbitrary random distribution over possible NK landscapes seems very misguided. I would be more comfortable with a worst-case analysis on a "reasonable" (hopefully as determined by experiment) subset of possible NK landscapes.
What is known about the typical structure of NK landscapes in biological domains? Also, are there examples of biological papers that do a worst case instead of an arbitrary random analysis on some non-trivial subset of landscapes? The only example I am familiar with is the gadgets used by Weinberger (1996) to show that the unconstrained model is NP-hard, but that is a trivial subset (all possible landscapes) and not of biological interest.

References
Kauffman, S. and Weinberger, E. (1989) The NK Model of rugged fitness landscapes and its application to the maturation of the immune response. Journal of Theoretical Biology, 141(2): 211-245
Weinberger, E. (1996). NP-completeness of Kauffman's N-k model, a Tuneable Rugged Fitness Landscape. Santa Fe Institute Working Paper, 96-02-003.

Artem. I have read several of your posts and found them quite interesting. I am quite unaware of the concept of evolutionary game theory (game theory in general). Can you suggest me a good read so that i can understand your problem better?
I know this is a not a valid comment . please forgive :P

@WYSIWYG Thanks! Coincidently I just wrote an answer where the second part talks about some basic references on EGT. Alternatively, take a look around my blog or just email me at lastnamefirstnamegmailcom

Very little is known about the structure of fitness landscapes.
H.A. Orr (2005; also Whitlock et al., 1995; Kryazhimskiy et al., 2009) explains that most experimental results do not actually attempt to measure the fitness landscape, but instead report just the average fitness versus time and average number of acquired adaptations versus time. This can't be used to discern epistatic interactions, or any combinatorial structure of the landscape. In general, the theory of adaptive walks has developed without reference to real data and even the most refined theories can only correspond in vague qualitative ways (see Kryazhimskiy et al., 2009 for the best example I know).
Szendro et al. (2013) surveyed the few recent experiments that conducted a methodical examination of all mutations in a subset of loci of model organisms, but most studies (6 out of 12) were able to empirically realize only small fitness landscapes of just 4 to 5 loci (so 16 to 32 vertexes), with the largest full fitness landscape having length 6 with all 64 vertexes examined (Hall et al., 2010), and the largest number of vertexes in a single study being 418 out of the possible 512 in a length 9 landscape (O’Maille et al., 2008). These are extremely small landscapes, and thus don't have much power in distinguishing proposed theoretical models.
After extensive searching, I have not been able to find examples of theorists doing worst case analysis of fitness landscapes. The closest to worst-case analysis is Orr-Gillespie theory (Gillespie, 1991; Orr, 2002; 2006; Kryazhimskiy et al., 2009) that assumes that the wild-type is still very fit after an environmental change, and so beneficial mutations are extremely rate. This allows the authors to introduce extreme value theory and consider just the asymptotic properties of distribution tails thus allowing a more general treatment with fewer parameters; in some cases leading to a full classification of adaptive trajectories (Kryazhimskiy et al., 2009). This approach is easier to relate to experiment, but unfortunately completely ignores the combinatorial structure (beyond first-order) of the fitness landscape and always just samples the next potential mutant from the tail of a distribution without taking into account how it is progressing in the landscape. Although Orr (2006) introduced the basics of fitness landscape structure, the structure was much simpler than the NK model; he used Perelson & Macken's (1995) block model with each block as completely unstructured beyond first-order.

References
Gillespie, J.H. (1991). The causes of molecular evolution. Oxford University Press.
Hall, D. W., Agan, M., & Pope, S. C. (2010). Fitness epistasis among 6 biosynthetic loci in the budding yeast Saccharomyces cerevisiae. Journal of Heredity, 101: S75-S84.
Kryazhimskiy, S., Tkacik, G., & Plotkin, J.B. (2009). The dynamics of adaptation on correlated fitness landscapes. Proc. Natl. Acad. Sci. USA 106(44): 18638-18643.
O’Maille, P. E., Malone, A., Dellas, N., Hess, B. A., Smentek, L., Sheehan, I., Greenhagen, B.T., Chappell, J., Manning, G., & Noel, J.P. (2008). Quantitative exploration of the catalytic landscape separating divergent plant sesquiterpene synthases. Nature Chemical Biology, 4(10): 617-623.
Orr, H.A. (2002). The population genetics of adaptation: the adaptation of DNA sequences. Evilution 56: 1317-1330.
Orr, H.A. (2005). The genetic theory of adaptation: a brief history. Nature Reviews Genetics 6(2): 119-127.
Orr, H.A. (2006). The population genetics of adaptation on correlated fitness landscapes: the block model. Evolution 60(6): 1113-1124.
Perelson, A.S., & Macken, C.A. (1995). Protein evolution of partially correlated landscapes. Proc. Natl. Acad. Sci. USA 92:9657-9661.
Szendro, I. G., Schenk, M. F., Franke, J., Krug, J., & de Visser, J. A. G. (2013). Quantitative analyses of empirical fitness landscapes. Journal of Statistical Mechanics: Theory and Experiment 2013(01): P01005.
Whitlock, M.C., Phillips, P.C., Moore, F.B.-G., & Tonsor, S.J. (1995). Multiple fitness peaks and epistasis. Annu. Rev. Ecol. Syst. 26: 601-629.

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Natural examples of XOR functions at the cellular level
We can often think of cells as a sort of circuit on macromolecules, and can show that they can accurately and robustly implement functions like $\text{MAJ}(x_1,...,x_n)$ (return $1$ if more than half of $x_1,...,x_n$ is $1$ and $0$ otherwise) under natural conditions (Cardell & Csikász-Nagy, 2012).
Not all functions are created equal. $\text{XOR}(x,y)$ is a boolean function that is $1$ if exactly one of $x$ or $y$ is $1$ and $0$ otherwise (i.e, if $x = y$). It is often generalized to a multi-input function parity (or odd) as $\text{ODD}(x_1,...,x_n)$ which returns $1$ if an odd number of $x_1,...,x_n$ is $1$. Notice that this is superficially similar to $\text{MAJ}$ but is doing its counting in base 2, which one would expect to be easier for say finite state machines.
However, in some ways, this sensitivity makes the function much more difficult to the point that Valiant (2009) writes:

[Parity] appears to be biologically unnatural. That is exactly the prediction of our theory, which asserts that evolution cannot be based on the evolvability of [the class of functions parity belongs to]

Synthetic biologists used to agree to some extent, with Tamsir et al. (2011) writing that the closely related XNOR (i.e. $\text{XNOR}(x,y) = 1 - \text{XOR}(x,y)$) is empirically impossible to implement. However, they were proven wrong when Bonnet et al. (2012) implemented XNOR among many other amplifying gates by exploiting the structure and process of transcription. Unfortunately, this is an example from synthetic biology, and I really want to learn ones (if any) that occur naturally.
Are there any examples of XOR or related gates implemented (without human engineering) at the cellular level? Are there any naturally occurring molecular pathways that compute something similar to parity? (i.e. something similar to the majority result, but for a more 'sensitive' function) I am primarily interested in empirical demonstrations, but I would be satisfied with theoretical examples that are appealing to biologists (i.e. not something purely comp. sci. like P-systems or something).

References
Bonnet J, Yin P, Ortiz ME, Subsoontorn P, & Endy D (2013). Amplifying Genetic Logic Gates. Science, 340(6132): 599-603. PMID: 23539178
Cardelli L, & Csikász-Nagy A (2012). The cell cycle switch computes approximate majority. Scientific Reports, 2: 656. PMID: 22977731
Tamsir, A., Tabor, J. J., & Voigt, C. A. (2011). Robust multicellular computing using genetically encoded NOR gates and chemical wires. Nature, 469(7329), 212-215.
Valiant, L.G. (2009) Evolvability. Journal of the ACM, 56(1): 3-22.

Benenson (2012) also offers a synthetic example. http://www.nature.com/nrg/journal/v13/n7/fig_tab/nrg3197_F6.html I'll leave the answering of your primary question about natural examples to the actual experts. I am but the greenest of dilettantes in this field.

@JonathanVanMatre thank you, that's an interesting paper. Although it seems like they are implementing XOR through several cells working together with NOR gates as primitives. I will take a look at it, maybe they discuss some natural counterparts. All the synthetic examples suggest that it isn't unreasonable to expect a natural one, I think.

What's interesting to me is that it's not hard to come up with XOR gate implementations that sound biologically plausible: gene X is activated by two separate activators A and B. When present at the same time A and B bind each other strongly in such a way that their DNA binding domains are occluded, decreasing the transcription of X. It would be a leaky XOR gate, but it seems pretty biologically plausible. But my cursory search didn't yield much on competing trans-activators that can heterodimerize...

Empirical examples can be thought of but whether natural examples exist or not depends on the usefulness of XOR gate in biological systems. Considering a typical application of XOR, I can't see where a cell would want a binary adder. If we find an application we would find the example too. Can anyone think of its application ?

@WYSIWYG what are the empirical examples you have in mind? Are they still from synthetic biology? Right now I am following some leads by looking at mechanisms of co-inhibition in T cells, but my lack of knowledge (and other commitments) are making my progress slow. I am not sure if we have to look for binary adders, necessarily. That is just a particular way of thinking about it. However, if we want to go the adders route then base doesn't matter, any prime will work, so an application could be time/season/period tracking.

@WYSIWYG Keep in mind, that a clock/counter is not that great an analogy, since we want the circuit to combine several different input wires/signals and not just track one.

reminds me of mcculloch-pitts model from the 1940s. one could probably find (somewhat forceful) critiques of this model in the literature (mostly as too simple).

@ArtemKaznatcheev.. by empirical i meant engineer-able. However I see a situation where XOR might find a role but am not sure if the gate exists.
Morphogen/Chemokine gradient: if A = left to right gradient, B = right to left gradient...and output is defined as cell migration/development pattern then a XOR gate is implemented as A=1,B=1 will not produce a gradient for the cell to respond.

@ArtemKaznatcheev.. In fact I also have a hunch that lymphocyte activation is a likely place where XOR logic is used. I found another example: can't call it a perfect XOR Gate.. but the study says that combination of multiple antibiotics is actually not doing the job well compared to single drug treatment. Somewhat close... *PS: please let me know how adders can track period and wrt any prime numnber (it just increases the number of bits right. Pls fwd me texts on this if you can.Thanks)

Many sex-specific genes exist in a pretty much XOR state. Same for cell fate specification. Delta-notch and neurogenin could be an example, though it's not cell autonomous.

When I think about your question of natural examples of XOR, it pushes me to think about what type of natural environments (i.e., evolutionary pressures) would lead to the selection of an XOR equivalent.
When we implemented a synthetic XOR by "double flipping" one transcription terminator as a type of gene expression "check valve" it was the case that I did not know of any natural examples of flipping terminators, whereas I know of several examples of nature flipping promoters.
Why do we have plenty of natural examples of flipping promoters but (unknown to me at least) as yet no charismatic examples of naturally flipping terminators?
Perhaps we haven't been looking in the right environments to find them?
E.g., for a terminator to exist in nature, there needs to be something that must  be expressed upstream of the terminator, and also something that should not be expressed downstream of the terminator.  Since there are plenty of terminators there must plenty of examples of nature selecting for terminators.  My favorite example is the "Tø" terminator in phage T7 that is just downstream of the major capsid gene (highly expressed) but just upstream of a minor particle protein (weakly expressed).
But now reason thru what would need to be true in order to select for terminator flipping.  I'd need all the requirements of a static terminator (above), and then another such pairing of selective requirements under different environmental circumstances for additional gene products encoded in the opposite direction on the complementary strand of DNA. Phew!
I'm not saying that it is impossible to imagine such a complicated coupling of selection requirements emerging in nature, but it definitely seems a much more improbable aggregation of selective pressures to co-mingle all within a single genetic loci.
I'm still nevertheless very curious and would be grateful to learn of any natural examples.  -DE

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Lineage selection in plasmid evolution
I've been reading through Paulsson (2002) and I am not sure what he means by "lineage selection" in the second to last section. The paper deals with plasmid replication, and mostly concentrates on the contrasting pressures from two levels of selection:

intracell selection - competition between plasmids in a single cell. A plasmid can undergo a cis-mutation and over-replicate, resulting in a higher intracell fitness than the focal plasmid. The plasmids reproduce.
intercell selection - competition between cells. Cells with a heavier load of plasmids will take longer to reproduce, and plasmids that produce a heavy load will have lower intercell fitness. The cells containing plasmids reproduce.

In this context, what does the third level of selection -- lineage selection -- mean? What reproduces? How do the lineages split or interact?
My guess
Does lineage selection simply mean group-selection on separate colonies of cells? In that case, how are new lineages formed? I would expect this group level to select for zero levels of plasmids (since they place no loads on the cells and thus these groups of cells will grow the fastest), but Paulsson (2002) suggests the opposite:

lineage selection could favor plasmid traits that help the population of plasmid-containing cells to fight plasmid-free cells.

Is there a more detailed discussions of this available than the one section in Paulsson (2002)? Neither the unit of selection nor either the evolutionary or genetic lineage Wikipedia articles address my question. The first only mentions lineage in passing, and the second two don't discuss models of selection.

References
Paulsson, J. (2002). Multileveled selection on plasmid replication. Genetics, 161(4): 1373-1384.

i read the paper casually. The lineage selection part is not very clear. I observe that the system has multiple optimum points (atleast for the intracellular selection. Fig 1). This might be the case when intra- and inter- cellular components are coupled and the lineage selection must be related to the selection of one of these optimal points.

i am not sure about it.. i'll read the paper in detail and see if it is the case.

He defines lineage selection as selection for traits which increase the fitness of a group of plasmids, rather than an individual plasmid with in a cell or a particular cell containing plasmids. He says that the unit of selection are "plasmid-host clades" : in other words the unit of selection is the group of closely related plasmids in separate cells. It is an example of a kin-selection though I haven't seen the specific terminology in widespread use. He likely doesn't use kin selection because the plasmids don't have well defined offspring, so he uses a broader term for kin--lineage. I might have preferred clade selection, but this term has its own baggage. I'm not sure (and neither is Paulsson) that kin selection is need to explain 'spitefully low loss' rates, since intra-cellular and inter-cellular selection both favor lower loss rates.

Thanks! So he is using lineage in the genetic sense as described by Wikipedia?

The terms lineage selection, clade selection and  species selection are sometimes used quite interchangeably, and are fairly often found in paleobiology and macroevolution, i.e. when discussing species diversity between lineages/clades/taxa.


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Are there any scientifically based predictions or theories of future human evolution?
Reading this question of the stack exchange got me thinking. I believe human evolution is an ongoing process and will not stop. Are there any predictions/theories about the phenotypes and genotypes of humans in the future? and how they may differ in a few thousand years compared to present day?
I remember watching a youtube video and in the video the user predicts that there will be two branches of human species; a short dwarf like species and a much taller species. I'm still skeptical about this claim. Is there any evidence to back it up?
One could argue that modern medicine is preventing natural selection. How will this effect human evolution?

Its pretty much impossible to predict what will happen in the evolution of species.  Evolution is a parallel search with millions (or in the case of humans 8+ billion) of threads.  Our adaptive capacities have never been fully understood and will always surprise us I think.
Of course that doesn't stop people from trying!  The prediction you mention is based on one man's ideas of dominant selection pressures on humanity now... for a men's TV show.  In Dr Curry's scenario, technology users, and economic disparity, producing Eloi and Morlock like dimorphism as in the HGWells book "Time Machine". This seems like hogwash to me.  All socioeconomic classes try to find high quality partners and height and attractiveness will be hard to stamp out in a large segment of humanity.
Economic elites breed slowly and even if they will try to skim the evolutionary cream of humanity off the top, there will be plenty of beautiful, tall and smart people who will lack economic opportunity in my opinion.
There have been more serious, IMHO, questions about whether medical technology, which lets the sick recover and may even compensate for genetically problematic traits.  There are no inoffensive examples I can think of so I'll take male pattern hair loss - apologies.  If medicine allows all men (and women) to grow a thick shock of hair regardless of our genes then the baldness traits might spread through the species.  Sure it could happen, but then most bald and balding people end up having children now anyway.
In fact since civilization has started feeding the hungry, making the hunting of wild beasts less important, causing the shrinkage of the male physique (we used to be much more muscular), inventing medicine and schools where smarts can be selected for, and giving us all more choice when it comes to mates, evolution has accelerated for human beings. The authors specifically cite social factors as being more important in our evolution now.

Do you have a reference for "..causing the shrinkage of the male physique (we used to be much more muscular)"? Considering that e.g. body size has increased due to better nutrition (at least in more recent times) it seems unlikely that overall physique has deteriorated. Also, even if we have become less muscular, this could simply be a phenotypic change due to how we live our lives (less fighting with wild animals) without an adaptive genetic change.

heres one - only a book review.  you'd want to look at the book   http://www.theregister.co.uk/2009/10/19/wuss_men/

Interesting, although some parts sounds like hyperbole. However, here is another popular account by the author of the book that goes further into the specific cases: http://www.huffingtonpost.com/peter-mcallister/pre-modern-man_b_836265.html. It also mentions that reasons (at least in more modern comparisons) are likely to be due to lifestyle. Comparisons with H. erectus and Neanderthals are more problematic since they represent different species, and it will be harder to infer that the changes are due to modern civilization.

There's a general thread on this in the literature - this requires at least a question on its own, but you have to remember that for their size, humans are just about the weakest primates around.  Even chimps which are much smaller can throw around hundreds of pounds easily.  There's a thread in the literature that in order to gain fine manipulation skills and dexterity we had to group muscles into smaller fibers with more nuanced innervation, resulting in lower strength.

Predicting future evolution is always extremely difficult (or impossible), and this is especially true for long-lived organisms such as humans. Therefore, your question is basically impossible to answer objectively. However, the question made me wonder about what research there is on the topic, and if there are any hypotheses or attempts to measure current selective pressures. A quick litterature search yielded a couple of interesting papers that you might be interested to look more closely at (along with hidden "gems" like "Do Women Prefer More Complex Music around Ovulation?"). They all touch on aspects of ongoing evolution or selection in humans.
Reed & Aquaro. 2006. Mutation, selection and the future of human evolution

Finally, it is frequently speculated that both positive and negative selection acting in modern humans is slowing down or coming to a halt because of our increasing insulation from the demands of the environment by the use of technology. The lessons being learned from studies in humans and other species, in fact, suggest that we will continue to be under certain forms of strong selection well into the distant future.

and

In summary, the maintenance of our genomes against deleterious mutations could have been a major selective component in shaping levels of human genetic variation. In addition to the probable role of rank-order selection (Box 1), the purging of deleterious alleles in gametogenesis might be a particularly efficient way to achieve this.

and

Furthermore, although selection against mildly deleterious alleles might be relaxed in modern humans, selection for the fixation of new alleles could be intensifying (and these could be detected with genome-wide data and statistical approaches; cf. Ref. [45]). This suggests a shift from the maintenance of our genomes against new mutations towards accelerated genetic change for a subset of new mutations (and possibly an associated shift from genetic drift to genetic draft dynamics [55]) as a theme for the future of human evolution.

Powell. 2012. The Future of Human Evolution

Abstract
  There is a tendency in both scientific and humanistic disciplines to think of biological evolution in humans as significantly impeded if not completely overwhelmed by the robust cultural and technological capabilities of the species. The aim of this article is to make sense of and evaluate this claim. In Section 2, I flesh out the argument that humans are ‘insulated’ from ordinary evolutionary mechanisms in terms of our contemporary biological understandings of phenotypic plasticity, niche construction, and cultural transmission. In Section 3, I consider two obvious objections to the above argument based on the growing literatures related to gene-culture coevolution and recent positive selection on the human genome, as well as a pair of less common objections relating to the connection between plasticity, population size and evolvability. In Section 4, I argue that both the ‘human evolutionary stasis argument’ and its various detractor theories are premised on a fundamental conceptual flaw: they take evolutionary stasis for granted, since they fail to conceive of stabilizing selection as a type of evolution and drift as a universal tendency that dominates in the absence of selection. Without the continued operation of natural selection, the very properties that are purported to reduce the evolutionary response to selection in humans would themselves drift into non-functionality. I conclude that properly conceived, biological evolution is a permanent and ineradicable fixture of any species, including Homo sapiens.

Keightley. 2012. Rates and Fitness Consequences of New Mutations in Humans

The human mutation rate per nucleotide site per generation (mu) can be estimated from data on mutation rates at loci causing Mendelian genetic disease, by comparing putatively neutrally evolving nucleotide sequences between humans and chimpanzees and by comparing the genome sequences of relatives.
  ...
  A genome-wide deleterious mutation rate of 2.2 seems higher than humans could tolerate if natural selection is "hard," but could be tolerated if selection acts on relative fitness differences between individuals or if there is synergistic epistasis. I argue that in the foreseeable future, an accumulation of new deleterious mutations is unlikely to lead to a detectable decline in fitness of human populations.

Nettle & Pollet. 2008. Natural Selection on Male Wealth in Humans

Abstract:
  Although genomic studies suggest that natural selection in humans is ongoing, the strength of selection acting on particular characteristics in human populations has rarely been measured. Positive selection on male wealth appears to be a recurrent feature of human agrarian and pastoralist societies, and there is some evidence of it in industrial populations, too. Here we investigate the strength of selection on male wealth, first in contemporary Britain using data from the National Child Development Study and then across seven other varied human societies. The British data show positive selection on male income driven by increased childlessness among low‐income men but a negative association between personal income and reproductive success for women. Across cultures, selection gradients for male wealth are weakest in industrial countries and strongest in subsistence societies with extensive polygyny. Even the weakest selection gradients observed for male wealth in humans are as strong as or stronger than selection gradients reported from field studies of other species. Thus, selection on male wealth in contemporary humans appears to be ubiquitous and substantial in strength.

You can't predict the evolution of anything because evolution is driven solely by the environment. It is the environment that squeezes species into to specific forms. We have has a much say in our shape and form as a whirlpool does and for the same reasons, both humans and whirlpools result form powerful outside forces.
In order to have shot at even making a credible guess about future evolution, you'd have to know what the environment around humans will be over the next 100,000 years at a minimum. About all you can say is the likelihood of this or that modification, based on existing physiology. The more that has to change to evolve a new structure, the less likely it will, even given strong selection pressure. We won't evolve wings or eyes in the back of head but we could get taller, shorter, hairier, larger brained, etc.
The idea that evolution is the result of some innate guiding or shaping natural force arose shortly after Darwin advanced the theory of transmutation of the species by natural selection. The scientific community got on board with whole transmutation of one species into another, but they view natural selection as to happenstance and taking to long to be the primary mechanism. Instead they came to believe that some force was driving organisms to become more complex, in a particular pattern, over relatively short periods of time 1,000 of years.
That is why, we call the concept "evolution" in the first place. It was not a word Darwin used or liked because it had existed since the 16th century. Literally, it meant "to unroll" like a scroll and implied a preset motion or sequence. Seeds were said to "evolve" into plants. Sailors and soldiers practicing repetitive drills, practiced their "evolutions". The word meant the unfolding of predetermined pattern, the exact opposite of natural selection.
Unfortunately, this erroneous mechanism would dominate evolutionary theory for 80 years until the development of synthetic theory in 1947. But by then, the idea of evolution being predetermined, fixed, with "levels", "stages", "higher", "lower" and generally progress, had been fixed in the public mind.
So you still see a lot of nonsense about the "next stage of human evolution" when under natural selection such a concept is simple gibberish. We will be what ever the environment shapes us to be.

It is an interesting question, and I definitely agree with shigeta's question about medical technologies enabling the transmission of certain negative traits that would probably otherwise be less frequent.
Remember, evolution is really just a numbers game of whose genes get passed on the most.  In general this was very strongly correlated with the fitness of that individual at being the best at getting food, attracting mates, and not getting dead.  At this point we've got a fast food joint on every corner, and most people in the developed world live to be able to reproduce as many times as they see fit regardless of any reasonable form of fitness.  Most people find a partner if they want one, and the incredibly fit do not procreate en masse like male leaders of packs of animals since polygamy is not an acceptable practice in many societies (notable human exceptions are cases like Genghis Khan who is thought to have fathered a ridiculous number of children [albeit this is not a great example of selection for a very nice trait]).
Just think about traits that people have who reproduce less, and traits people have who reproduce more, and we're evolving towards the latter.  There is an absolutely hilarious (and depressing) intro to a movie based on taking these sorts of arguments to one extreme.. but I'm not sure this is the right venue to post it :)

If you can reproduce, you are fit. Period. The idea that the "wrong" people reproduce is simply elitism and various bigotries dressed up in the scientific guise of eugenics. Historically, it's always been the case that the wealthy reproduce at higher rates than the poor. It is still the case, though the gap as narrowed in the industrial age. Nevertheless, the idea that the "wrong" people are reproducing is not only completely unscientific but the basis of some of the worst evils ever. Yet still it's a very common idea, usually in the social/political classes you'd least expect it to be.

What if life was simply testing all possible genomes. The viables survive while the worst die. Thus it should have begun with small genomes and becoming always longer, like a brute force process acting since billions of years. This but would mean that it is not evolved but simply tested DNA, also genetical modern technologies could use this way ?

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Flower identification (Singapore, April)
I saw some flowers growing by the roadside today, and was wondering about the species of this plant.

The plant also appeared to be fruiting, and it produced small fruits that formed small clusters.

This is called "Red Powder Puff" or botanically Calliandra haematocephala. See the images (from the Wikipedia article):

What you identified as the fruit appears to be the buds:

Some more information can be found here.


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Alternatives to NCBI BLAST during US government shutdowns?
Many molecular biologists are used to going to NCBI BLAST for quick, hassle-free BLAST searches of their genetic or protein sequences.
However, during the last American government shutdown in 2013, BLAST was rendered unusable due to lack of funding.
The incumbent president is also threatening to shutdown the government if funding for the Mexican border wall is not approved by the Democrats.
What are some alternatives for NCBI BLAST that are reasonably fast, easy to use, and would not be rendered unusable in the event of American government shutdowns? Ideally, the tools should encompass all of the standard BLAST sub-functions (pblast, PSI-blast, etc).

b.nota is correct - Just further adding to his answer. The International Nucleotide Sequence Database Collaboration (INSDC) is a consortium between DNA Data-bank of Japan (DDBJ), EMBL-EBI and NCBI. Contributions to each of the 3 databases are shared on daily basis.
(Thanks to @KonradRudolph) Since EMBL-EBI is not directly accountable to any single government either financially or in terms of research directions so a (temporary) shutdown equivalent to that of the NCBI is vastly less likely. Rather, like CERN, it’s an international treaty organization and thus probably a lot more robust.
BLAST
Answering part 2 of your question: YES! BLAST is available in both DDBJ and EMBL-EBI on following links:

BLAST - DDBJ
NCBI BLAST+

Scope
Here is what INSDC's website says about its scope:

INSDC covers the spectrum of data raw reads, though alignments and
  assemblies to functional annotation, enriched with contextual
  information relating to samples and experimental configurations.

Following table (taken from INSDC website) may help you have better understanding about respective data types comparison for 3 contributors:

It’s worth noting that EMBL-EBI isn’t directly accountable to any one government either financially or in terms of research directions so a (temporary) shutdown equivalent to that of the NCBI is vastly less likely. Rather, like CERN, it’s an international treaty organisation and thus probably a lot more robust.

BLAST can be localized to your machine. There are tutorials, such as  Run-Blast-Local provided by NCBI. Note: you will need to download any/all databases you want to BLAST against locally. Other options for identifying ORFs and trying to identify potential genes include:  USEARCH, VSEARCH (both claim to be as fast, or faster).
If you download entire databases, for example the nr db, running BLAST locally will be far slower than through a browser. I imagine creating customized, more specific databases would speed this up greatly (though I cannot confirm as I didn't get this far in my research).

While this is certainly a legitimate alternative, I don't imagine that a majority of molecular biologists (as opposed to bioinformaticians) have the requisite skill to install all of the packages on their own.

@MarchHo Thank you for the helpful criticism. The link provides an brief how-to instruction to localize BLAST and includes a support email for any who require additional assistance. I should have included this information in the answer. I don't mean to claim this is by any means easy, you are indeed correct in putting forth that this method isn't without its challenges. Just providing additional solutions that I know of :)

The SequenceServer software (which I help make) can also  help set up personalised point-and-click BLAST databases (it is free an open source). It can be helpful for a bioinformatician running it locally on their computer. But it can also be installed on a shared server for access through the web browser. (OR, there is also a cloud BLAST hosting service for those who want to set it up by pointing and clicking. )

If the university also has the informatics department, they can setup BLAST server for the university no problem.
The server only needs to capture the input from the form and render the output as plain text, an easy task that can be implemented with the wide range of programming languages, server frameworks and operating systems, from Java to .NET, from Apache to node.js. Just restrict IPs for campus only to avoid abuse from the side.
Asking informaticians would eliminate the problem that may be difficult to run BLAST locally for each biologist separately. This can even be made an assignment for students, later putting the winner on the web.


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Are there any drawbacks to having a fixed-Köhler microscope?
I am considering to buy the Zeiss Primo star microscope. There are two variants: one with so called "Full Köhler" illumination and one with "Fixed-Köhler" illumination. Are there any drawbacks to having it fixed? When I would not want to have Köhler illumination?

IMHO: there's hardly any reason why you should't use Köhler illumination. It's the method of choice to achieve bright and even illumination, in the entire FOV, permitting max. resolution. In a well designed system.
Köhler has only one drawback: often it turns out to be impossible to achieve even illumination at low power in the entire FOV. Usually, but not aways, the manufacturer has made provisions to achieve propper illumination at low power at the condenser level.
Allow me to add that I'm not a fan of the Primostar stand, which is a microscope build on order for Zeiss, probably by Meji.
Compared to the older Black, grey and white Zeiss Standard stands, it's a toy...

I wonder where that -1 came from


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3 end RNA seq library construction
I have tried to make cDNA libraries from FFPE tumor blocks (highly degraded RNA) using the 3' end RNA seq protocol provided by West lab. Here is the link for the same.
http://med.stanford.edu/labs/vanderijn-west/Protocols.html
After PCR enrichment, a gel purification step follows. My trouble was, the fragments always gave rise to a smear rather than a band between 200-300 bp. Can anyone provide any suggestions as to why this may be happening?
Thank You

RNAse contamination?


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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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Maximum RPM in zero-g before losing consciousness, spinning head-over-heels
There are more than a few scenes in Gravity that I find dubious. Specifically the ones where people are revolving very quickly, either about their own center of gravity or at the end of a rather long pole. I'd guess we'd need to know how long the pole was, but I'm more concerned with a person themselves, just flipping around out there (and I suppose we'd need their height, or does that cancel out?). How fast can they spin until it's night-night? Is it reasonable to assume they should've passed-out in at least one of those scenes?

I think people can easily endure head-over-heel revolutions in space such as seen in Gravity. I am no mathematician (let alone physicist, both of whom could answer this more accurately) but here is my reasoning (faulty though it may be).
You are assuming that someone would pass out from lack of blood supply to the brain.  Given we have absolutely no problems normally at 1 g (the force of gravity on earth), the average non-couch-potato person can tolerate forces of up to 20 G for less than 10 seconds, to 10 G for 1 minute, and 6 G for 10 minutes before passing out.
But g is very dependent on (as you stated) distance from center. It's also very dependent on revolutions per minute.
$$g=\frac{R\left(\frac{\pi\times rpm}{30}\right)^2}{9.81}$$
or
$$R=\frac{9.81 g}{\left(\pi\times rpm\over30 \right)^2}$$
g = Decimal fraction of Earth gravity
R = Radius from center of rotation in meters
π = 3.14159
rpm = revolutions per minute
The average North American male is 1.75m tall. That means the distance of the top of the head and bottom of the feet (if stretched out at full length) from center is under a meter (.875m). At 60 rpm's (that's pretty fast), solving for the above, g = 3.52.
g = [.875({3.14159x60}/30)^2]/9.81 = 3.521 (so just over 3.5G)
Gravity at the top of the head and the bottom of the feet would be 3.5G, while the gravity at the center would be zero G. The heart can easily compensate for that for a while. An astronaut, trained for increased Gs, can do well for longer.
Much worse than too little blood to the head is too much, which is what I would be worried about. Eventually, slightly less than half the blood volume would end up below the waist with the feet feeling the most pressure, and the rest above, with the brain being engorged with blood, which can cause hemorrhage (not taking into account here precise fluid physics). I'm not sure how this would play out in space over longer periods of time, but survival would be the norm for the scenes we see in Gravity.
An Air Force physician named John Stapp was the first to determine just what humans could take in the way of G forces. On his final run, firing nine solid-fuel rockets, his "sled" accelerated to 632 miles per hour in five seconds, slamming him into two tons of wind pressure, then came to a stop in just over one second. A witness said it was "absolutely inconceivable anybody could go that fast, then just stop, and survive." But Stapp did—in fact, he went on to live another 45 years, dying quietly at home in 1999 at the age of 89—and he experienced a record-breaking 46.2 G's. For an instant, his 168-pound body had weighed over 7,700 pounds.  Stapp's efforts put him on the cover of Time, and he was called "The Fastest Man on Earth." More importantly, his work led to greatly improved safety in both planes and cars, and he gave us a much-improved understanding of human tolerance to G forces.
All About G Forces

Very interesting that you would have to flip three times a second to put you into the one minute danger zone; not as dubious as I thought.

Nice fact too :)

I think "too much blood to the head" is in fact the problem that would be experienced, since centrifugal force would force the blood away from the axis of rotation and thus towards the top and bottom of the body. Per this, the tolerance limit for that would be only ~2G, making 60rpm readily fatal. That tolerance is less time-dependent than most. Of course, the rush of blood to the legs as well may play with that result, as may the high centre-of-mass of a human; I'd also be interested to see the effect of the spinning on venous return, cardiac preload etc.

@Watercleave - According to xkcd, Dr. Stapp would not have survived (even though he references Stapp's work. His stick figure model doesn't mention time.

@Watercleave - I alluded to this in my answer; I also mentioned that more like half the blood would go to the head; that factors in as well. xkcd is incorrect. Refute me with NASA's numbers (which xkcd references but doesn't use) which states that -4 - -6Gz (that's 6G blood to head position) would be uncomfortable but tolerable for 6 seconds. -3Gz doesn't mention blackout at all. Also, it doesn't change my conclusion: that for what we see in Gravity, the spins would be survivable.


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TV's so loud when I turn over
Scenario: I'm about to fall asleep with the T.V. on. Having completely forgotten that it was, no longer even hearing it, just before falling asleep I turn over with a 'fresh' ear and it's blaring. If I roll back over it will be noticeable, but quiet again. Waking hours my ears are fine, no worries. Is this some weird sleep induced brain shut-down going on?

I've noticed a similar thing. I think your ear adapts to the sound level it is being hit with, so when you turn over, the ear that was used to hearing absolutely nothing comes up, adapted to find the weakest signals. You can do something similar with your eyes. Cover one for a few minutes, then open it and close the other. The room will seem quite bright. Or, look through a cardboard paper towel tube with one eye for a while. The view through the tube will get much brighter, as that eye is being hit with considerably less light.


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Questions about the Evolution Theory
I'm trying to understand more about evolution theory.
(I am coming from a mathematical background)
What i understand till now is that the "improvement" of the dna is a purely random development and the Selection criteria if the improvement was not negative is by surviving.
The better the improvment was the higher the likelyhood of surviving is.
What i don't understand is that the likelyhood that something useful comes from random changes in the dna is very low?
This reminds me of the http://en.wikipedia.org/wiki/Infinite_monkey_theorem it has surely a finite likelyhood but considering the complexity i still doesn't understand how for example wings of birds evolve.
Consider a pre-bird without wings, to get wings it has to have interstage with some useless pre-wings and then it has to learn how to flight.
Maybe someone can help me solve these mysteries :)
The other thing i am wondering is the smallest living element is the cell.
How did the first cell evolve?
Thank you very much

This question has a large answer but in short, mutations occur at a certain rate, which can depend on the environment and how exposed organism is to mutagenic factors but there are intrinsic mechanisms for creation of variation such as SNPs and chromosomal crossover. Many mutations don't have any negative impact on survival (more importantly passing your genes). The ones that do will get selected against but the ones that increase chances of survival will remain and tend to become prevalent amongst the species over time. Cell is the smallest living unit in an organism. Look at the RNA world.

Your two questions (1. How can useful features initially evolve, 2. How did life start) are two of the largest debates in biology, with endless arguments going back and forth throughout academia and laydiscussion. It's not currently possible to definitively answer either of them, and people have written entire books trying to summarise the state of the debate at that time. Google these to your heart's content - some keywords of potential interest include "origin of life", "intelligent design" and "RNA world" - but unfortunately Bio.SE is not a suitable platform for discussing this.

Welcome to BiologyBeta.SE!
On stackExchange sites, an OP should always limit his/her post to one question and should make his/her question is not too broad. But before you split up your question I invite you to have a look to some other post that will give you some answers. For this reason your question will very likely get closed as too broad. But I am giving some indices below. Also your post is a bit poorly written. This also lead people to close posts. Please come back with better posts, show some efforts in seeking for some information and it will be my pleasure to help you!

Origin of life

There are already a bunch of posts on the origin of life for example. Note that the origin of life is not a field that is part of evolutionary biology as evolutionary biology only explain the evolution of life and not its origin. As a mathematician you may prefer saying something like the domain of definition of evolutionary biology does not include the origin of life just like the shannon's theory of information says nothing about the euclidian geometry.

What i understand till now is that the "improvement" of the dna is a purely random development and the Selection criteria if the improvement was not negative is by surviving

Hum… that's sounds very weird. If I didn't know I would hardly recognize that you talk about evolution. You should have a look to some introduction to the field. Also, you should not confound the concepts of evolution, natural selection and mutations that I guess you confuse. A good, extremely simplistic view of evolution is that mutations occurs and create variance in the population. This traits are heritable. The variants that replicate the best increase in frequency in the population while the other variants will decrease in frequency up to the point to disappear. This is called natural selection.

Consider a pre-bird without wings, to get wings it has to have interstage with some useless pre-wings and then it has to learn how to flight

You also seem to ask a question about how some traits may come to exist while what seem to be necessary intermediate would not be beneficial. This question has been answered probably a thousands of time as it is a common creationist argument.

Because your questions really sounds like creationist arguments I am a bit afraid that you are not trying to understand evolution but you wondering whether evolution does occur or not.
Note also that evolutionary biology is a very big field. You cannot expect to have a more or less good understanding of the whole science of evolutionary biology in less than a year. But if you are trying to just understand the very basic, sufficiently to persuade you that evolution does occur, then few weeks will probably be enough if you show some effort
Please don't forget the questions you may have. Seek by yourself for more knowledge and if you can't find something, then you're really welcome to come back to this site with an accurate question.
EDIT
Have a look to the definition of scientific theory. Also, please read @Chris comment below.
You misunderstand the meaning of "direct observation" that canadianer used. Observations we do in evolutionary biology are just as valid as those that has been made to confirm the theory of gravity. The only point concerns the easiness of understand these observations for non-literate in the field.
Yes, you are totally right. Just like the theory of gravity, the theory of evolution does not explain everything. It only applies to a subset of the phenomenons existing on earth. The theory of evolution is true, we know for a fact that evolution occurs but our theory is not global enough to explain things like the big bang or the surface tension and will never do so. The theory of evolution will never prove or disprove the existence of God as well (supposing you're concerned about that) because again it is not within its scope and will never be. However, the sociological impact of this theory tells much about the human behavior and our difficulties to accept something we know to be true if it contradicts some pre-establish believes even when these pre-established believes are not based on any logical developments.
Your question has been closed because it is too broad. The issue also is that your questions concern much more than evolutionary biology and biology. It also concerns the very nature of science and this is a common reason why creationist missundestand evolution. They don't (only) missunderstand evolution but they missunderstand what science is.

thank you very much. That intermediate changes might have some other function is something i did not thought about, but it sounds reasonably. I want to understand Evolution-theory more because i have the feeling i have no idea about it. In mathematics i learned that asking the critical question leads to far better improvement than looking at the obvious examples and that is often the point where some of the "theories" fail. And in my personal opinion as long as something is not proven (might be never the case) you should always look at the critical points without the bias evo is true/false

Direct observations of populations changing were and are made and then the theory of evolution was created to describe the process. There is no debate about evolution being true or false. What you're saying sounds the same as watching an apple falling from a tree, creating a theory of gravity to describe it and then having a debate about whether apples falling from trees is true or false.

why is it then called theory?

to make your comparison more correct i'd would say it's more about if the theory of gravity is right/wrong. While Newton's Law is true it is only partial true as an approximation for a more general law. (and Newton's Law was discovered through Direct observations) So maybe even while Evolution seems to be true it might not explain the picture fully.

@jonsonBen See my updated answer. Hope that helps!

@jonsonBen Just because it is called theory, it doesen't mean it is theoretical and can not be proven. The opposite is true. A theory describes the theoretical foundation of a special part of science. As does Newton with its theory of Gravitation or Einstein does with its Theory of Relativity. What you are looking it is the term "hypothesis". This can be proven wrong or right. If the first is true, scientists set up a new hypothesis to work with. Standard procedure, no drama included.

What i don't understand is that the likelyhood that something useful
  comes from random changes in the dna is very low?

Well, in that most changes are neutral, sure.  But EVERY organism on the planet has mutations.  It doesn't matter if the odds are low.  If you have billions of organisms in a square meter of soil, how likely do you think it is that not a single mutation in a single organism will be beneficial in that environment?

Consider a pre-bird without wings, to get wings it has to have
  interstage with some useless pre-wings and then it has to learn how to
  flight.

Ah, another Creationist who thinks that the universe can not possibly contain anything that s/he can not personally imagine.  There might be uses for intermediate structures that you just can't think off off the top of your head  (like gliding).  There might be intermediates paths that you just can't think of.  There might be other structures that worked in concert with the intermediates, and then faded away as things changes, much like you build an arch with a scaffold, and then remove the scaffold.  Just because you personally can't imagine the possibility of a scaffold doesn't mean such things are literally impossible.
Have you even tried googling "bird wing evolution"?

The other thing i am wondering is the smallest living element is the
  cell. How did the first cell evolve?

Come on.  That's a completely different question.  Surely someone who thinks they understand the problems of evolution better than professionals who have studied the data for years know that lipids spontaneously formed closed cells, right?  And knows that RNA can autocatlyze reactions, yes?


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Transcranial Magnetic Stimulation on science fair
My friends and I would love to make a TMS machine and apply it to make famous "god helmet". We know that magnetic stimulation may cause visions of angels, gods etc. My question is: what are the dangers?

You should primarily consider that TMS therapy is administered to human patients by licensed clinicians and physicians, who are (1) qualified to deliver medical procedures and (2) qualified to monitor patients for adverse effects that could occur such as seizures. Even if it were an animal you would still need quite a bit of licensing and approval from a governing body like an IACUC.

TMS may evoke simple visual percepts or motor responses, but I've never heard of complex perceptual changes elicited by TMS.  Further, this site isn't meant to assist you in making potentially harmful devices.

I'm voting to close this question as off-topic because OP requests assistance on building a potentially hazardous device.

I would not consider this question off-topic on the grounds of it asking about a potentially harmful device. I however, would consider this question as slightly broad. Moreover, questions on legality are not really on topic here. You may try to have a look at the responses to the linked article and also the articles citing it. As @CMosychuk has pointed out, carrying out these procedures are not suitable/allowed for something like a science fair. You can however volunteer for the experiment yourself.

@Christiaan I edited my question. Now it fits the rules. Can you revive my question?

@AliceD every device is potentially hazardous. EVERY.

@user46147 - I think the question lacks the necessary focus. To perform a risk analysis there are standard operating procedures in place. Risks can occur at the electrical, electronic and physiological level. This question cannot be answered in any meaningful way.


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Biological reason for "deadlift face"?
Always when I deadlift at the maximum load, my face looks more or less like this:

or this:

The same applies for when I do other heavy-weight exercises.
But what biological mechanism causes that? Face muscles, to the best of my knowledge don't participate in the mechanical system that contributes to the lift. Also lifting doesn't cause any uncontrollable emotions, that would cause my face to go >:( Furthermore, I don't see any biological gain my organism gets from a "deadlift face". It doesn't increase oxygen intake or improve cooling.
So why do I uncontrollably flex my face? I suppose it is something about my nervous system going into overdrive, but I have no idea what's the actual mechanism.
I did some research, but google only directs me to dubious "fitness lifestyle blogs", and I have no idea how to word my question in a way that would make sense on google scholar.

On this site, you need to show evidence of your efforts to solve the question. Google ugly gym face or something similar, and if you still have any questions, edit your post to show the specific problem you have.   Many people take offense when informed that they need to show their attempt to answer this question first. Isn't this a Q&A site? Yes, but it's an "advanced" Q&A site, so to speak. This requirement is puzzling to many. Every site has a culture. This is ours. Thanks.

@anongoodnurse ah sorry. I tried some research, but google just returns some "fittness lifestyle" dubious blogs. And I don't know how to express it in scientific wording to do google scholar search.

Did you actually try ugly gym face? Because that search was spot on for me. It’s so strange that almost everyone who’s asked to google something can’t find what I find easily. It’s a real mystery to me. Anyway, if you don’t show your research, you won’t get an answer. Sorry.

I don't make that face when I do my one rep max so it's not biologically necessary. I don't see it as any different from someone who tenses up when doing something where tensing up is of no benefit, like playing a musical instrument. The only difference is in this case is that it doesn't hurt either way so no one tells them to learn not to do it. Not all things you automatically do have benefit.

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


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Giant inflatable laboratory in the jungle. How to find it?
When I was a child (circa year 2000), I watched a documentary (in English) about some biologists doing research about jungle (perhaps Amazon). The biologists lived in a base which was a huge inflatable structure, that was resting on top of the trees. The base had some labs in it and living quarters.
I can't find anything related on Google. It's just spam about inflatable castles.
Can someone tell me what was the name of the research project from the documentary I watched?

Can you remember what language it was in, what year it was made, anything specific about what was being studied, who was in it?

It's not the BBC "Life in the Canopy"?

I’m voting to close this question because it is not about biology as defined in the [help] — specifically it isn't about a biological mechanism, process, or research technique. In addition, you are asking multiple questions, which would be reason to close even if this were on topic. Please consider reviewing the [help] starting with [ask], what is on-topic and what is not.

@tyersome it is about history of biology, because giant inflatable research base is a historical achievement. Also, it is a research technique of establishing a lab in a difficult environment. Also I removed the extra questions.

@user46147 if this question were to remain open, it would be helpful to know when you watched this documentary, and which country and language you watched it in.

@bob I added the info you requested.

Thank you for removing the extra questions, but I still think this is not appropriate here. There is a site for history questions — [HSM.SE] — I don't know if your question fits their criteria, so please check their help section for suitability. If you do decide to try there, please delete your question from this site before reposting because cross-posting is impolite. Alternatively, you can request migration of this question by flagging your post for moderator intervention and explaining what you want and why. –

After more intense search, I found the following research article ( https://doi.org/10.1002/ppp3.10125) by Margaret Lowman.
She discusses canopy research, stressing that forest canopy is poorly researched topic. She outlines the history of previous research on that topic, and points to the spectacular research of Frances Halle from Institut de Botanique in Montpelier.
His team managed to launch a huge effort involving inflatable rafts, slides and dirigibles, that has been named "Radeau des Cimes" (Raft of the Peaks in English).
The structure facilitated canopy sampling and hosted 50 researchers.  Over time, the inflatables have surveyed the rain forests of Cameroon, Panama, Brazil, Gabon, and Australia [copy from the article linked].
Here's a picture from radeau-des-cimes.org :

The colors of inflatables match my memories, so I consider the search a success.


text:
Do any predatorial animals attempt to appear smaller?
There are many animals that have behaviors or characteristics to make themselves appear larger than they are as a defense mechanism, such as butterflies have large eye patterns on their wings.
Are there any animals that do the opposite? That attempt to appear smaller in order to lure their prey closer?
I'm more interested in physical characteristics but behavior that does this, also counts.

Many carnivores crouch closer to the ground with ears flattened when stalking prey

@ScottStensland yes that's correct however that's in order to remain unseen, I'm more interested in behavior/characteristics that are meant to be seen by prey to lure them, similar to the angler fish's light

In order to answer your question, two things must be demonstrated: First, we must demonstrate that the prey animal has perceived the predator. Second, we must demonstrate that the prey animal believes that it has perceived a small animal (which poses no threat).
There are several ways that a predator might achieve these outcomes. The first way is to present a small part of its' body as an independent animal, and the rest of its body as something innocuous, like a rock. There are many examples of this type of deception: you've already identified anglerfish lures. My personal favourites are frogfishes. Several other examples are discussed in the Wiki on Aggressive Mimicry.
Another way is to present the whole body in a way that makes it appear small, for instance by presenting a silhouette with a small apparent area to the prey. This has long been thought to be part of the foraging strategy of some ambush predators which have bodies with a small cross-section, such as pike and dories.
In addition to visual deceptions, some predators may use other signals to be perceived as animals that are smaller than themselves. Atkinson (1997) suggests that predatory Northern Shrikes impersonate the songs of smaller Passerine birds in order to lure them into striking range. This behaviour would also qualify as a predator attempting to be perceived as something smaller than it really is in order to gain prey.

This kind of deception can happen at various levels. Mimicry (which you already mentioned), Camouflage, distractions, deceptions, display behaviors. These are not just for predation or avoiding predator but also for reproduction and avoid conflicts. There are many examples of this kind of behavior, I know few of them. All are not exactly reduction in size but something similar to lure prey.

Hunting Strategy of the Margay to Attract the Wild Pied Tamarin
Zone-Tailed Hawk a Mimic of the Turkey Vulture
Fireflies who mimicks flash responses of the prey's own females.
Motion camouflage of dragonflies
Fake death by opossums
Assassin bug's fake vibrations to lure spiders
Octopuses occasionally stroll around on two arm
Tactical concealment in primates


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What is the biological age of grafted plants?
Suppose you graft a piece of an existing 'old' plant onto a host plant. Will the graft continue to grow having the same biological age as its parent? In other words, would the graft die at the same time as its parent plant? Or would the process of grafting result in some sort of rejuvenation of the grafted daughter plant? Or alternatively, would the host plant carrying the graft determine the biological age of the graft primarily?
PS: Personal experience-based (anecdotal) answers are more than welcomed

@J.Musser - wouldn't you happen to have a clue about this given your reputation of epic proportions on Gardening.SE :) ?

Funny I would stumble upon this and see your ping. Yes, I have done a lot of grafting and know what will happen, but I may not be able to find resources to back me up. It would all be experience. If that's fine, ping me, I'll answer. (ps: I like this question :P will vote it up when I get more votes (I am a heavy voter))

Also, if you ever need me, don't hesitate to ping my in a chat room. Basically, if the name doesn't autocomplete for ya, it won't ping. I'm almost always in our chat room, but if not, I'll be in GL's chat room.

@J.Musser - I'm not sure what you mean with more votes but I bountied my question - hit me without references! :)

I have answered a related but not identical question previously "Do trees age on a microscopic level?": http://biology.stackexchange.com/questions/2055

In my experience (in common with the experience of everyone I've talked to who could be considered an expert on the subject), taking old wood and using that as a scion when grafting new trees rejuvenates them, and they grow as new trees.
I'll take apple trees as an example. As you can see from the table here, there is a distinct age after which the tree begins to decline. Now, that's not concrete (I've seen some apple trees last over 100 years (didn't plant those myself btw)), but generally, an apple tree will lose vigor and productivity before it reaches 50 years of age. This tree's 'immune system' also goes down, and it becomes susceptible to many diseases. You'll rarely see such a tree, as orchardists generally replace them rather fast.
But to the point of your question. When you will graft an apple tree, you will generally bud graft it, as described here. That article (which is spot-on) says:

Select a healthy branch of this year's growth from your desired variety of tree. Look for a plump leaf bud about halfway down the branch. Leaf buds are close to the branch where fruiting buds tend to stand out more.

Note that it says nothing about the tree's age, simply stating that the wood must be healthy. That's because old wood/young wood produce the same result in the new trees. I was using a 40 year old razor russet to graft onto all the Malling V rootstocks I had for that variety. And of course they grew as expected, as a young sapling should. I've heard of a nearby nursery taking budwood from a 100 year old tree that still looked good.
Additionally, you can use a rootstock taken from an old plant, and also a scion from an old plant, and the new plant created will grow as a young sapling. Here's how the rootstocks I use are created: You cut down a tree at ground level, and it sends out a lot of shoots. You pile soil over it, but allow the ends of the shoots to stick through. These shoots will root into the soil, and can be cut at the base, and planted out for grafting later. This way, you can have 1000's of identical (cloned) rootstocks. You can also get rootstocks from old trees. Here's a diagram of the process.

About herbaceous perennials, I've found (to some people's surprise) the same thing. The scion grows as a young plant again once grafted. I found this out because I graft heirloom tomatoes onto hybrid tomato rootstocks (the latter are seedlings). Usually, the scions will be from seedlings, but at times I take the scions from a large mature plant.
Just so you know, an indeterminate tomato plant will, once mature, flower and fruit until frost. A determinate tomato variety will produce a large crop all at once, and then die back (this is the kind preferred by owners of mechanised (machine harvested) fields).
In my tests, you could take the scion from an old determinate plant that was through fruiting, right before it started dying back, and successfully use that for grafting the new plants. These new plants' growth was identical to the growth of grafted plants whose scions came from seedlings, and they began to flower and produce fruit at the same time. Of course, actual seedlings did not have the vigor of the grafted plants, and were behind in growth.
Off-topic for your question, but possibly still of interest, I've found that cuttings and layers (not scions) taken from old plants (both woody and herbaceous), and rooted, would grow as young plants again.

If you want expansion on any point, let me know.

THANKS! So, erm (I feel a bit overwhelmed :-), there is quite some jargon in there (which is absolutely totally fine! I love your answer) and I will have to re-read your MOST interesting answer a few times to grasp (when I have more time), but for now, can I warp your information to "Grafting rejuvenates the graft". In addition, Would you have any idea how the graft is rejuvenated (i mean, is this DNA level, or hormonally regulated etc?)? The latter question may be worth a new question, though :) Thanks again!

@ChrisStronks I could research that for ya.

@ChrisStronks Does this answer your new question?

@ChrisStronks Here's a related thread (by me) that may interest you: http://biology.stackexchange.com/questions/2050/why-do-some-trees-have-a-life-span-while-some-dont


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What percent of your blood can you lose before you need a transfusion
Losing a little blood is okay. If your a normal healthy person, and got into an accident, how do they know if you need a transfusion or if you'll be okay? This is hypothetical.

You may find http://whqlibdoc.who.int/publications/2010/9789241599221_eng.pdf and http://www.compliance.iastate.edu/iacuc/policies/docs/blood-collection-guidelines.pdf useful.

Typically transfusions are indicated for hemoglobin < 7 g/dL (for adults normally: 12-15 grams per deciliter [1]) or < 8-10 g/dL if there is cardiac disease where diminished oxygen carrying capacity cannot be compensated by increased cardiac output.
The answer above is theoretical because there is no accurate way to measure blood loss in the clinical setting - it's usually a mess.
The most useful parameter to assess intravascular volume in the immediate term is blood pressure. Again, the actual number is variable but a 30% drop from baseline in the acute setting is bad.
Another less acute indicator of hypovolemia is urine output (normal is .5-1 ml/kg body weight/hr, dropping below ~35 ml/hr therefore is an indicator of hypovolemia.)[2] Hypovolemia is often corrected with sterile saline fluid and adding packed red blood cells only as needed to keep hemoglobin in the above required range, unless someone is actively bleeding (trauma, bleeding ulcer, etc.) in which case "whole blood" (or packed red blood cells, fresh-frozen plasma and platelets) is given.[3]
[1] McPherson: Henry's Clinical Diagnosis and Management by Laboratory Methods, 22nd ed.
[2] Oliguria &  Volume Depletion
[3] Fluid Resuscitation and Volume Assessment

Welcome to biology.stackexchange. Can you please expand your answers with some references and also explain the parameters you name? It is then easier to understand for people who are not specialized in the field.

I'm confused about the last sentence - whole blood? I took a look at the paper cited and don't see that, nor have I heard of it. Blood isn't generally stored that way. Perhaps you mean packed RBC + platelets + FFP....but that's different from "whole blood."

@Susan - One can order units of whole blood, but yes, FFP + packed red cells + platelets is more readily available and easier to transfuse. see http://clinicaltrials.gov/show/NCT01227005

What percent of your blood can you lose before you need a transfusion

According to Wikipedia: starting with Class III (more than 30 % of circulating volume loss), hemorrhage requires transfusion.

Class I Hemorrhage involves up to 15% of blood volume. There is typically no change in vital signs and fluid resuscitation is not usually necessary.
Class II Hemorrhage involves 15-30% of total blood volume. [...] Volume resuscitation with crystalloids (Saline solution or Lactated Ringer's solution) is all that is typically required. Blood transfusion is not typically required.
Class III Hemorrhage involves loss of 30-40% of circulating blood volume. [...] Fluid resuscitation with crystalloid and blood transfusion are usually necessary.
Class IV Hemorrhage involves loss of >40% of circulating blood volume. The limit of the body's compensation is reached and aggressive resuscitation is required to prevent death.

Of course this applies to a healthy person. If suffering from anemia or other blood conditions, smaller amounts of bleeding may require transfusion.

how do they know if you need a transfusion or if you'll be okay?

In most situations it is hard to estimate how much blood was lost. So in medical practice some indicators are used. These include (according to Puget Sound Blood Center):

hemoglobin / hematocrit ratio and/or values lesser than 7 / 21
small hemoglobin correlated with clinical signs (symptomatic anemia)
low O$_2$ saturation
acute blood loss of more than 30 % (when it can be observed)

But how can the doctor tell when the patient has lost that much blood?

@anongoodnurse a significant drop in blood pressure, along with a commensurate increase in heartrate, is often used as a "back of the envelope" measure of blood loss.

@MattDMo - My point is that the OP asks, in trauma, "how do they know if you need a transfusion or if you'll be okay?" This answer gives no indication of how the trauma doctor would assess this.

@anongoodnurse I agree.


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What is the evolutionary explanation for bat's echolocation
The bat's ability for echolocation is amazing (so are other the abilities of other animals). I was wondering how all of it came to be.

This is an interesting question.

https://www.youtube.com/watch?v=Z_E3zxx2l9g < might not take much

The main reason for bats to "develop" their echolocation system was the avalability of an almost empty niche: Hunting insects at night. Birds are not able to hunt without light and here is where the bats come in. They are able to hunt at night and also to live and orientate in environments where they are protected over the day: Caves. Bats at night are also protected from predatory birds.
There is are a few interesting sources if you want to dive deeper into the stuff:

The evolution of flight and echolocation in bats: another leap in
the dark
Echolocation in bats
Evolutionary aspects of bat echolocation

Not a major issue, but owls and nightjars might disagree with your assessment of birds' ability to hunt insects at night.

They still need some light - bats can hunt in total darkness.

They developed this ability because there was an empty niche? So what, they hired an MBA to find a market opportunity and set an R&D budget? There are lots of "niches" in the animal kingdom - your answer doesn't explain how they are evolutionarily determined and filled

This happens in the usual way: Mutations occur and don't have a negative effect. At some point they prove advantageous, which put selective pressure on mutations which lead to a better adaptation of this new niche. So for example (speculative here) bats were able to navigate better because of mutations in their hearing. This led to a shift of their hunting habits more to the evening, which resulted in the survival of more bats better adapted to this (because less got caught by predators, more food was available etc.). This led to a further selection of animals adapted to this kind of living.

the question isn't "does mutation occur" but:  how did this particular mutation occur?  Randomness isn't a sufficient answer.

Why isn't randomness a sufficient answer for you? Mutations occur randomly, some of the proof advantageous, some are neutral, some negative.

I think your answer would be enhanced if you extracted some of the deeper results from your sources.

Remember, evolution says things don't initially develop "for a reason" -- they develop at random, non-harmful mutations are kept in the gene pool, and eventually a selection event occurs (opportunity to exploit another food source or avoid a hazard) which selects for the mutation in some subset of the population. Over the kind of timescales evolution works on, that's enough to take something that is harmless, turn it into something that is just barely useful (though not necessarily for what it's now used for, eg feathers), and then continue to randomly vary it so it works better or differently or whatever.
Echolocation by itself isn't so remarkable -- we generally can tell about what size room we're in by listening to the echos around us. It's focused echolocation that was a breakthrough.
Late addition: In fact, it is possible for humans to learn to echolocate well enough to get an accurate picture of their surroundings. Some blind individuals have demonstrated this under MRI imaging of their brains. It's not common, but this may be because not enough respect has been given to the technique -- just as ASL was not respected until deaf linguists were able to explain why it was so much better than the alternatives.
So maybe what's special about bats is not the ability, but their reliance upon it.
https://en.m.wikipedia.org/wiki/Human_echolocation

It would be frat if you provided some references for your response.

References: The keyword to search for is "punctuated equilibrium".


text:
Can Mono-Cell or other organism self-replicate?
I have a question regarding how organism replicate them self to create an other organism,
We know that in animal reign, we need a male and female that will generate a new being.
what I want to know is if there is a micro organism that can create another one without a partner of the same kind? and in that case how this organism can do that?
hope my question was clear!
Thanks!

The short answer is yes, there are single-celled organisms that can reproduce without another "partner". Probably the most famous example is that of bacteria.
What you're talking about is known as asexual reproduction. In bacteria, the process is known as binary fission, where one bacterium (known as the parent cell) divides into two organisms (known as daughter cells). These two cells will be genetically identical (barring any mutations) to the parent cell, because there has been no combination (for lack of a better term) of DNA, as there is in sexual reproduction.
The process works the same way it does in cells in multicellular organisms, such as humans: DNA "unwinds" (again due to lack of a better term) in the center of the cell, complementary bases are added to each of the now-separate strands (adenine with thymine, guanine with cytosine), the other parts of the cell are duplicated, and, gradually, the bacterium splits in two. The process can be very quick, compared to the nine months humans spend in the womb.
Asexual reproduction is not unique to single-celled organisms, though. While it is prevalent (and easy) in bacteria, some multicellular organisms reproduce asexually. Some plants are capable or this via self-pollination, and there have been some reports (albeit rather dubious) of certain "common" animals reproducing asexually.
There are advantages and disadvantages to asexual reproduction. One advantage is obvious: no mate necessary. As long as an organism has enough energy and nutrients to reproduce, it can. Also, the process is quick, and easy. There are some disadvantages, though. The big one is that there is no recombination from multiple DNA sources - that is, the resulting organism will have exactly (again, barring mutations) the same genes as its parent - for better or for worse. If an asexually-reproducing organism has a defect that still allows it to reproduce, chances are, its offspring will have that defect.
Some sources:
http://plato.acadiau.ca/courses/biol/Microbiology/Replication.htm
http://www.yourarticlelibrary.com/biology/asexual-reproduction-in-animals-characteristics-occurrence-and-types/11727/
http://www.mpipks-dresden.mpg.de/~mbsffe09/talks/Krug.pdf
http://www.britannica.com/EBchecked/topic/498542/reproduction

I disagree with your statement that asexual reproduction is known as binary fission in bacteria. Some bacteria reproduce by budding and some eukaryotes and archaea reproduce by binary fission.

@canadianer Are you saying that binary fission is not unique to bacteria, that it is not the only method used by bacteria to reproduce asexually (which I knew but did not put in), or that it is not correct terminology?

Ok, does it happened in nature that the resulting organism have different DNA then the parents?

If there is one parent, and there are no mutations, then the offspring will have the same DNA as the parent. If there are multiple parents with different DNA, then the organism will have different DNA than the parents.


text:
How come degraded eyesight still holds with a mirror?
When you use a mirror to look at something, you can position it at an angle arbitrary to your face and still look at an object far away. My question is, for degraded eyesight, how come the picture is still degraded in the mirror? Is it because of an imperfect mirror? Is it theoretically possible to have a mirror that when looked at an angle with perfect scattering to give you better vision than without the mirror, just looking regularly with degraded vision? I am just wondering, it seems like a photonic process, but i don't know enough about the eyes to turn them into any sort of functional system

No, if your eyes are defective, the quality of an image cannot be upgraded with a mirror.

You need to clarify the question - it would help to be a little more concise and say why you think it should help to use a mirror

I asked this same question to my high school physics teacher when we were going over optics. I'm nearsighted, and wondered why I could see clearly from 6 inches away, but if I looked at a mirror from 6 inches away things were still blurred. The answer has to do with the angles of light entering the eye instead of distance.

It's been too long since physics to have a good answer, but I know that if you look at an object in a flat mirror, the light coming off the mirror would be identical to light coming a real object in the same position. The angles of the light rays are the same. Therefore, no matter how close the mirror is to your face, your eyes treat the image as if it's coming from 10 feet away, or however far the object in the mirror is away from the mirror. Bent mirrors will change this, that's why you get the "OBJECTS IN MIRROR ARE CLOSER THAN THEY APPEAR" warning.
I made a diagram to to try and explain it better.
The eye is looking at a mirror, the light from the arrow on the left of the mirror reflects off the mirror and toward the eye. The eye sees an image that appears as if it were behind the mirror, on the right.

The working of a mirror is not what the OP is asking about. The question is whether a defective eye can see a clear image reflected off a mirror (i think).

If the mirror is shaped to correct the image, then yes, just like how lenses can adjust the light so that it enters the defective eye in such a way the eye focuses it into a good image, a mirror could be made to do the same thing. However, getting the focal length right will be very hard and you'd have to put your eye in the exact same position relative to the mirror every time you use it. Flat mirrors will not fix the image and defective eyes will still see the images poorly.

Degraded eyesight can mean two basic processes:
1)  Degradation of the imaging optics in your eye that focus light onto the retina such that light is not focused correctly, or
2)  Damage to the retina itself so that light is focused, but signals to your brain are not generated in response to light.
What these two processes have in common is that they are problems with your eyes ability to process and interpret light.  Placing a mirror close to your eye (but outside of it) does not directly compensate for either of these problems because, other than transforming the coordinate system, it doesn't actually do anything to the light or to your eye.
Possibly what you are thinking of by "degraded" eye sight is simply being near or far sighted, which is the specific case where your vision still works normally, but your eye does not under some conditions (nearby for farsighted, etc) due to a loss of accommodation (the physical flexing the lens of your eye that adjusts its focusing).  In this case, a curved mirror can be chosen that operates just like eye glasses.


text:
Regarding the kingdom Animalia, which phylogenic tree is more common: Molecular Comparisons or Body-Plan Grades
In the picture below, which I obviously do not own:

it depicts two different phylogenic trees, one which is based on molecular comparisons and another one which is based on body-plan grades. My question is which is more common or accepted in the current Biology world?
Image reference: http://www.zo.utexas.edu/faculty/sjasper/images/32.12.gif

Molecular comparisons are more reliable. BTW ctenophora has been identified as a sister clade to both porifera and cnidaria.

@WYSIWYG Correctly speaking Ctenophora are a sister group to Porifera+Placozoa+Cnidaria+Bilateria

@har-wradim .. yes you are right.. missed it..

Long story short, use sequence information if you can.
The long story long:
Sequence information and the trees generated from them are strictly more reliable than morphological characters. For instance: sharks are pretty much the same shape they were millions of years ago, but they've been accumulating genetic differences 'invisibly' that allows us to group the different kinds of shark accurately. Where genetic data is unavailable (paleontology as a rule, certain kinds of field taxonomy where it's cheaper to code the morphological features of each new beetle than sequence them all) morphological trees are still used. So in terms of which tree type is more common: It depends.
In terms of which tree type is more accepted, it's genetic data by a landslide. Genetic data by and large is much less affected by homologous structures and convergent evolution. In addition, it works on species that all look pretty much identical (imagine trying to code hundreds of bacterial species that are all closely related). Using highly conserved cellular machinery, trees for very distant species can be constructed. Using unconserved noncoding sequences trees for very closely related individuals trees can be constructed with a reasonable degree of accuracy.
Some examples: Mitochondrial Eve would be impossible to date with morphological characters. There's just not enough morphological variation between humans.
Opabinia is a really good example of how hard it is to classify things based on shape, especially when they're a weird shape.
Something you can do yourself: Human  and Thermodesulfator(seq) are about as morphologically distinct as two living things can be. One is you, and one eats carbon dioxide and breathes sulfate and hydrogen. It lives at the bottom of the sea and would be more at home in a cup of hot coffee than outside it. Nevertheless, the two species show ~50% sequence similarity using 16S, twice as much as would be expected by chance and easily enough to classify a third thing as more closely related to one or the other. Try it yourself if you like.