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Are mutations random?
The following claim

Mutations are random

or just the use of the expression

Random mutations

are very common among lay people.
The claim is very common among lay people. The claim is often made by OPs (such as here, here for example) but also in answers (such as here for example).

What does it mean exactly?
Are mutations really random?

A bit of a straw horse? However I have taken it by the horns (biology was never my strong suit) and provided an answer that explores a rather different aspect from you.

genetic recombinations are fairly random, but mammals have more efficient mutations than birds, owing to their 2x times bigger genomes. when the chromosomes devide and combine, segments shuffle around a bit like when you mix up colored socks in a draw. the mutations are carefully balanced, not random at at all, as in randomly growing a nose on your elbow.

@comprehensible No offense but outside the fact that birds have smaller genome than mammals, I don't think anything from your comment makes any sense.

@David You're right! Thanks for that. I've removed my link to wikipedia from my question (and my previous comment). I would not think anyone would argue that the claim is not a common one but I did quickly link to three SE posts who talk about "random mutations".

OK. I've deleted my comments on Wiki as they are now redundant.

Short answer
The claim is unclear but is essentially misleading and wrong. However, IMO, for lay people, it is a good approximation to just think that mutations are random!
Here, on Understanding evolution is a great source of information on what it means to say that mutations are random
Long answer
What is a mutation?
A mutation is an alteration of the DNA sequence. There are different types of mutations, consider for example the following Single Nucleotide Polymorphism (SNP)
Original Sequence

ATTATCTG

Sequence after mutation of the 3rd nucleotide

ATGATCTG

Note that mutations can have much more drastic effects such as the duplication of a very long sequence of DNA for example.
You might want to have a look at What is the definition of a mutation? and eventually Effect of mutation on phenotype.
What can be random?
A variable can be random. So is the term mutation a variable?
IS "MUTATION" A VARIABLE
Consider first this discussion about the term house. You can measure the height of the house or the number of windows and both the height of the house and the number of windows so that both the number of windows and the house of houses are variables but house itself is not a variable.
A mutation is an event but, just like with the house, there is no obvious number associated with the term mutations. The number of mutations occurring in a reproductive event is a variable. The effect size on fitness of a mutation is a variable. So claiming that mutations are random is unclear as we don't know what property of the mutation the claim is referring to.
WHAT IS RANDOM
Fully discussing the concept of randomness will require doing quite a bit of math and philosophy. I will not attempt to do so and will intentionally make some oversimplifications here.
The concept of randomness only makes sense if we formalize a model. The outcome of flipping a coing may seem random to you but this is true only if you assume you don't know the forces at play on the coin (the movement of the thumb, the speed of the wind, etc...). A physicist would be happy to consider a coin flip being a perfectly deterministic (deterministic = not random) process.
If a process is deterministic, it means that for a given input there is a single possible output. If a process is stochastic, then there are several (potentially an infinite number) of possible outputs. Now, stochastic does not mean fair or uniformly distributed and therefore a process can be stochastic and yet we can have some predictive power on what range of values the outcome will likely take. For example a weighted die/dice may turn up certain numbers more often, but it's still random, it's just that the distribution of expected outcomes is not uniform.
So, to talk about the claim mutations are random, ideally one would need to fully specify a model of consideration.
RANDOM AS DIRECTIONLESS
Often by random, people mean "directionless" (or "fair"). This is clearly not what the term random means but I will still discuss the case of "direction" (or "fairness") as it is often what people mean. If a mutation is directionless, it means that this mutation is not more likely to increase the value of the variable than to decrease it. For example, if the variable of interest is the height of the individual, assuming that mutations are truly directionless, a mutation is not more likely to increase the height of an individual than to reduce it.
Is the number of mutations random?
VARIATION IN MUTATION RATE
The mutation rate varies dramatically among species and along genomes roughly speaking from a rate of $10^{−2}$ to a rate of $10^{-10}$ mutation per nucleotide. For example microsatellites (repeated sequences) are highly mutable.
EFFECTS OF NEARBY SITES
Note also that the probability of a given nucleotide to mutate depends also on the exact nucleotides that are around it (Rob Ness; Personal communication).
PLASTICITY FOR MUTATION RATE
The mutation rate is also a plastic trait (and is therefore under selection) in some species (of plants and bacteria typically) (Chary et al. 1993; Bjedov et al. 2003). The environment affects the mutation rate and the environment can be chosen by some species (avoidance) or even constructed by others (niche construction).
AGE OF THE PARENTS
In multicellular organisms, the age of the father correlates with the number of new transmitted mutations as well. See the post Gender and age-specific mutation rate in plants (and its references) for more information.
EPIGENETICS
Epigenetic changes (do not concern all species) can also affect the mutation rate and even influence what new nucleotide the old nucleotide will be mutated into (with a given probability).
CONCLUSION
Many things affect the mutation rate. However, the exact number of new mutations an offspring will carry is not perfectly deterministic.
Type of mutations
Mutations are more likely to be transitions than transversions. But again, it is not a perfectly deterministic process.
Effect of mutations on fitness
DISTRIBUTION OF FITNESS EFFECTS
Different mutations have different effects on fitness. We talk about the Distribution of Fitness Effects (DFE).
The DFE varies from one sequence to another. In conserved sequences, mutations tend to have a higher impact on fitness.
ARE MUTATION EFFECTS ON THE FITNESS DIRECTIONLESS?
No, most mutations are deleterious or neutral. Only few mutations are beneficial.
Effect of mutations on the phenotype
Again, some phenotypes are more sensitive to new mutations than others. The increase in phenotypic variance due to mutation at every generation is called the mutational variance.
ARE MUTATION EFFECTS ON THE PHENOTYPE DIRECTIONLESS?
It can be the case, but it is not necessarily true. When mutations are not directionless, we talk about mutation bias (see for example Eyre-Walker 1998, Harr and Schloterrer 2000 or Shah et al. 2010).
Conclusion
Yes, there is some randomness in many of the variables associated with mutation events. However, it would be wrong to think that we have no predictive abilities in the number of mutations or effect of mutations, it would be wrong to think that a mutation is as likely to increase fitness than decrease it and it could be wrong to think that a mutation is as likely to increase a phenotypic trait than decreasing it.
Related posts

Are evolutionary mutations spontaneous?
What are the major causes of mutations in DNA?

Source of information in evolutionary biology
Understanding Evolution by Uc Berkeley is a good, short and very introductory course to evolutionary biology.

I think you could add to your discussion of "what is random" some recognition that "random" does not necessarily mean "uniformly random": a weighted die/dice may turn up certain numbers more often, but it's still random, it's just that the distribution of expected outcomes is not uniform. You touch on this later but I think it's a really key part of what "random" means to a biologist/statistician versus what it means to a 'random' individual.

@BryanKrause I added a paragraph (3rd paragraph) including a sentence form your comment. Please feel free to edit if you can improve that. I agree with you it is important to clarify this point to the readers. Thanks

It would be more considerate to other answers if you could set out your answer using a smaller size of type for your headings (and perhaps fewer of them). Try using caps or italics at the default size in your hierarchy instead. As it is I and others have to scroll more than three screens-full on my laptop to get to the next answer (admittedly two screens-full and my own).

@David I'm sorry your laptop has a small screen! Reproaching someone of not being considerate because his/her answer is too visible feels rather strange. Also, changing the title sizes won't change much to the overall length of the answer unfortunately. But anyway, I did change all titles. It rather decrease the quality of the format I think.

Thank you. The quality of the format is limited by the extent to which one can manipulate the underlying HTML. Even on my 27in iMac your answer still takes up over two screens. But very large type is ugly and not what you would see in a professionally printed document.

The claim is unclear but is essentially misleading and wrong. - No, if something is unclear to you, it is not misleading and wrong.  Only clear things can be misleading and wrong.

Mutation is an event causing an alteration in the DNA sequence where the mutation occurred.  - It's nonsense. It means: Mutation is an event causing an alteration in the DNA sequence where the event causing an alteration in the DNA sequence occurred. //// An event causing an alteration in the DNA sequence is not the same as mutation.

@user1425 Thanks! Indeed the phrasing was wrong. I am not sure I fully understand what your issue with it was but I changed the phrasing to something that, to me at least, seems correct.

What has been meant historically by random mutation?
I am not an evolutionary biologist, so I was surprised that the poster — whom I believe is — does not discuss the origin of the term. As original conceived ‘mutation’ could have had nothing to do with DNA, as DNA was not established as the genetic material until the Avery experiment in 1943. It is more reasonable to thinkg that a mutation was thought of as some unspecified heritable change in the genetic make-up of an organism.
I did a Google Books ngram search for “random mutation” with the result shown below:

Perusing the books that came up, I found two snippets from the 1907 Proceedings of the American Catholic Philosophical Association:

The pure chance that causes mutation, we are told…

and

[…de]termined in advance. From which random mutation can be distin[guished]

Unfortunately, more of the context is not available there (the completions in the second snippet are my own deduction) but is evident that ‘random’ is being used — not in a strict mathematical or statistical sense — but in opposition to ‘determined’. It was, of course, all to do with evolution and religion. Indeed that type of concept of ‘random’ has a hard scientific pedigree: Einstein, albeit in another context, maintained that “He [God] is not playing at dice”. (Original German: Jedenfalls bin ich überzeugt, daß der nicht würfelt.)
Another example is a biology text book from 1937:

To some biologists these evolutionary trends cannot readily be fitted
  into a random mutation-natural selection explanation of evolution.
  Consequently, to account for them some of these biologists have
  suggested orthogenesis hypotheses, ..

And although I had never met the term orthogenesis, the Wikipedia entry suggests it is a religious or quasi-religious antithesis to mutation and random selection in which evolution is directed by some (supernatural?) force.
How would the term be viewed by a modern molecular geneticist ignorant of history?
Perhaps a modern scientist, unaware of the historical usage and uninterested in the historical and long-settled antagonism to evolutionary theory would regard random mutation as meaning something like the following

That there is an equal chance of any base-pair in the genome of an animal undergoing a mutation, hence there is an equal chance for genes of the same length to undergo mutation.

Are Mutations really random?
Yes: in the historical meaning of the term — there is no evidence for a directing force.
No: in the modern sense of the term, there are factors that can make particular regions of DNA more susceptible to mutation than others.
The poster, in answering his own question, mentions this point but does not elaborate on it. Being, perhaps, more concerned with biology at the molecular level, I shall give a few examples from my own knowledge, and encourage others to contribute more.
1. CpG dinucleotides mutations
The paucity of these in the human genome is thought to be because of their methylation to 5-methylcytosine, which slowly deaminate spontaneously to thymine.
2. Trinucleotide repeat mutations
For example, CAG repeats can expand in length due to mismatches in crossing-over.
3. Somatic hypermutation in immunoglobulins
Perhaps this is not strictly relevant as it occurs in somatic cells, but it is thought to operate on the DNA, and it is of interest in that it targets a particular region of particular genes.
4. Mutational hotspots

Mutation frequencies vary significantly along nucleotide sequences
  such that mutations often concentrate at certain positions called
  hotspots

I take this quotation from the summary of a review by Rogozin and Palov in Mutation Research. The interested reader is directed to his university library etc. for the full text, which is not freely available.


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Bird brain-eating Mantis - how does it crack the skull?
The New York Times' Science article Birds Beware: The Praying
Mantis Wants Your Brain is a good read and is well researched. Apparently the larger Mantises have been documented to occasionally kill and eat (parts of) birds on six continents.

The mantis was clinging with its back legs to the rim of the feeder, holding its feathered catch in its powerful, seemingly reverent front legs, and methodically chewing through the hummingbird’s skull to get at the nutritious brain tissue within.
“It was staring at me as it fed,” Mr. Vaughan said. “Of course, I took a picture of it.” Startled by the clicking shutter, the mantis dropped its partially decapitated meal, crawled under the feeder — and began menacing two hummingbirds on the other side.

The article continues:

James V. Remsen of the Museum of Natural Science at Louisiana State University and his colleagues documented 147 cases of mantis-on-bird predation in 13 countries representing all continents but Antarctica — not surprising, Dr. Remsen said in an interview, since there are no mantises on Antarctica.
Hummingbirds were the most common target, but mantises also went after warblers, sunbirds, honeyeaters, flycatchers, vireos and European robins. Large species like the Chinese mantis, which grows to four inches in length, were the most avid avivores, and females were responsible for virtually all the bird-killing observed worldwide.
In two reported cases, females feasted on birds while copulating with males. Sometimes the mantises would tuck in through the bird’s breastbone, but more often they went for the head, Dr. Remsen said.
“They bite in and eat the brains,” he said, “which might imply this is something they’re professionals at.” (emphasis added)

Question: How does the mantis break through the skull? I'm guessing it is smooth and much larger than the insects mouthparts, so it can't crush it. Does it cut through somehow? Or maybe go in through the ear? (Yuck!) What "tools" does the mantis have at its disposal to break through a bird's skull?
note: The link is to Bird Predation By Praying Mantises: A Global Perspective, Martin Nyffeler, Michael R. Maxwell, and J. V. Remsen, Jr., The Wilson Journal of Ornithology 129(2):331-344. 2017, https://doi.org/10.1676/16-100.1

below: "An unlucky hummingbird caught by a mantis at a feeder in Colorado." From here. Credit Tom Vaughan/FeVa Fotos

The mantis doesn't need to crack the skull to eat the brain. It can get to the cranial cavity through an easier way: the eye socket.
Have a look at this image of the ruby throathed hummingbird (Archilochus colubris) skull:

Source: http://wildlife.ohiodnr.gov/species-and-habitats/species-guide-index/birds/ruby-throated-hummingbird
You can see the huge eye sockets. This image (not a real skull, but a plastic cast) shows that even more clearly (also Archilochus colubris):

Source: http://www.boneroom.com/uploads/4/8/1/1/48118243/s521972503441136676_p1061_i1_w640.jpeg
According to the original paper of the research, which was linked by the NY Times article and by your very question (Nyffeler, Maxwell and Remsen, 2017):

Bigas et al. (2006:237) described the feeding behavior of the mantids in the mist-nets:
“The modus operandi of the mantis seems to be to approach the bird,
  which is always hanging downwards, and then enter the cranial cavity
  via one of the eyes, feeding on the brain tissues.” (emphasis mine)

If you look at the image you shared you can see that the mantis' mouthparts are positioned at the side of the hummingbird's head, which corroborates the claim that the mantis uses the eye socket to get to the brain tissue.

Sources:

Nyffeler, M., Maxwell, M. and Remsen, J. (2017). Bird Predation By Praying Mantises: A Global Perspective. The Wilson Journal of Ornithology, 129(2), pp.331-344.
Bigas, D., J. Piccardo, And J. L. Copete. 2006. Praying mantis killing passerines in mistnets. Dutch Birding 28:237–238.

Excellent answer, thank you! The image of the hummingbird skull is very helpful, it's nothing like what I imagined (probably a small human skull with a beak cartoon style).

@uhoh Nope, it's very different! Have a look at this image (not a real skull, but a cast): http://www.boneroom.com/uploads/4/8/1/1/48118243/s521972503441136676_p1061_i1_w640.jpeg The eye socket is huge.

I see what you mean. I think this is more what I was thinking of; http://calvinisticcartoons.blogspot.com/2012/03/anesthesiologist-discovers-ancient.html or perhaps this; http://tralfaz.blogspot.com/2014/07/skeleton-bird-dance.html Far too much TV when I was young, although I did learn physics from Wile E. Coyote and the Road Runner.

@uhoh That's great! By the way, if you want to know more about mantises, have a look at this extremely serious and scientifically accurate video: https://www.youtube.com/watch?v=0aSCPmabRpM

I'm going to dream about mantises tonight I just know it. I've managed to loose an hour already just watching one video after another from that channel. OK focus...

source: Stack Exchange

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

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Spider with brown zig zags on abdomen and black head
Found this spider roaming around my room the other day.. can someone tell me the species?
Location: Central KY, USA

Also, here's a video of him moving around in a glass candle lid, where you can get a really good look.

As far as I know you've found a male steatoda triangulosa or triangulate cobweb (weaver) spider

More info:
https://en.m.wikipedia.org/wiki/Triangulate_cobweb_spider
http://lancaster.unl.edu/pest/resources/triangulatespider.shtml

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


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How are fMRI responses to auditory stimuli measured?
How can fMRI experiments be conducted which measure the response to auditory stimuli (e.g. music) when the apparatus makes such loud, nasty, and distracting noises? Are there quieter MRI tomographs in the meanwhile, or must the stimuli (transfered by earphones) be louder than the noise of the machine? How to measure the effect of a whishper then?

I could have found this article earlier, but as things go, I didn't. But possibly it contains most of what can be said to this question:
Jonathan E. Peellej, Methodological challenges and solutions in auditory functional magnetic resonance imaging, Front Neurosci. 2014; 8: 253


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identify some kind of vine
I have found this plant in Trabzon, a city in Turkey. I found it near the highway. I assume it isn't planted intentionally, but maybe left after previous ornamantel plantings. It smells good I think. I am interested in it because of the nice scent. Please could you help me to find what species is this.

edit: and I forgot to add its fruits. I want to plant this vine, but if there are better varieties, I can plant them instead.
Sadly flowers lost their conditions because i collect them 2days ago. and i transported them in a plastic bag.

i can provide photos from different angles, if thoese arent clear enough

Please add the location where you found it and if you found it in the wild or in a garden.

This is a clematis, probably clematis vitalba.
This plant is native to Europe and Turkey. It also occurs on the westcoast of the USA and Australia/New Zealand, but it is probably introduced there. Source occurences
Picture from Dutch wiki:

Many clematis species have a very nice smell, and both the flower and the fruit are also nice to look at. That is why clematis species are grown in garden often, with countless varieties. They differ in color (most are white, pink or purple), in flower size and in flower time (spring/summer).

this answer is great, i was planning to plant it but i see there were better varieties with more spectacular fruits. but i dont accept this answer yet. because maybe you could want to improve your answer after i edited my question.

It's a very un-remarkable clematis, the wild type. it looks like a bush. children smoked the stalks in old times. There are much more suitable garden varieties. clematis can develop a stalk 5cm wide after enough time, they are my favourite climber along with yellow clematis, passion fruit and wisteria. clematis seeds grow very easily.


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Why do buffalos not leave the lion alone?
In the Buffalo Kill Lion - The Stronger is The Winner video the buffalos seem to be attacking an incapacitated lion.
Why would they do that?
They seem to risk injury for no gain (they don't eat lions).

The gain is one less lion to worry about.

@JAB: I have serious doubts about math capabilities of buffalos ;-)


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What of Gould's contributions to evolutionary biology are still accepted in the mainstream?
I have been reading Daniel Dennett's Darwin's Dangerous Idea, in which he picks apart many of Stephen Jay Gould's criticisms of neo-Darwinism, particularly in the chapter 'Bully for Brontosaurus'. Turns out Gould wrote a lengthy refutation back, and they ended up throwing slurs at each other for a few years afterwards.
I am interested to know what the current state of mainstream opinion is on Gould's interpretations, particularly on panadaptationism and gradualism. Has the field yet come to any firm conclusions on who was right after all?

His main contribution was making biologist consider that population size affects how fast selection changes a population, but he tended to imply this was some form of categorical difference and not a spectrum. But this was greatly overblown my media into some sort of insistence that they could not be the same. large population slow change and small population fast change are both points on the same spectrum. Nobody was right becasue both sides were not really saying the other could not occur they just emphasised their own area. Gould main problem was the idea of stasis in punctuated equilibrium that large populations somehow did not keep evolving this was a point he contested without ever really being able to provide evidence for. His own evidence often fit both interpretations. Since then it has been pretty thoroughly refuted by genetic studies, better resolution*, and modeling of stabilizing selection, all populations change, large ones just change slower, often with less direction. Gould himself later accepted this, but insisted on keeping the terms punctuated equilibrium and more oddly "stasis" for these periods of reduced change, this led to more misunderstanding especially with the public and media. Many scientist felt it was a sign of being unwilling to truly accept the evidence.
He also contributed a lot to our understanding of evolutionary development and how evolutionary baggage effects future adaptations. We often forget this but without his constant pushed of the importance of constraints and development both would probably be much more poorly understood. Panadaptationism was probably given more service by than many ever though it deserved, but Gould was right that that are far more aspects to selection than many considered. It just was not as popular an idea as his attention implied, but that is part of science harping on bad ideas is not really bad in science, it just starts to get old when the idea never had a lot of traction. It is however understandable considering Gould's own focus.
He has a serious problem(probably not unfounded) with sociobiology but probably pushed too far by implying searching evolutionary history for influence of our behavior was pointless. As much good as he did for understanding physical adaptations he seemed to have a blind spot when it came to behavioral adaptations. He mellowed about this in later years but still seemed to resist it. Sociobiology tended to be over applied, often without evidence, it was easily the worst offender with panadaptationism. Gould was right to push back against speculation but he often treated all behavioral science the same regardless of rigor.
Dennit who primarily researched evolutionary aspects of human behavior and publicly speculated a lot, of course ended up as a stanch opponent. But then as the more rigorous evolutionary psychology arose from sociobiology Gould seemed unable to see the difference which quickly led other to stand against him and probably did more than anything to produce his negative image. I know it is the thing that put me off his writing.
The other issue that I, as well as many other paleontologists, had with him was his resistance to the application cladistics and other computer based analysis. Both extremely important tools in understanding evolution, especially once to could be applied to genetic material. He always seemed to treat it as not real science, which always struck me as weird considering how much he emphasised rigorous investigation. He struck me a brilliant mind falling behind the technological curve and becoming disapproving of it. To myself as a young scientist he seemed to resist anything new regardless of rigor despite his own emphasis on rigor.
In short he was hard working scientist. He improved our knowledge in some areas while being unhelpful in others. He was a scientist who got a huge amount of media attention, which few scientist can do without sooner or later showing normal human flaws. Now take all this with a grain of salt, this is all my own personal impressions from observation of his work in paleontology along with reading his (and just about every other) book about evolution. I have not read many of his paper outside of paleontology. I say this becasue speculating on the beliefs and motivations of the dead has always struck me as dishonest especially without laying your cards on the table.

I wanted to give special mention to resolution and darwin finches, darwin finches undergo different selection every year depending on rainfall, large and small (specialized) beaks during wet years and medium (generalist) beaks during dry years, this changes every breading season with the amount of rainfall on any large scale this would appear to be no change as they tend ot average out, but with better resolution we can see many many small directional selection pressures adding up to no net change on a large scale.


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What causes this eggplant scar?
This eggplant fruit is featuring a big scar. What causes such a scratch? Is it a disease or maybe the fruit was hit and then it healed the crack? Is it correct to call it "Eggplant scab"?

do you know if that is where it lay on the ground? if not, it's probably due to the fruit being bred to grow very big compared to it's wild version.

@comprehensible - no idea. I got them from the fruit shop

perhaps someone threw a grenade near it when it was in the trenches, or it fell off it's motorbike when it was doing 30. even more likely is that it was in contact with planks/rods/a stem/the ground/some stones. perhaps try brushing it with a toothbrush.

return it and get a new eggplant

I like com.prehensibe's comment.Melons get cracks like this on the places where they sit on the ground. Melons are cucurbits too,this looks like it happened where the eggplant sat on the ground. Wash it off,it's still good.


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What if Staphylococcus Aureus are extinct?
What if Staphylococcus Aureus are extinct?
Can it be good for human or bad for human?
Thanks for your answer in advance.

thats a homework question isnt it.

Of course not. I have nose infection and it was caused by my razor. I am curious how I can prevent bacteria in this kind of situation (when I am not protected by skin).

It is almost entirely parasitic and has not physiological or ecological effects that could not be replaced easily by another bacterium. It is responsible for immeasurably more infections that protections of humans, therefore it is a disease vector, not a beneficial bacterium.
If it went extinct, humans may suffer from increased population pressure, that would be the only worry.

I know this has been closed already, but could you please provide a reference?

There are millions of references, i.e. A large proportion of the population (60%) harbours S. aureus intermittently, and the strains change with varying frequencies. Such persons are called intermittent carriers. Finally, a minority of the people (20%) almost never carry S... it's not possible to find a study about benefits of aureus, it's always benefits of treatments of the desease.

So this is a very helpful answer. It means scientists don't have to hesitate to kill S.aureus as many as they can.

thanks, the over use of antibiotics is what creates super resistant variants. excess and low hygiene and un-natural human cities and social structures probably cause most S. aureus problems.


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Criticism of the significance of fMRI studies
On the german Wikipedia page on fMRI I read the following

"There is some critisism of the basic assumptions and possible
  insights gained from fMRI studies which is based on a constructive
  component of the visualization of measured data, whereby it is more
  the ideas and expectations of the researchers than the actual
  processes that are visualized." (translation by me)

Can these "basic assumptions" and "expectations" be made more precise, and the way how they are reflected in the "constructive component", and how the constructive component in turn is reflected in the visualization (which doesn't necessarily show the averaged but true activities of neurons)?
Especially:

What do typical "basic assumptions" concern? The processing of single neurons, the inner connectivity and processing of groups of neurons, the collective processing of different groups of neurons, the interwovenness of neurons and blood vessels?
What is a specific typical "basic assumption" in the context of fMRI?
What is a typical "expectation of the researcher"? Finding a correlation between two regions of activity while performing a task?
What is a typical "constructive component"? A method of statistical analysis? Or something else?
How does an inappropriate "constructive component" typically lead to false fMRI visualizations?
Do fMRI researchers regularly check if a BOLD signal really (or most probably) reflects neuronal acitivity at that spot - and don't display it if not?

Not anywhere close to an answer, but you should probably be made aware of the dead salmon fMRI experiment.

I've heard of it.

Are you familiar with the expectation of one question per question? I like fMRI analyses. This is unfortunately too broad.

What is too broad? My question or your liking of fMRI


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Can a novel protein domain arise de novo in nature or did all protein domains evolve from a single ancestor?
I know there is extensive research into the taxonomy and evolution of protein domains and many connections are, and are continuing to be, found between numerous domains. However, as far as I can see, new domains always arise from preexisting ones. I have seen no paper, in any field, showing the development of a new protein domain from a random piece of DNA which just mutates a start codon and synthesizes a new protein with no apparent function. I know this is theoretically possible but has anyone seen any evidence it has happened in any form of life in any geological period of time? OR are there some other mechanisms that could generate novel domains from non-coding DNA that I have overlooked when searching the journals?
My thinking is that, if de novo protein domain generation doesn't occurr, does it mean that all protein domains are a kind of "progeny" of a single domain that arose at the onset of life as we know it (or maybe even was the first lifeform on Earth). It seems very strange to me that this hasn't been pointed out by now since it's a relatively simple deduction. Thus, I'm asking either for a reference paper showing evidence for the evolution of de novo protein domains from a random piece of DNA that somehow managed to turn into a gene or for a reference to a paper discussing the idea that all proteins originate from a common ancestor existing at the onset of life and even, possibly, a single domain as old as life itself?

You're right, it doesn't work this way. Which is why you've never seen a paper on it. "I'm asking either for a reference paper showing evidence for the evolution of de novo protein domain unknown by now from a random piece of DNA that somehow managed to turn into a gene" You won't get one; that's not how it happens.

Then how does it happens @anongoodnurse? Please, explain how we can get a brand new protein domain and even possible new family of domains if there is no previous domain it came from? As far as I know all domains come from previous domains, all genes evolved from previous genes and all proteins from previous proteins. But if that is true does it mean all domains, all proteins, all genes, the entire biodiversity evolved from a single ancestor gene, which coded a single ancestor protein and may be it had a single ancestor domain? Am I right on track or am I missing out something important here?

I've trimmed down your question a little bit, I hope it's still okay for you. I think it is interesting and will try and look for some literature.

Yes, there is no problem. I think it's better this way, too. :)  I hope I could know do novel domains rise from random pieces of DNA or all proteins and genes just like the cells they are in come from a single ancestor? Of course we could speculate about LUCA containing all the genes necessary for the entire biodiversity but even then the question remains: Did LUCA itself had its genes and proteins evolved from a single gene with a single protein and may be a single domain? I'm thrilled to know could we trace all biodiversity to just one molecule, even more-to just one domain?

Yes. Novel protein domains can arise de novo in nature. The evidence is quite solid as those new domains show all the expected mutation patterns and statistical properties (expected for something evolving from DNA that doesn't yet encode for a domain). E.g.: see the following meta-analysis, which also describes how those new domains behave relative to older ones, and how they integrate into proteins: Toll-Riera et Mar Alba 2013, BMC Evolutionary Biology, "Emergence of novel domains in proteins":  https://bmcevolbiol.biomedcentral.com/articles/10.1186/1471-2148-13-47
If you are additionally interested in new genes, the following mini-review: http://www.sciencedirect.com/science/article/pii/S0960982214001547#bib20 .
If you are additionally interested in in-vitro evolution, which is directly observable within the life-span of single humans, the following review: http://www.sciencedirect.com/science/article/pii/S0022175904001309

The link is dead for the first article. Could you write the titles/authors/etc for these articles?

Maybe the link isn't dead but rather my useless network is acting up. In any case, full citations would be appreciated.

note that presently NPG appears to have server problems (even nature.com is down), which also applies to the journal above.

@tsttst, if you could provide a list of the journals you targeted in your search and can provide me with a list of keywords I would give the price to you. It would be also useful if you can name the search engine you used. My background is in theoretical biology and the origins of Life, so, I'm not really good at genetics and modern fields connected to proteomics and may be have been using the wrong keywords, so, if you can tell me the 2 lists-of related journals and keywords I will be greatly thankful. I wish to know how to search better and if you can help me I will vote for your answer.

@YordanYordanov: I knew that the topics covered by links 2 and 3 would exist and concluded that they would be thematically close, if something on de novo evolution of domains existed. Since the latter seems to be a fascinating and important topic I concluded that it would be covered tangentially by reviews on topic of link 2 and 3. Thus I looked for first review in google scholar on topic 2 within a good journal ( main npg or cell press ) and would read it - hoping to satisfy my and your curiosity on topic 1. Indeed the first review would contain cognate citation towards specialist article.

Thank you very much @tsttst. :) I will give the reward to you for your efforts.

@YordanYordanov: thank you, and good luck and fun for your future research. No effort spent on my side as I also wanted to know the answer after seeing your question


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Importance of germline and somatic genomic mutations to the purpose of treatment in cancer
Is there a hierarchy in the sets of genomic mutations (somatic and germline) to the purpose of treatment in cancer?
Can they be considered at the same level in the context of targeted therapy or are there reasons to prioritise one set vs the other?

A) There isn't really a fixed hierarchy that is applicable across the board - alterations are often binned into actionable targets and non-actionable ones. In terms of customised cancer vaccine for immunotherapy (Eg - www.sciencemag.org/news/2017/04/personalized-tumor-vaccines-keep-cancer-check ) , more antigenic mutations tend to be prioritised.
B) Sometimes there are reasons to prioritise mutations over others even for small molecule targeted therapies. For example, one would want to target mutations that are clonal rather than subclonal where possible, so that the bulk of the tumour, rather than a small fraction of the cells in it, are targeted. Alternatively where one has, for example, a resistance mutation arising from prior therapy (You see this with EGFR T970M mutations) it is an indication for next generation EGFR inhibitors that specifically hit the resistant mutation.


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Biological meaning of taking zero as coefficient of the Laplacian in mathematical models of cell motility
Several mathematical models from theretical biology deal with various forms of cell motility (for example, cancer growth) or evolution of populations.
The equations that make up such models usually contain (among others) a Fickian diffusion term of the form $$- \delta \Delta u(t,x),$$ where $u$ is the cell (or population) density.

To fix some ideas, consider the following examples.

A chemotaxis model:

$$\partial_t u(t,x) = \delta \Delta u(t,x) -  \nabla \cdot(uK\star u),$$
where $K \star u = \int_\Omega K(x,y)u(t,y)dy$, for a certain kernel $K$.

A model arising in population dynamics:

$$\partial_t u(t,x) = \delta\Delta u(t,x) + u(t,x) \left(\lambda - a\int_\Omega u(t,y) dy\right).$$

Biologically, what is the meaning of a situation where $\delta = 0$ (that is, where there is not Fickian diffusion governed by the Laplacian term)?
Is there any interest in studying such situations?
Can you point out some references on this topic?

I'm not familiar with these models, but is it even proposed that there could be situations where that constant is zero? Note that biology is not math, and much like physics, sometimes certain assumptions aren't bothered to be stated, because there is no biological interest in equation results outside those naturally observed. (also links to papers are always nice for people to follow the situation you are describing)

@BryanKrause For example, there are many models governed by equations of the kind $$\partial_t u = \delta\partial_{xx} u + \mathcal{I}[u],$$ where $\mathcal{I}$ is an integral term that accounts for nonlocal interactions and nonlocal diffusion of particles (cells). My general question is: does it ever make sense (biologically) for particles to not mode randomly, that is, to have $\delta = 0$?

No, it doesn't make sense. You would be talking of drift in a common direction with no interactions or offsets, all cells in the field moving in synchrony.

@Jay I think this needs more context before you can get a good answer, i.e. a more specific model. I could imagine, e.g. a model where cells are not motile on their own (e.g. no drift or diffusion) but interact at a distance (via chemotaxis, etc.). This could lead to diffusion-like terms that aren't the simple Laplacian here, and thus delta = 0. I think Hans Othmer and others have worked on deriving these models from single-cell starting points, which would be a useful guide.

@AJK I edited my question.

@Jay: your question implies that the excerpts of the models would be biologically meaningful. However, if you would model individual entities rather than large groups of entities (where you imply that every entity would have to have 0, which could easily be theoretically and biologically unreasonable,....), differential equations wouldn't be a valid approximation. In this case theoretical biologists would usually change to exact stochastic models (such as Gillespie) where you'd mode a trajectory according to transition probabilities.

@tsttst $u(t,x)$ describes a unit area on a surface at a given time, and not so directly the particulates themselves. That being said, "if you would model individual entities rather than large groups of entities.." isn't applicable to this collection of equations; e.g., the difference in modeling the physics of a moving car vs. modeling traffic flow. Also, you mention to use stochastic models instead, however, those equations do contain stochastic models, as indicated by integration over the sample space $\Omega$, in both the chemotaxis and population dynamics models.

Just so we're on the same page..

$u(x,t)$ is a concentration/density function that describes the number of particulate species (bacteria, gas molecules, etc.) at point-in-space $x$ and time $t$. And although it may be an obvious statement to make.. with $u$ having the parameters $(x,t)$, this indicates that particulate concentration values are dependent upon both position and time.

$\delta$ is the diffusion coefficient of the particulate concentration, defined as a proportionality constant between particulate diffusion and the overall particulate concentration gradient. Particulate diffusion can be regarded as local behavior, whereas the overall particulate concentration gradient describes the behavior of distribution for the entire particulate concentration, and of which may be affected by forces other than the particulate's response to an attractant/repellant gradient, including temperature, pressure, and/or other environmental variables. An in depth understanding of this coefficient can be obtained by reading sections 2.1 & 2.2.

Your questions

Biologically, what is the meaning of a situation where $\delta = 0$?

Well, if you did in fact read the recommended sections, you may already have realized that it's just not possible for $\delta = 0$, unless you're considering concentrations of mass that simply can't diffuse throughout one another, but even then $\delta$ would be considered as $DNE$.
To reference a portion of 2.1 & 2.2:

Molecular diffusion, strictly speaking, cannot occur under conditions in which both the net flux and the [concentration gradient] are simultaneously zero. If the [concentration gradient] is uniform, then in general fluxes are different for different species, and the net flux is not zero. If the net flux is zero, a small [concentration] gradient must exist in order to counter the tendency for the different species fluxes to be different.

That being said, the diffusion coefficient can be an extremely small value - of which is based on the nature of the particulate(s) undergoing diffusion, and the medium for which they travel throughout - but it's never zero. See here for a series of tables that contain diffusion coefficients for common substances at standard conditions.
And as for the biological meaning to $\delta = DNE$.. the only conclusion that could be made is that the mass concentrations under consideration can't diffuse with one another, for whatever reason. Whether or not there's meaning beyond this, I believe that would be dependent upon what's specifically being studied.

.. that is, where there is not Fickian diffusion governed by the Laplacian term?

This statement however, does have biological meaning to it. When $\delta \Delta u(t,x) = 0$, this means there is a zero net flux occurring at point-in-space $x$ at time $t$. Which is to say that - the number of particulates of a given species entering a given region of space over a given time interval is the exact same as the number of particulates of the same species leaving that exact same region of space over the exact same time interval. When this is true for all regions of space within the [biological] system, it means that the system is in a steady-state, and/or has reached equilibrium.
Note: Equilibrium and steady-state systems are not the same, however, the differences involved aren't relevant to the scope of this discussion, and so nothing further will be said about this.
When a biological system is in a steady-state, and/or is in equilibrium, that can carry significant implications. Perhaps the most ubiquitous example that also first comes to mind are the steady-states of ion channels, with the effects of cell activation/non-activation being the implications. Another example could be pretty much any chemical reaction that reaches equilibrium.

Is there any interest in studying such situations? Can you point out some references on this topic?

Yes, there are many occurrences where these states are studied, of which you may already be aware of. Regardless, here are a few that seem worthy enough for me to provide in this response:

Steady-state Distribution of Bacteria Chemotactic Toward Oxygen

Equilibrium of Two Populations Subjected to Chemotaxis

The Hodgkin-Huxley Model

In summary
The biological meaning of $\delta \Delta u(t,x) = 0$ usually deals with scenarios where the region(s) in space experiences a flow of mass that has equal incoming & outgoing rates for a given particulate species. Most of the time, this is indicative of a steady-state, and/or equilibrium, and this can be confined to local regions, or globally throughout the system.
And I'd also like to offer a slightly different perspective. Normally, the diffusion coefficient is a temperature & pressure dependent function. However, if you're considering situations with STP/NTP, the diffusion coefficient can truly be treated as a constant. When this is the case, the Laplacian term is analogous to the heat equation. By taking this perspective, the Laplacian term [being zero] is stating that there is no loss or gain in heat (species-specific particulate motion) when considering a region of space over a defined time interval, and the overall model would describe the change(s) in motion (heat) for the entire system. From there, biology could explain as to why the "heat" behaves the way it does, of which would involve the mechanisms & behaviors of an organism with respect to its reaction(s) to an attractant/repellent.
And lastly, for the sake of inclusivity, the other terms in these models generally represent behaviors that are external to local interactions, and each may carry differing effects, such as birth/death rates in population dynamics, or particulate concentration movement that's perpendicular to the axis to which the concentration gradient moves upon, as is the case with the second term in the chemotaxis model. So then, when the Laplacian term is not contributing to any change, i.e., when there is a zero net flux, these other terms will then be the only candidate contributors to any potential changes in the system, whatever those changes may be.

References

A Mathematical Model For Chemotaxis
Keller-Segel Models for Chemotaxis
Gaseous Diffusion Coefficients
Fick's Second Law

I think this ignores a central aspect of the question, which is that there is a second term, which is not just the Keller-Segel chemotaxis term. Secondly, I think it's confusing to claim delta can't be zero. delta = 0 in KS corresponds to a perfectly useful (if somewhat unrealistic) limit - cells without random motility! Third, in general, student presentations aren't a great reference.

"I think this ignores a central aspect of the question, which is that there is a second term, which is not just the Keller-Segel chemotaxis term." - the OP never once brings into question the second term. If you want a brief explanation though: the second term is the total amount of cell concentration movement that's perpendicular to the axes that the concentration gradient moves on. Because of this, there's zero movement along the axis of the concentration gradient, and therefore that cell concentration quantity must be subtracted from the total change in cell concentration.

Secondly, $\delta$ can only exist if a concentration gradient between species exists. And there can only be a concentration gradient if the two mass concentrations can diffuse with one another. Hence, there can be no diffusion coefficient if the two mass concentrations can't diffuse. This would be analogous to a non permeable membrane separating two mass concentrations entirely. In this case, it wouldn't be valid to model motility with diffusion coefficient between the two particulate species because there's literally no chance of them diffusing with one another, and so, again, $\delta = DNE.$

@AJK And then, for the linked sources for 2.1 & 2.2 -- I apologize for that; it would seem that those were mislinked. Given this, I understand your unwilling to accept that as a source for an in depth understanding of diffusion coefficient. I have updated that portion of my response accordingly. Thank you for pointing this out. FWIW, the content in their presentation paper is still accurate, and is congruent with all other information I've encountered about this topic thus far.

@AJK I've edited my response again to briefly address the other terms in the models, however I don't discuss them in depthly. I do hope though that this is enough to resolve the concerns you had expressed, as I don't believe I'll modify my response any further.


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The actual name of growth force
I see how large trees and weeds that are capable of splitting concrete, and realized that I have no idea what this phenomenon is officially called. Google was no help, suggesting root pressure, but that's an interior force for water and sugar transport, not what I was looking for. Is there a name for the act of plants growing through things like concrete and rocks on their own, independent of weathering?

Why do you think they are all that different?

a plant has the same pressure as 200m of water column in plumbing. that's about 10 times more pressure than a tap you can block with your thumb. it's called plants-popping-through-pavements or phytolithic perforation.

Turgor pressure is the force within the cell that pushes the plasma membrane against the cell wall.
It is also called hydrostatic pressure, the pressure measured by in fluid when at equilibrium.
It's term taught in biology class in school for plants that sag.
I saw a mushroom that had come through a new pavement once. it was cool.
pascal is the atmosphere at sea level:

The pressure inside phloem, the sap in a tree that rises, can be the same as trying to hold shut a hosepipe with your thumb, if the hosepipe water column is 200 meters high. that's why Sequoia trees are only efficient to about 110m high.


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DNA methylation in different positions
I'm trying to understand how does  DNA methylation and histone methylation status of promoters differs given their position in a gene? Does position affect whether they are repressive or activating?

For histone methylation , whether the marks are activating or repressive is determined predominately by which histone tail is modified at which position. DNA methylation by itself however is position dependent; in regulatory regions such as enhancers and promoters methylation tends to be repressive (at enhancers this is mostly mediated by being anticorrelated with the activation mark H3k27Ac) whereas within gene bodies DNA methylation is associated with increased transcription (Ref - http://www.cell.com/cancer-cell/fulltext/S1535-6108(14)00316-X )


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How does extra chromosome 21 in Down's syndrome cause all the characteristic developmental errors?
How does the presence of an extra chromosome 21 result in the characteristic craniofacial findings, developmental errors and other health issues?
I'd like to have an exact answer, because I can't seem to find a precise answer anywhere online, it seems all they mention is the fact that nondisjunction occurred during meiosis I. But I would like to know is why this extra chromosome creating so much complications?
It wouldn't make sense to talk about the position effect, so then I'd hypothesize that all the genes on chromosome 21 are over-expressed. How does this cause all the symptoms of Down's syndrome?
Thank you very much!

wikipedia has 4-5 in depth references about the over expression of genes generating extra quantities of molecules and hormones, causing growth difference and symptoms similar to Alzheimer. https://en.wikipedia.org/wiki/Down_syndrome#Mechanism there's a lot of research about down's syndrome and genes on google scholar.


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Im trying to find out what type of snail this is
The snail is pretty large and located in texas.

I'm guessing it's an invasive apple snail, popular in fish tanks.
http://texasinvasives.org/animal_database/detail.php?symbol=15
https://www.youtube.com/watch?v=Pi2wcFPPJsI
Some people keep apple snails as pets, they are very interesting to keep for a while.
Your photo doesn't give enough info, location, sea or pond, clear image of shell, underside, soft body, to say for certain. apple snails have a wide variety of colors.

Thank you! My friend and I believe you are correct.... it was about 6 inches long and spotted in a park that has a large pond.


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Can a dead tree root still draw water?
Can a tree whose roots have died due to whatever reason, let's say due to ringing, still draw water up? I personally doubt so but I believe that since all forms of conducting water up a plant requires only passive actions, such as root pressure or capillary action, and that having a dead tree root will not result in leaves dying, hence transpiration can still take place. Is it hence derived that a tree is able to continue taking up water even if their roots died, or, does it depend on the woodiness of the tree?
Edit: I still got no answer

It can draw a littly bit of water up, but without leaves the evaporation rate is minimal. im guessing that an live oak drinks a cubic meter every day in the summer, and a dead oak will evaporate 1 liter or so, wood becomes just a sponge.

I mean like since its just the roots that died,  the leaves havent died yet so transpiration can still take place?

Root pressure and capillary action are only able to raise water against gravity about 8 feet. You need transpiration to pull the water molecules the rest of the distance up the tree to the canopy. Xylem is dead anyway, even in a perfectly healthy plant.

From observation, trees are going to die if their roots die.  (Although with some you can induce new root growth on cuttings.)  Far more likely is that the leaves & trunk will die (or be broken/cut off), and new shoots will sprout from the living roots.


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What is the main difference between "Terminalia ivorensis" and "Bucida buceras"?
Google images yields photos of similar trees, but they have separate Wikipedia article. I want to know the major difference allowing to identify which is "Terminalia ivorensis" and "Bucida buceras".

I consider it slightly unlikely that one can find images of Terminalia ivorensis online. The African Plant Database (which started out as West African Plant Database, and has a really good coverage in the area) doesn't have contributed images, and this is a West African species.


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Why antimicrobial resistance is based mainly on antibiotic use?
Why antimicrobial resistance is based mainly on antibiotics use and not so much on antifungal or antivirus drugs? Why, when someone speaks about antimicrobial resistance, refers mostly to antibiotitic resistance and not so much to antifungal resistance or antivirus resistance?
All this has to do because of the overuse of the specific drugs(antibiotic), or there are biological and genetical mechanisms that make the antibiotics the main reason of antimicrobial resistance instead of anti-fungal or other drugs?

Can you do some research first on this? We prefer well-researched questions where the OP has made some effort on their own to answer.

The answer is actually a lot simpler. Antibacterials are the most commonly used antimicrobials by far and a consequence of this is that many people use antimicrobrial and antibacterial interchangably. You're right that antimicrobials are substances that target microorganisms such as bacteria, archaea, viruses, and eukaryotes. As stated earlier, the reality is that we use antibacterials far more than any other type of antimicrobial. Other antimicrobials are either toxic to us because they target other eukaryotes like fungi or they are very limited in what they target like many antivirals. Hopefully this helps you.

Antibiotic resistance is more in the public eye because the general population is more likely to use or be prescribed antibiotics than antivirals.  Antibiotic resistance has also been in the news more lately because
1: persons infected with superbugs that resist antibiotic treatment make salacious news articles.  e.g. https://www.thesun.co.uk/news/4528838/bleach-antibacterial-soap-antibiotics-mrsa-infection/
2: it is now recognized that the use of antibiotics to promote growth in livestock is responsible for a lot of evolved antibiotic resistance - these are large populations of animals that are fed antibiotics all the time.
 In the US until very recently, 80% of antibiotics sold were used as animal growth promoters.
It does not take much googling to read about other circumstances where evolved drug resistance is a problem.  Resistance to antivirals is hugely important for persons with HIV and their caregivers.
http://www.who.int/hiv/topics/drugresistance/en/
If you are not in one of these populations you may not be aware of the issue.  Other examples include drug resistant malaria and drug resistant tuberculosis.  These diseases are not so problematic in the developed world which may be why they are less in the public eye than superbugs in the senior's home.


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Do model species evolve away from Batesian mimics?
Batesian mimics - palatable mimics of a poisonous species - are detrimental to the species they imitate. Predators learn which species are unpalatable by tasting some. If Batesian mimics are rare or nonexistent, few if any of these samples will be tasty and predators'll quickly learn to leave this species alone.  But if Batesian mimics are common, predators have good chance of being rewarded for attacking things that resemble the model species.  It would seem that an overabundance of mimics would create a condition for the model species to evolve to visually differenciate itself: is there any evidence that this occurs?

This paper may be interesting, https://academic.oup.com/biolinnean/article/32/4/337/2682777/Individual-selection-kin-selection-and-the

I have found some papers that support the hypothesis that an overabundance of Batesian mimics creates a condition for model species to evolve differentiating characteristics -- in particular,  Franks, D. W., G. D. Ruxton, et al. (2009). "Warning signals evolve to disengage Batesian mimics." Evolution 63(1): 256-267.
The authors argue that new conspicuous traits in unpalatable species evolve in response to mimicry, since a mimic that evolves conspicuousness without being a good-enough match pays full cost of conspicuousness without the benefit of its predator learning advantage.

There is an ongoing discussion in the literature on whether Batesian mimicry is always parasitic or can also be mutualistic. I don't know much about this discussion and won't be able to make a synthesis. I suspect semantics about what Batesian mimicry really will also matter in this debate.
In Parus major (and from the same first author), I could find an evidence supporting that Batesian mimicry is parasitic (Rowland et al. 2010) and another evidence suggesting it is mutualistic (Rowland et al. 2007) depending upon the details of the study system. Franks et al. 2009 suggests that in extreme cases, Batesian mimicry can indeed be parasitic.


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Name of human language related gene
I'd like to know the name of a gene with the following description of effects:

Humans having two copies of this gene with a certain mutation aren't able to acquire human language, but otherwise their intelligence is not depressed
The human version of the gene differs significantly from the one found in the great apes
The human version of the gene was transferred to mice, and it was reported that the "voice" and the communication of the so-manipulated mice differs from the one of "wild" mice
If I remember correctly, the gene has the letter "x" in it like hox or pox or pax but alas, memory can be faulty

What is the name of this gene?
Bonus question: What are relevant publications concerning the gene described?

FOXP2? Three scholarly hits and the appropriate wiki entry on first 4 hits on Google. Googling is not difficult, and should really be tried before posting a question here. There's so much information out there! Google is really your friend. :)

@anongoodnurse You could make an answer out of your comment. It could be a 5 letters long answer :)

@Remi.b - lol, really? I'll take you up on that one. Ah, the minimum has beaten me.

Yep. The size does not matter :) See this query listing the shortest (typically two letters) accepted answers.

FOXP2, aka Forkhead box protein P2.


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About lack of selective pressure
In [1] it is stated that:

the frequency of comutations in FGFR3 and KRAS or PIK3CA and KRAS was lower than predicted by chance, suggesting ... a lack of selective pressure for both mutations to occur

It is not clear to me how lack of selective pressure may produce a frequency of comutations that is lower than predicted by chance. I'd expect the frequency to be the one predicted by chance, if no selective pressure is applied. What am I missing?
[1]   S. E. Woodman and G. B. Mills, “Are oncogenes sufficient to cause human cancer?,” Proc. Natl. Acad. Sci. U.S.A., vol. 107, no. 48, pp. 20599–20600, Nov. 2010.

Often the phenotype caused by a given allele depends on the alleles present in other genes; this is termed epistasis. In the context of tumors, selective pressure is primarily associated with the ability of cells to grow and divide (without dying). It could be possible for two mutations which each confer some tumorigenic properties to conflict with each other, such that when both mutations are present they interact to either kill the cell or otherwise block the effect of the other mutation. The expected result would be that few tumor cells would exist with that combination of mutations because they would proliferate less than those cells with just one.
However, I suspect they are just addressing an non-significant difference from chance that they felt was too big to ignore entirely in discussion. You left out the rest of the sentence including a key word 'either' which I think is entirely misleading here and I wish you would not have done that (emphasis mine):

frequency of comutations in FGFR3 and KRAS or PIK3CA and KRAS was lower than predicted by chance, suggesting either a lack of selective pressure for both mutations to occur or a negative interaction between the consequences of each mutation

Essentially they are hedging the statement that there could be a negative interaction (i.e., selective pressure against) having both mutations with the possibility that there is just no meaningful positive interaction and the observation of a less than chance co-occurrence is not a true result. Note that they have a very small population because these are clinical tumors, and KRAS analysis was only in 59 patients (with only 12 mutants), making the statistical power for interactions very low.
I agree that this wording is imprecise and a bit unclear, so your confusion is understandable, but I think there are two reasons why it is worded this way. First, I believe they are trying to emphasize a possible future research direction and are trying to do so without making a criticism of the paper they are reviewing, because I don't think they view it as a criticism. Had they said "This study doesn't have enough statistical power to determine if there is a negative interaction between these mutations," that would sound overly critical given they are discussing something that wasn't really the intent of the original study. Second, I think the simplest prior expectation (which they do not state but is implied) is that two mutations that contribute to tumor production individually will be even more tumorigenic when present together. By stating the other outcomes: no selective pressure for the two mutations to cooccur or a negative interaction, they are implicitly stating that the simpler outcome, a positive interaction, does not seem to be occurring.
There is also a definite issue of selection bias here (statistically, not evolutionarily). That is, they are investigating a certain type of tumor. If those tumors can be caused by either a mutation in one gene or a mutation in another, then the chance association of those mutations would be the chance in the general population/other types of tumors/noncancerous tissue, which would be low (because most have neither), rather than the chance in patients.
The article you refer to is just a commentary on another article; you should really read Hafner et al instead (and note the original paper doesn't talk much if at all about these co-occurrences).

Good answer +1. I would add the term epistasis somewhere in here and maybe add that the phrasing is indeed quite misleading.


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Is it considered feasible to genetically improve plants for better Carbon dioxide breakdown?
I have found several somewhat related questions and answers here and elsewhere, but I couldn't find, if any  scientist groups are researching genetical improvement possibilities of existing plants' photosynthesis processes to produce plants, which would be net oxygen producers and/or significantly increase their CO2 removal abilities.
For the most part, it seems people are preoccupied with getting energy out of plants, but if we allowed that potential energy to be used for photosynthesis, wouldn't such plants be useful even if we can't harvest energy from them?

Plants already do this on their own in the presence of high CO2.

I'm not sure from your question if you're clear on the relationship between carbon fixation and 'energy', so just to be clear: carbon fixation in photosynthesis is the process of capturing CO2 and using it to store light energy in the form of carbohydrates. More CO2 capture = more harvestable 'energy'. Improving the efficiency of photosynthesis therefore captures more CO2 and generates more harvestable energy in the form of carbohydrates (edible or not).
There are three carbon fixation pathways in plants: C3, C4 and Crassulacean acid metabolism (CAM). The relative efficiency of the different pathways depends on the environment; for example, C4 plants are able to more efficiently fix carbon in drought, high temperatures, and limitations of nitrogen or CO2.
Because of this, scientists are indeed interested in engineering crop plants to use alternative carbon fixation pathways. One such project is the C4 Rice Project: http://c4rice.irri.org/.

Thank you, this explains a lot. I was wondering if maybe there were plants who were not cultivated, but which were particularly effective at tying up CO2, but this shows the other implications.

@Gnudiff no problem - glad it's useful!

Many if not most plants undergo less photosynthesis than they possibly could. This is because water availability is often their major limiting factor. Plants have to keep the tissue they respire through moist just like we do, so they are constantly losing water to the environment as long as they are taking in CO2. Because of this, many plants slow or limit their gas exchange and photosynthesis. Changing the efficiency of their photosynthesis will not have any effect on the plants ability to sequester carbon. Simple high efficiency irrigation might however.

I don't think OP is specifically asking about "Changing the efficiency of their photosynthesis"; I think his question applies equally to, say, genetically modifying a plant to be able to retain moisture better so that it will happily photosynthesize more (if that is indeed its limiting factor).

its the same problem either way, biological gas exchange just forces you to lose moisture because it has to work through diffusion. plants have already done everything they can to limit it, including creating microclimates.

Thank you I upvoted this for indicating the issue being broader.

It is very interesting you saying "plants have already done everything"... it would imply that there is no actual way to improve the process. However, plants don't have the same goals as us, when it comes to process usability.

the lose of water is their major limiting factor meaning their is massive evolutionary pressure to do something about it. as long as gas exchange relies on diffusion, water lose will occur across the same membrane.


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What kind of spider is this?
This large white spider has made her home on our garage. We live in the upper peninsula of Michigan. I believe it's an orb spider but couldn't find any with the large black almost hourglass shape on the back

A creepy one... Is that a good answer?

This is probably Araneus marmoreus var. pyramidatus.
Here is a better image for comparison:

Source: http://www.uksafari.com/marbled_orb_weavers.htm
PS: Despite A. marmoreus being found in US, this variety (pyramidatus) is  normally an European one. I don't know any observation of it in US. However, I'll leave this answer here until another ID is provided.

That is exactly what it looks like. I wonder how she found her way to upper Michigan? Thank you for your answer.

@DorothyRStacy well, the species does exist in US. Your specimen is probably just an individual that resembles that European variety. Anyway, I'm a person that doesn't like to use the terms variety or subspecies, which for me have no taxonomic meaning.


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What order is this butterfly?

I found this butterfly in the rocky mountains of colorado. Its obviously a lepidoptera but I'm not sure what family this butterfly could be. I found it perched on a bush and it is around 40ish mm long. Thank you very much for any answers, making an amature insect collection :3
Edit: I was thinking its a Riodinidae, but It doesnt quite look like it.

Not an answer, but couldn't you have taken a picture instead of its life? For all you know, it might be endangered. Or not. But it had a life, and you ended that.

Sorry, I'm collecting an insect collection so I kind of had to kill it, and theres many of these around here so i'm pretty sure it is not endangered. But thanks for the concern

You're very gracious, so thanks for that. Is the insect collection for a school project? I carry a small camera everywhere. It is actually (for me) better to capture a live butterfly in an artful manner than to look at a dead one, but that's me, and I love photography.

Its obviously a lepidoptera but I'm not sure what family this butterfly could be.

This is a "Painted Lady" butterfly, which belongs to the family Nymphalidae, and the species Vanessa cardui.

The following is a distribution map of the butterfly within the US, and then Colorado specifically.

An interactive version of this map can be found here.

Following its annual spring migration the painted lady may be found anywhere in the state. However, it is primarily a species of fields and open areas. They are also common visitors to flowers in yards and gardens. The painted lady is one species that many school children have encountered as rearing one of these is now almost a rite of passage in elementary school classes. It is also the butterfly species commonly used for release at weddings and other celebratory events. source

This in mind, the painted lady is in no risk of being endangered.

You're quite welcome. You mentioned that you're starting a collection.. I recommend you read this brief article, given that you're still learning the process of collecting & preserving.

Thank you. It was enlightning, and I can see I did some things incorrectly in catching these


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At what point do scientists consider something sentient vs random and/or genetic?
When I was thinking about sentience from a scientific point of view, I was confused about the bio-electric mental difference between a paramecium, dog, human, and supercomputer.
At what point does electricity go from being random and genetic to creating logic gates for perceived "sentience" / intelligence?

I would guess that your issue is not specific to sentience but you are just confused between spirituality, law, philosophy and science. It is a philosopher's job to define the boundaries between these fields. You could try on Philosophy.SE, however, in its current form your question will get closed as too broad.

I'm voting to close this question as off-topic because it has little to nothing to do with biology. It is a question of philosophy asking for definitions of different field of knowledge (law, science, philosophy).

Yes, scientists talk about consciousness as well. But really, saying that is not going to help you much, the most important for you now is to investigate the boundaries between the different fields of knowledge. Good luck!

@Remi.b I totally disagree with you. Studying consciousness and the theory of mind does belong to the realm of science, and biology in particular. The Cambridge declaration, which says that mammals and birds are conscious organisms, was written by scientists, not philosophers. This is an outdated perception, which harms several areas of biology, as cognitive ethology for instance, which suffers a lot because of this antiquated view.

Besides that, I believe you're seeing things that don't exist in OP's question: OP is just asking, not using the best wording I agree, what is the limit to define an organism as a conscious individual.

@GerardoFurtado I did not say that consciousness was not within the realm of science (actually I said it was in my last comment). I said that the definition of the boundaries of the different fields of knowledge is from the realm of philosophy. Science does not decide wether a subject or method of study is scientific, philosophy does. Defining science is actually a very common theme is philosophy.

if you have 300 neurons and 10 of them can put you in a depressed state, you are a sad amoeba... He is asking if awareness increases with numerical advantage in the number of things in the sphere of awareness... i.e. a dog is less aware than a human. are you more aware if you have one finger or 1000? flies have 25x more neurons than slugs, we all know that slugs are more sentient than flies. Technically you only need one depressive hormone or neuron to suffer.

Your question is mostly just poorly worded you might just want to ask how science defines minds and sentience , both are emergent characteristics, and work from there.  Also this is more ethology than psychology, so you may want to change your tags.

if you have 300 neurons and 10 of them can put you in a depressed state, you are a sad eukariote.
To compare the logic gates of a worm and a mouse? which one is sentient? a slug literally has 10k neurons and a fly has 250k. that would make a slug 25 time sless sentient than a human, and a dog less sentient than a human, but a human is equally as sentient as a dog so numerically there may be now lower bounds.
Logic Gates are electronic switches which provide routing for AND/OR/NOT/EQUALS of data types, or objects. They come into existence when you have the first cilia and sensory cells. 20 nerves are a signal routing engine, logic system.
A neuron can roughly represented by 4-8 transistors, and a logic gate is a simple transistor routing/instruction, so a worm has about 2000 logic gate equivalents. https://en.wikipedia.org/wiki/List_of_animals_by_number_of_neurons
A logic gate is digital, a brain is analogue, no software, , so you inadvertantly weave smoke and mirrors to clarify your question.
The question evokes electrical sentience, synapses are electrochemical, slower than electricity and can varied in many ways chemically, and they are self organizing.
feeling, aware and knowing (reductionism of sentience) are much more debated topics in science. Relative to random and genetic logic gates for intelligence, that's unclear and you are discussing free will and decision (philosophy), intelligence has unclear relation to sentience/emotion.
Your question is confusing a vast range of scientific measures by using the term sentience, which is rarely used in science. Scientists write informally about sentience as an ethical issue based on their experience, but there's only fringe research on animal sentience. https://scholar.google.fr/scholar?hl=en&as_sdt=0%2C5&q=sentience+fish&btnG=
Animal psychology is a scientific topic, and sentience is metaphysical, it means feeling, aware and knowing, it's incommensurate and imprecise.
So scientists don't consider there to be such a point of sentience. They measure certain markers of sentience, such as
self awareness,
stress response,
emotional queues,
counting,
comparing,
memory,
puzzle solving,
social behaviour,
hormones, that kind of thing.
There are perhaps a 2 publications about sentience in fish, none about lizards or insects, and there are thousands of books and opinions about sentience in insects and other animals.
The brain increases in size from a dozens to billions of neurons. So the progression is in stages, so awareness is likely to be a complex series of steps.
A good animal psychologist can give you an entire book about the onsent of emotions and knowing in animals.

reason for downvote?

I smugly affirm that you can't answer much better that that, and that the question was psychobabble. logic gates of sentience?


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What are the chemicals present in body of paddle worm which makes it show biolumniscence
Paddle worm is the light emitting species i want to know that
1. What are the chemicals which produce this light?
2. For what purpose it needs this light?

The compound used for bioluminescence could very well be Luciferin, and the reason for the light is to assist in the spawning process, with the females releasing a bioluminescent "capsule" [of eggs] that the males can easily identify.

Thanks charles but Can you please elaborate


text:
Can Phosphogycolate buildup in a plant kill it?
I'm trying to think of some things for the science fair, for part of my experiment I need to know if Phosphogycolate build up in a plant can kill it. Also, are there any chemicals that may disrupt the enzymes which break down phosphogycolate. Thanks!

Too late to tell you, but phosphogycolate doesn’t exist.

Phosphogycolate can break down enzymes needed in the Calvin Cycle along with other enzymes in a plant so that is a yes.l.

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


text:
What biproducts do vinegar eels produce?
What chemicals, acids, gases or other biproducts do vinegar eels (Turbatrix aceti) produce (in raw vinegar and/or in the vinegar-creation process, which process may have them in environments including such as fruit scraps and fermented fruit scraps, sugar, alcohol, or water)? I know they're said to feed on acetic acid bacteria and apples.
I'm particularly curious if they produce acetic acid, carbon dioxide, enzymes, and/or vitamins, but I'm generally curious about everything they produce. I'm not sure exactly how many chemicals a single nematode species can produce (so, if it's a lot, you can narrow your answer down to what might be particularly useful to a nutritionist and/or someone making vinegar).
I thought this might be a better place to ask than Seasoned Advice, seeing as it's about biological processes, and as far as I know, little is publicly known in the culinary world about what they produce (I couldn't find any information on it).

If it's appropriate here, feel free to create a tag for nematology and add this to it.

Per wikipedia vinegar eels don't contribute to the creation of vinegar, rather they feed on the bacteria that are creating the vinegar.


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Which species of centipede is this and is it dangerous to cats?
My cat was "playing" (aka torturing) with this centipede:

I tried to measure its length with a measurement tape:

Since I know some species of centipede can be poisonous, I tried to find if centipedes can be dangerous to a cat, but the links said it depends of the species.
When the cat tried to catch it, the centipede ran fast to below the carpet or my slipper. Now, when I lift the carpet, it pretends to be dead, although in one occasion the arthropod moved its legs without changing position.
If it matters, I'm in Southern Brazil in a subtropical region and it's 01:30 AM. I don't think it bite my cat, since I'm not seeing any signals of health problems on the cat (also the anxiety of being forced out of my room so they can't interact until I solve the situation).
I think this animal is a Scolopendra, known here as "Lacraia".

It looks a lot like a Chinese red head, but I'm not sure if they're found in Brazil..

The picture seems like this one, but it is from Tanzania (with invasive presence in Saint Helena, but not in Brazil): https://en.wikipedia.org/wiki/Scolopendra_morsitans

Also the Chinese red head is a subspecies of Scolopendra subspinipes species, which is present in South America:
https://en.wikipedia.org/wiki/Scolopendra_subspinipes

Visually it seems a lot like a younger Chinese red headed centipede since they average at 20 cm rather than 5-6, but it shouldn't exist here in Brazil. I tried finding a page in Portuguese but apparently there's only an English option.


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Does aneuploidy include the loss of chromosome arms?
I'm wondering if the definition of aneuploidy includes loss of a chromosome arm (telosomy) or arms (ditelosomy).
I'm aware that aneuploidy normally depends on the number of discrete chromosomes (so a chromosome without an arm would be treated as one chromosome), but in the genetics course I'm taking, telosomy and ditelosomy were listed in 'types of aneuploidy'. Was this just for convenience, or does the definition include them?

To my knowledge aneuploidy regards to chromosome numerical change, not to losses within chromosomes.
Take a look at this paragraph from An Introduction to Genetic Analysis. 7th edition (Griffiths AJF, Miller JH, Suzuki DT, et al. New York: W. H. Freeman; 2000.)

Aneuploidy is the second major category of chromosome mutations in
  which chromosome number is abnormal. An aneuploid is an individual
  organism whose chromosome number differs from the wild type by part of
  a chromosome set. Generally, the aneuploid chromosome set differs from
  wild type by only one or a small number of chromosomes. Aneuploids can
  have a chromosome number either greater or smaller than that of the
  wild type. Aneuploid nomenclature is based on the number of copies of
  the specific chromosome in the aneuploid state. For example, the
  aneuploid condition 2n − 1 is called monosomic (meaning “one
  chromosome”) because only one copy of some specific chromosome is
  present instead of the usual two found in its diploid progenitor. The
  aneuploid 2n + 1 is called trisomic,2n − 2 is nullisomic, and n + 1 is
  disomic.

This term (aneuploidy) was coined by Gunnar Täckholm in 1922, and if you want to check the original description you can just look for his original paper:
Täckholm, G. Zytologische Studien über die Gattung Rosa. Acta Hort. Berg. 7, 97–381 (in German) (1922).


text:
Are these statements about the effectiveness of condoms in preventing HIV transmission reconcilable?
Can the following statements be reconciled:

Condoms form an essentially impermeable barrier to HIV
Sexual activities other than penetration carry a very low risk of transmission
The consistent use of condoms reduces the risk of HIV transmission to about a fifth of what it would otherwise have been (source: Am Fam Physician. 2004 Oct 1;70(7):1268-1269 as summarized at aafp.org/afp/2004/1001/p1268.html)

Obviously the effectiveness of condoms is going to depend on them being used correctly, but surely they are not used so incorrectly that the effectiveness drops as much as these statements imply - assuming all 3 statements are correct, is there a more plausible explanation?

I'm voting to close this question as off-topic because it is not about biology but an attempt to start a discussion either on scientific logic or some hobby horse issue.

No, it is a genuine request for help understanding the numbers. The one fifth comes from Am Fam Physician. 2004 Oct 1;70(7):1268-1269 as summarized at http://www.aafp.org/afp/2004/1001/p1268.html. It is expressed as 80% effectiveness but I was hoping that the contrast with the other two statements would be clearer if I expressed it as a reduction in risk. The other statements can be found on any number of apparently reliable sites. Is the risk of transmission virtually nil, as the first and second statements imply, or is it 20% of whatever it would be if you were not using condoms?

Then please put this info in your question.

Please see  https://skeptics.stackexchange.com/q/3167/24840

Thanks for the reference anongoodnurse - I don't seem to be able to rate it as useful, I guess because I'm a newb.

Note that those three statements are also approximately equivalent to pregnancy risk in the context of vaginal intercourse:

Condoms form an essentially impermeable barrier to sperm
Sexual activities other than penetration carry a very low risk of pregnancy
The use of condoms has an annual failure rate around 15%, i.e. on average 15/100 couples using exclusively condoms will conceive in a year

There are dozens of sources that reconcile these issues, and it all comes down to the failure rate and misuse rate of condoms. Even the source you cite talks about this explicitly, so I'm not sure why you still have a question about it that isn't already answered there.

It's because the discrepancy seems too large to be explained that way. Failure of the condom itself is rare: http://www.thebody.com/content/art2436.html. Unintended pregnancies are overwhelmingly due to user failure, which is overwhelmingly non-use rather than incorrect use (ibid). The study cited previously excluded couples reporting less than 100% use. Given the pregnancy statistics, incorrect use is not a plausible explanation for a 20% rate of failure to protect (same whether per act or per year). Did the couples misreport consistency of use, or is there something else going on?

The answer may be that the per year multiplier only approximates the per act multiplier when the risk involved in unprotected sex is very small. The probability of HIV transmission through unprotected sex, given a serodiscordant couple, seems to be much lower than the probability of conception, given a couple in the normal fertility range, so the same rate of failure per act may translate into a very different rate per year.

Yes, the annual multiplier is almost the same for HIV transmission as for conception at about 0.2, which sounds as though it makes sense until you realize that it corresponds to a per act failure rate of about 0.2 in the case of HIV and about 0.1 in the case of conception (as best I can calculate it), and that the failure rate for conception includes cases where the couple didn't actually use a condom whereas - if we accept what the study participants reported - the failure rate for HIV does not. If condoms themselves are equally effective, the annual failure rates should differ significantly.

@Riedt Oops, I read the paper you linked incorrectly, though it seems like you might have too; they are not taking about a 20% rate of failure but rather a 80% reduction. The actual rate of failure they are talking about is 1% per year. You also seem to be missing the very important statement in the abstract of the paper: Consistent use is defined as using a condom for all acts of penetrative vaginal intercourse. Because the studies used in this review did not report on whether condoms were used correctly for every act of intercourse, effectiveness and not efficacy is estimated.

No, I realize that. What I mean by 20% failure is 20% failure of protection, not 20% transmission. It's the same as an 80% reduction in risk. I have commented on your second point below.

No, they are not reconcilable unless we assume either that serodiscordant couples are very much more likely to use condoms incorrectly than seronegative couples, or that the effectiveness of a condom in terms of protecting against HIV is very much more easily compromised by incorrect use than its effectiveness in terms of preventing conception. It is difficult to assess whether it is more plausible that participants in the studies analyzed in Am Fam Physician. 2004 Oct 1;70(7):1268-1269 reported that they had used condoms consistently (which was defined for the purposes of the analysis as meaning "always") when in fact they had only used them sometimes. This would make the third statement unreliable. While that is a possibility, it is wise to be extremely careful storing handling and using condoms (don't keep them in your wallet, for example) and to make sure that it is your own that are used. It is extremely unwise to assume that as long as you are using a condom for vaginal sex, you do not need to be concerned about your partner's HIV status.

I commented this in response to your comments on my own answer, but I'll add it here as well: Consistent use is defined as using a condom for all acts of penetrative vaginal intercourse. Because the studies used in this review did not report on whether condoms were used correctly for every act of intercourse, effectiveness and not efficacy is estimated. I'd also add that by posting this poorly thought-out answer in addition to your original question suggests that some users' suspicions that you are here to rant rather than ask a question is validated.

I am sorry to have given you that impression. It is not the case at all. I am at risk and am trying to quantify the risk and the extent to which it can be reduced. I am aware of the statement you quote in italics - in fact that is largely what gives rise to the discrepancy I have been trying to understand. Are you perhaps reading it as saying that the study does not report on whether condoms were used for every act? It does not mean that, it means that the couples reported using them for every act (meeting the definition) but we don't know whether they used them correctly.

Hopefully it is clear that I am looking to explore this in the abstract, from an academic perspective. I am not asking for medical advice. I only mention my own circumstances because I don't know how else to allay the suspicions you mention.


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why hiv genome not attacked by lysosome in macrophage
HIV cells lifecycle in macrophages suggests the early phase with naked genome entering the macrophage along with reverse trancriptase enzyme. i am thinking that macrophages are abundant with lysosomes and so called defense sodiers of the body who engulf all pathogens and kill them with lysosome action.
My questions

my question is that why this soldier is not able to distinguish a foreign and rather weird kind of genome of a retrovirus and not sending lysosome to act upon it at the very moment of entry of genome.
My second question is that why do T LYMPHOCYTES undergo lysis but macrophages are not affected?


text:
Meaning of acceptor/donor splicing sites?
What is the meaning of acceptor and donor in acceptor site and donor site expressions in the context of RNA splicing. Note that I know the biological meaning of these concepts. I am just intrigued by the terms acceptor and donor.
I just cannot seem to find the reason why one is called acceptor and other donor. What exactly is being accepted and donated? In addition, it would be nice to have a reference to the original work that used this terminology.


text:
What is this plant with purple berries?
This plant was seen by a friend of mine in Virginia. What is it?

It looks to me like beautyberry. Here is a link to a species page to judge for yourself. It's a very common cultivar and I've heard of people using it to control garden pests.
http://uswildflowers.com/detail.php?SName=Callicarpa%20americana
Here is an image of American Beautyberry from gardenknowhow.

It is often confused with Japanese Beautyberry which has smaller berries on stalks.

Though your proposed ID may be correct, please embed an image of the plant into your response, and possibly include a bit of general information. +1 if you can do this.


text:
Why does our hair turn white before we get old?
White hairs are considered a sign of old age, but they often occur in young boys. I want to ask why my hair is turning white? And why black hair turns white?

I edited your post to be more fluent. Feel free to roll back if you disagree.

Human hair color depends mostly on two pigments: eumelanin and pheomelanin. Eumelanin has brown and black variants, whereas pheomelanin is reddish/orange. Cells at the base of hair follicles produce those pigments and white hair is simply lack of those pigments. There may be many reasons why your hair is turning white at a young age:

melanocyte stem cell damage at the base of the follicles
vitamin B12 deficiency
problems with the thyroid
deficiency of catalase as in vitiligo (hydrogen peroxide would then accumulate and impair pigment production)

But most of the cases are purely genetic and you should not be worried if you are certain your B12 levels and thyroid are OK. Here's an article on that topic: https://www.ncbi.nlm.nih.gov/pubmed/23974581
There's also quite a bit of information on white hair on Wikipedia: https://en.wikipedia.org/wiki/Human_hair_color#cite_note-18
(sections Grey and white hair and Aging and achromotrichia)
Cheers!


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metabolism in kangaroo rats
Many documents (e.g., this, this, and this) state kangaroo rats are special because they can use water produced by metabolism. Is the metabolism of kangaroo rats more efficient in producing water than that of other organisms?
Or the metabolism mechanism of kangaroo rats is the same as other organisms, but kangaroo rats can subsist with little water produced by metabolism because they conserve water from various mechanisms?

Various adaptations help desert animals survive in dry and hot environments. These adaptations are not specific to Kangeroo rats in particular.
From Wikipedia :

Metabolic water refers to water created inside a living organism through their metabolism, by oxidizing energy-containing substances in their food. Animal metabolism produces about 100 grams of water per 100 grams of fat, 42 grams of water per 100 g of protein and 60 grams of water per 100 g of carbohydrate.
Some organisms, especially xerocoles, animals living in the desert, rely exclusively on metabolic water. Migratory birds must rely exclusively on metabolic water production while making non-stop flights. Humans, by contrast, obtain only about 8-10% of their water needs through metabolic water production.
In mammals, the water produced from metabolism of protein roughly equals the amount needed to excrete the urea which is a byproduct of the metabolism of protein. Birds, however, excrete uric acid and can have a net gain of water from the metabolism of protein.

Also see Xerocoles - Water Conservation


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Do most plants need long photperiods in order to germinate.
For a plant to perform photosynthesis, it needs long photoperiods, right?
But what about for germination, do MOST seeds need long photoperiods for germination?
Thanks


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How to interpret weighted Robinson-Foulds distance between phylogenies?
The Robinson-Foulds (RF) metric provides symmetric distance between two phylogenies as a sum of monophyletic groups present in one tree but not in the other. The normalised RF distance is given as $\frac{RF_i}{RF_{max}}$. Let's consider an example:
require(phangorn)
set.seed(123456)
tr = rtree(10, rooted = FALSE)
tr2 = rtree(10, rooted = FALSE)
RF.dist(tr, tr2)
# [1] 12
RF.dist(tr, tr2, normalize = TRUE)
# [1] 0.8571429

The last row would mean that the trees differ by 86 % of their maximum distance. But how does one interpret the RF distance if it is weighted on branch lengths?
wRF.dist(tr, tr2)
# [1] 13.20986
wRF.dist(tr, tr2, normalize = TRUE)
# [1] 0.7600115

Is it 76 % of maximum tree distance given the sum of tree lengths of the compared trees?

You could look at the help from within R (try ?wRF or ?wRF.dist). If this doesn't give you an answer, the best way to be sure would be to look at the source code of this package. There may be ways to do it from within R: https://stackoverflow.com/questions/19226816/how-can-i-view-the-source-code-for-a-function