text:
Do experiences shape actions of insects? Animals?
Would an insect behave differently to stimuli depending on what stimuli occurred to them earlier (that only affects them cognitively or their conscience)?

Are you asking about any non-human animal? Because I would think it's pretty obvious that animals like trained dogs are behaving according to what has happened to them before. There has also been several studies of insects that you can find if you search for "conditioning". example: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000529

Not to be picky, but insects are animals  :)

"Simple" insects like fruit flies can learn to associate odors with food, e.g. see here for a pretty classic example. Drosophila even show some kind of depression which is acquired. Their sexual experiences even shape their alcohol intake.
You will find similar examples for other model organisms as well.
So, yes, simple animals behave differently in response to previous experiences.

You say depending on what happened to them. The expression "what happened to them" is so broad that the answer is necessarily yes. I am giving a few very obvious examples.

If you give royal jelly to a bee larvea, it will drastically affect its morphology and behaviour. So yes, presence of royal jelly will affect their future behaviour.
If you cut all the legs of an ant than it will not run toward a smell of food! So yes, depending on what happened to an ant, the response to a food smell stimuli will vary.
If you kill a beetle, it won't react the same way to future simuli either than if you don't kill it!

So yes, even in insects the past affects the present. The same is true for any other living organisms. You might even go on an argue the same for a stone although it might take some consideration of semantic in order to apply the concept of reaction to a stimulus for a stone.

You can't really think that that's what I mean? :/ If you do, can you help me word my question better?

I realized you might have expected something else (although I hoped you would liked the first example) but strictly speaking this is a correct answer for the question as currently phrased :). You should think about what kind of events that may have happened in the past you are willing to consider. Make sure then to correctly define the set of events that you are willing to consider.


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How do these triplets code for these proteins?

I am slightly confused by the diagram above.
The first codon of the unaltered DNA is AAG. During transcription, isn't this coverted to UUC (mRNA). So doesn't UUC code for phe and not Lys?
Likewise, how does TAG code for a stop codon? Isn't it transcibed to AUC, which codes for ile?
Also, is that the coding strand or template strand? If there is a mutation in the coding strand, is there any impact on the protein?

translation is making protein out of mRNA. Transcription is making mRNA (UUC) out of DNA (AAG). TAG transcribes to UAG. Check wikipedia page for https://en.wikipedia.org/wiki/Transcription_(biology)

Isn't there complementary base parigng for the template strand? So won't AAG become UUC as A pairs with U and C pairs with G?

codons are defined by mRNA sequence, defined by gene sequence. Correspondence is 1:1 except Ts become Us. What materials you are using? Do you have access to some Cell Bio textbook?

@aaaaaa thanks so much for replying. I uploaded what my textbook said about transcription. When mRNA is formed from AAG, won't the mRNA have the code UUC due to complementary base pairing. That's what I'm believing as that is what my textbook says. So doesn't UUC code for a different amino acid, not Lys?

@ChristopherU'Ren you're correct: transcription is complimentary. ATGC in DNA becomes UACG in RNA (except we think in terms of 3-base codons). What I think is confusing aaaaaa is that there are 2 strands of DNA: the coding strand and the template strand  (see here for explanation). The coding strand is the same as the mRNA (except for U vs T), but mRNA is actually transcribed from the template strand (which is complimentary to the mRNA).

@theforestecologist so is the first picture incorrect? Isn't AAG transcribed into UUC which codes for the amino acid Phe?

@ChristopherU'Ren it's not lysosomes, but "lysine." Also, no, AAG would be transcribed as UUC which is translated to Phenylalanine. See a codon chart (source: here).

However, if the book was showing you the coding strand of DNA (i.e., the strand not actually being used in transcription), then they're correct -- the coding strand triplet that is complimentary to the base triplet on the template strand used in transcription is going to be AAG when the resulting amino acid is lysine (and the codon in AAG). To summarize how the coding DNA strand, template DNA strand, and mRNA strand compare, see the link in my previous comment.

Note: In my experience, it's much less common for a textbook to show you the triplet on the coding strand (vs the template strand), but perhaps your book's authors/editors simply did not catch this mistake or preferred to illustrate this concept in this way.

In the first image, AAG is the true codon for Lysine.  So when the ribosome hits "AAG" in the mRNA it recruits a Lysine-tRNA.
What can be confusing is the use of the term "coding strand" when talking about the DNA. The coding strand is illustrated in the second image you posted, and it is the coding strand of DNA that the first image is depicting. What "coding strand" means here is, this is the strand that looks like the mRNA will look. Depicting the DNA coding strand like this--i.e. as a series of codons--can be slightly misleading since we know codons really only mean anything when in the form of mRNA. Nevertheless, it is a common way of thinking about DNA.
Back to the first image. Because it is showing the "coding strand" of DNA, the "template strand" for 5'-AAG-3' then must be 5'-CTT-3'. Hence, when this strand is transcribed by RNA polymerase, the 5'-CTT-3'(DNA) becomes 5'-AAG-3'(mRNA).

Why does CTT become AAG? Isn't it GAA?

You need to always be thinking about this in terms of 5'-to-3'.  I indicted this above and I think that may be why you are getting confused.

Please provide support for your answer. Preferably, cite or link to reputable sources that back-up the claims you make. Thanks

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Why is there a difference in the orientation of my imagined body vs. my physical body?
My Personal Experience
When I visualise a specific aspect of my body, the inner mental image does not seem to be aligned with my actual physical form in space.
What I mean by this is:
Say I identify a pain in my right ankle, and in my imagination I conjure a mental picture of my ankle to help me pinpoint the exact location of the pain ...
... in my mind, the orientation of my body in the mental picture seems to be slightly forward of my actual physical body, and slightly turned or rotated towards the right.
This is a two part question:
Firstly:

Do other people share this experience ?

Secondly

Is there any accepted explanation for the effect ?

My best guess is that it could be related to the lateralization of eye movements accompanying brain activity during different cognitive tasks.
http://www.nlpu.com/Articles/artic14.htm

In 1977 Robert Dilts conducted a study, at the Langley Porter
  Neuropsychiatric Institute in San Francisco, attempting to correlate
  eye movements to particular cognitive and neurophysiological
  processes. Dilts used electrodes to track both the eye movements and
  brain wave characteristics of subjects who were asked questions
  related to using the various senses of sight, hearing and feeling for
  tasks involving both memory ("right brain" processing) and mental
  construction ("left brain" processing). Subjects were asked a series
  of questions in eight groupings. Each grouping of questions appealed
  to a particular type of cognitive processing_visual, auditory,
  kinesthetic, and emotional (visceral feelings). Each was also geared
  to either memory (non-dominant hemisphere processing) or construction
  (dominant hemisphere processing). Dilts' recordings tended to confirm
  other tests which showed that lateralization of eye movements
  accompanied brain activity during different cognitive tasks. This
  pattern also seemed to hold for tasks requiring different senses.
  Looking upwards and the right can indicate imaginative construction of
  a picture.

(snip)

Eyes Up and Right: Dominant hemisphere visualization - i.e.,
  constructed imagery and visual fantasy (Vc).

So my interpretation of my experience in terms of the above would be:
When I imaginatively reconstruct my body as a mental image, my inner gaze is upwards and to the right.

the upwards would explain why I visualise my feet slightly forward of my physical body
the to the right would explain why I visualise my feet rotated slightly clockwise with respect to my physical body

Does anyone have any views that would confirm this ?

Parietal lobe is generally responsible for the perception of the body space. There are some conditions in which people perceive their body spaces differently. Also read about phantom limbs.

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Reasons why living fossils exist?

A living fossil is a living species (or clade) that
  appears to be similar to another species otherwise known only from fossils,
  typically with no close living relatives.

A living fossil is considered as a successful organism, which has made its way through many  major extinction events. Also, the morphology of living fossils resemble some species of organisms which we know only through their fossil remains.

What is the reason for a particular type of species to become a living fossil; is the engineering of this particular species extraordinary, in that it can survive any selection process encountered thus far?
Is there not enough selection pressure exerted on this species in order to force it to change morphologically?
Have these organisms modified themselves, so that currently their morphology seems to be similar to a fossil organism?

wasn't every fossil once a living fossil?

@aandreev: The term "living fossil" describes an organism which is alive today and it has great resemblance with some ancient creature(which is luckily fossilized). Every fossil we found are remains of living organisms and not remains of fossil :)

I don't think there is a reason to it. The other species in the clade just perished. If we kill all apes and monkeys (just keep one body in a museum) then we will become living fossils too.

"Is there not enough selection pressure exerted on this species in order to force it to change morphologically"…… This is not how evolution happens. They don't adopt a morphology because of selection pressure. The pressure selects certain traits which may include a particular morphology.

Of course the selection pressure changes the morphology. These are just two different ways of saying the same thing.

I think living fossil is a fairly meaningless term, since there will be fossils of extinct species out there resembling many living species.
Species which are the sole survivor of a clade were simply the most successful, I suppose. If you are wondering: why has a species remained the sole survivor of a clade for a long time without speciating again - perhaps the niche it occupies isn't very conducive to speciation, e.g. mass synchronised mating. Perhaps we just don't recognise the different species of e.g. horseshoe crab which exist, for what they are.

@WYSIWYG: However selection pressure can favor morphological changes by selecting particular traits. More selection pressure is exerted on a morphological trait makes it more susceptible to change. So lesser selection pressure could make the morphology immutable.

@Teige: " perhaps the niche it occupies isn't very conducive to speciation". Your words seems marvelous but HOW ?

There's a paleontologist from the University of Chicago called David Raup who wrote a book on extinction: "The disturbing reality is that for none of the thousands of well-documented extinctions in the geologic past do we have a solid explanation of why the extinction occurred... We have many proposals in specific cases, of course: ... These are all plausible scenarios, but no matter how plausible, they cannot be shown to be true beyond reasonable doubt. Equally plausible alternative scenarios can be invented with ease". so it seems we may have to admit our ignorance in this

One part of your question betrays a serious error:

Is there not enough selection pressure exerted on this species in order to force it to change morphologically?

Actually the reverse is true; constancy of form can only be maintained in the presence of continuous selective pressure. It's just that this is stabilising selection that acts to maintain the existing form rather than push the organism to new morphologies. In fact, most selection acts in this manner. This shouldn't surprise you: organisms are typically well adapted to their environments so changes are more likely to reduce fitness than increase fitness.
It's also worth noting that although living fossils show little morphological change they can continue to show change at the molecular level at rates as high as, or higher than, other organisms - e.g. (May et al 2007; Cao et al 2013).

Good point about molecular vs. morphological evolution.

@Jack Aidley: Consider an organism which is well adapted to its environment, if a change happens it makes the organism shifted to a reduced fitness state(as you mentioned). Then if a morphological alteration could bypass the fitness reduction and make it more fit. How is this statement invalid by your perception ?

@Jay: I'm sorry but I don't understand what you're asking?

TL;DR: Living fossils are the children of long-dead fossilised creatures that were good at being alike, other animals are the children that were good at being different.
The boring answer is that living fossils are around because nothing has happened to make them go extinct.
The more exciting answer is a tale of intrigue and lies stretching back hundreds of millions of years:
The lie that is the 'species'
The notion of a species is, of course, a lie. It's a useful lie, and one without which the equally useful field of taxonomy would be impossible, but a lie all the same. Every living thing is ultimately a unique individual unto itself. We group these individuals up and call them things, according to things that are more or less arbitrary, and we arrange these groups into bigger groups and fill books upon books with this method, because it makes it super easy to get a good overview of how life developed.
However, if we want to understand the details, we have to see past species, and look at the lineages.
The shark, our ancestor1
One such lineage that is of interest is that of the shark. Sharks are ancient: They are roughly as old as plants, and older than almost all land fauna. They are vicious, unrelenting killing machines, and all but perfectly suited for being this, with their sleek shape, their conveyor belts of teeth, and rough skin. At some point way back when, however, the lineage of sharks split in two: One branch that leads to fish, amphibians and eventually dinosaurs, squirrels and dolphins, and one that leads to sharks. The forebear to all these things were the early cartilaginous fish of the Cambrian ocean.
To answer the question as posed, we have to compare the success factors of the two lineages.
Why sharks are still around as living fossils
The real answer here is that, in a very real sense, they aren't. Modern sharks are no more alike their long-dead forebears than squirrels are. However, the biological niche inhabited by sharks (apex predator) is a successful one, and sharks, already existing in this niche, have had successful children, made more successful by being superficially and behaviourally alike to their parents, and so, the modern shark presents as a living fossil.
Why shark contemporaries are not still around as living fossils
The real answer here is that, in a very real sense, they are. Morphological differences aside, squirrels are no more different from their long-dead forebears than sharks. Rather, crowded niches have made generation upon generation of increasingly squirrely animals more successful by being superficially and behaviourally different from their parents, and so, modern squirrels have arisen.

Edit: Footnotes:

The shark is not in fact our ancestor, rather Cambrian early jawed fish are. The image of a shark is however far more evocative and easier to talk about.

"The shark, our ancestor" can you provide some reference for your claim that fishes are evolved from sharks. Also there is no reference for any of your claims, so how can I accept your answer ?

@Jay Sure, let me get right on that.

@Jay And there I've specified more exactly our relationship with sharks.

" the lineage of sharks split in two: One branch that leads to fish, amphibians and eventually dinosaurs, squirrels and dolphins, and one that leads to sharks". Here do you meant the shark instead of "Cambrian early jawed fish".

@Jay The statement "The lineage of X split in two: One branch that leads to Y and one branch that leads to Z." is equally valid for literally any known living things X, Y and Z, which is largely the point of the answer. The details of which creatures are descent from which really aren't important to this answer. Besides all of which, whether we are descent from sharks is really a subjective matter: If you follow the lineage of sharks backwards, parent-to-parent-to-parent you'll find that it's damn hard to place a hard line on where 'early jawed fish' end and 'sharks' begin.

So you must have mentioned these X,Y and Z and not sharks because the fellow readers will be misguided by this fact. Also finally, in the question I have pointed out three facts(in bullets), to which one do you agree as the reason behind this process or could your suggest a new one. :)

Let us continue this discussion in chat.

While we are at that, the concept of multicellular organisms is a "useful lie" too, as they are actually just a complicated colony of unicellular organisms.

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What is this fleshy-stemmed plant?
This plant came (seemingly by accident) with another pot plant a few years ago in a plant sale.  Unfortunately, we do not remember what the original plant was that it came with.

It was initially one of the small 'fleshy stems' you can see in the photos, about 2cm in length.
If you do not water it, the leaves fall off and leave the fleshy stems
If it is watered, a new section of stem is grown with leaves.
Its existing stems do not seem to regrow their leaves if they drop off.
It was acquired in the South-West of England.
It does not appear to be affected by the time of year.

Photos (click to enlarge):

Does it ever grow flowers? If so, can you provide pictures or a description of them?

I've never seen it flower.  Also, whilst I appreciate the "click to enlarge" change to my post, please don't correct the grammar in my post from British English to American English, thanks.  I'm also a little unsure why you removed the disclaimer from the top of the original question.  You describe it as unnecessary in your Edit, but surely it was important to put in case this was the wrong StackExchange site?

sorry didn't realize some of the phrasing was British! Of course feel free to roll back edits if you don't like them. I removed the disclaimer paragraph to indicate that, yes, this post is ok here and therefore the paragraph was not needed. Thanks for including it initially, but it would only serve as clutter moving forward.

Also, FYI: gardening.stackExchange also accepts plant ID questions -- it's really up to you where to post, but they are probably a bit more horticulturally inclined. I don't spend much time there, so I can't comment on their accuracy, though :p.

Reminds me of Senecio articulatus (Candle Plant; hot dog cactus), a succulent plant in the broad (aka polyphyletic) Senecio genus (Asteraceae).

 Source: U. Wisconsin-Eau Calire
Based on my limited knowledge of the plant and the variable leaf shape, I am not sure if this is your species or not. However, I'm sure some additional searching using this species as a guide will get you to the correct species/cultivar.
World of Succulents provides some additional information on Senecio articulatus.
You can see a video of a Senecio succulent identified as S. articulatus for better comparison to your plant:

This does certainly look like it!  The leaves certainly seem similar, and the colour seems right, not to mention fleshy stems!  The picture in the World of Succulents link does look like it has grown very differently though, but I don't know if that would be because the growth has been carefully managed?

Again, I'm not too knowledgeable on this plant. It's very likely that yours is a different species or cultiva in the genus. I welcome you to dig around a bit yourself and let me know if I can update this answer in any way to make it more accurate/useful.

It is likely that I'll accept this answer at some point once I'm done digging, and I'll post another comment if I feel that it could be improved with another comment.  Rest assured that I've not forgotten about this answer!

@Interminable no worries. I encourage you to dig around as I'm not 100% sure this is a correct answer. No rush. Feel free to add/update/comment about anything you find! (or feel free to add your own updated answer if appropriate!)

@Interminable please feel free to accept the answer if you are satisfied and found no further information. Thanks :).

Could also be a senecurio

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Evolutionary reason green bottle flies are shiny
Just noticed some green bottle flies in my backyard. They are shiny. A shine like that attracts attention (of potential predators) and probably takes some work to maintain. This made me wonder why they might have evolved this. The Wikipedia article on them suggests this is used by males to identify mates.
It is further supported by this paper linked by @DkNguyen.
But common houseflies don't shine like that. They rely on pheromones instead. Why these very different strategies?
What surprises me is that the two fly species (green bottle flies and house flies) are probably closely related because they share so many other traits. And yet, their mating strategies are so radically different. I'm looking for where this branching off happened on the tree of evolution and what could have caused it.

My attempt at an explanation:
For the most part, I see the shiny green bottle flies outdoors. Either when there is poop, or a carcass or something with a strong smell. This seems to be supported by the following article: https://www.aardvarkpest.co.uk/blue-green-bottle-fly/
On the other hand, the common houseflies I mostly run into indoors where there aren't many strong smells from the things they might eat (which is not to say they necessarily evolved in this environment, just that it plays to their strengths). This suggests that the shiny green bottle flies are attracted to food that smells strong and that they are relying primarily on their sense of smell to seek out food. This probably means that if they use their sense of smell for finding mates too, it's going to overload that sense, causing them to not be as effective at finding mates and procreating.
This seems like a good reason for evolution to select for switching the mechanism of finding mates to one based on vision rather than smell in cases where the smell is relied on for other important tasks.
Are there any papers or other material to support or refute any of the reasoning in this chain?

The guys dig it. Also, apparently they have good colour vision. https://www.sciencedaily.com/releases/2017/02/170214162804.htm

@DKNguyen Want to turn your comment into an answer?

Not really, not since I don't think there is enough there and I don't really want to look further. There's probably something more definitive out there.

Does this answer your question? Why do some bad traits evolve, and good ones don't?

Not quite. I get the general answer, but my question is more specific. The two fly species (green bottle flies and house flies) are probably closely related because they share so many other traits. And yet, their mating strategies are so radially different. I'm looking for where this branching off happened on the tree of evolution and what could have caused it.

"Probably closely related" — is there some reason you haven't looked this up? Since one of the expectations on this site is that posters demonstrate prior research, doing that might improve this questions reception. However, the page linked by MaximilianPress is in all likelihood the best answer you will get — evolution has a large random component so trying to say why these two flies do things differently could require reconstructing the entire evolutionary and ecological history of these two flies and their ancestors ...

Look up references that support that the two are closely related? I felt that was quite obvious, but I can do that. Also, while it might be true that MaximillianPress's answer is the best I'll get, I don't think answering this one is as hard as you're making it out to be. One plausible theory is that the common ancestor relied only on pheromones and that they were exposed to an environments where the smell signal was compromised (perhaps because of what they were eating), forcing them to slowly abandon the smell mechanism and switch to a more visual mechanism.

Also, I think the fact that evolution is random is besides the point. It wouldn't work any other way. That's not an excuse to throw up hands and say "well, its random" :)

They are in different families — I don't off the top of my head known how many millions of years of separation that represents, but flies have been around for 100s of millions of years and families represent some of the deepest levels of separation. 2) This means that there have been a (large) multiple of 10^8 generations (with random mutations) since the last common ancestor. Does that help you understand why the assumptions behind your question are naive?

I didn't know these two things, so thanks for pointing out. But still, I feel these alone don't say much; turtles and crocodiles have been fairly unchanged for 100s of millions of years and a mind boggling number of generations as well. I feel most traits of green bottle flies and house flies like the way they fly, speed at which they process information, lifespans, etc. have hit local optima and the way they look for mates is one of the few traits that separate them. Maybe I'm still naive, but I find the answer I posted satisfactory.


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Can toilet or sewage aerosol transfer eggs of human parasites?
Flushing a toilet produces hundreds of thousands of tiny droplets containing viruses and bacteria (source).
Additionally vomit and feces of infected people sometimes contain extremely high concentrations of viruses or bacteria.
Similarly, sewage water produces droplets and was proposed as the transmission mode in the SARS outbreak in Hong Kong in 2003.

Apart from viruses and bacteria being transferred through toilet and sewage aerosol, can human parasite eggs be transferred as well given the droplet size?
I'm interested in the aerosol, not the relatively large droplets that land on the toilet itself.

Common small protozoa that are present in infective loads in stool have not been documented in toilet aerosols. The size of the organism is going to be an issue here. As you can see from this table from the CDC, intestinal parasites (and ova) of concern to human health are larger than most droplets. Compare, E. coli and Shigella (0.5 - ~2 $\mu m$). Salmonella tends to be a litter larger (up to 5$\mu m$), but I expect those 5 $\mu m$ specimens are not the ones transmitted through aerosols. Cryptosporidium would probably be the most likely candidate, and that's one shown in the first linked study to not be present in aerosols. I wouldn't say it's impossible, but certainly transmission through aerosolized particles is less likely than for the smaller viral and bacterial organisms.


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Is Norway spruce (Picea abies (L.) Karst.) isohydric or anisohydric species?
Question from a thesis defense list ask me this. But I can't find the exact answer on the internet or in books. In my thesis, I described isohydric plants, for example maize, lupin, pea, poplar. This plants response to a decrease in soil water in same way. How Norway spruce response to decrease in soil water? As a isohydric plant or anisohydric?
Thank you for your time and help.

Welcome to Biology SE. Please Edit your question and re-post it, with little more details.

What do you think and why?

According to this report, maize, lupin, pea, and poplar are all anisohydric.

@augurar According this study:

For this reason, in these species leaf water potential is a better indicator of soil moisture than gs. Isohydric species (e.g. maize, lupin, pea, poplar), on the other hand, close their stomata in response to a decrease in soil water and/or an increase in VPD, controlling plant water potential.

@Hawk81 I think you are right and that was a mistake in the report I linked -- one of the papers they cite lists maize and poplar as isohydric.

This review paper states that spruce is isohydric, citing Physiologie und Ökologie der Gehölze by Lyr, Fiedler, & Tranquillini:

Spruce appears to reﬂect an isohydric strategy (Lyr et al. 1992), reducing stomatal conductance at early stages of soil drought.

It's important to note that this is not a binary distinction, isohydric and anisohydric are two extremes in a spectrum of how plants respond to drought.


text:
An example for N50? Why do we need it?
I'm trying to understand N50 on the wikipedia. But I was unable to get a sense of the definition:

Given a set of contigs, each with its own length, the N50 length is
  defined as the length for which the collection of all contigs of that
  length or longer contains at least half of the sum of the lengths of
  all contigs, and for which the collection of all contigs of that
  length or shorter also contains at least half of the sum of the
  lengths of all contigs.

Is there a simple example that illustrates this definition? Furthermore, why do we need this statistic? What does it really tell me? Do we want a higher or less value?

Contig or scaffold N50 is a weighted median statistic such that 50% of the entire assembly is contained in contigs or scaffolds equal to or larger than this value.
Mathematically:

Given a set of sequences of varying lengths, the N50 length is defined
  as the length N for which 50% of all bases in the sequences are in a
  sequence of length L < N. This can be found mathematically as follows:
  Take a list L of positive integers. Create another list L' , which is
  identical to L, except that every element n in L has been replaced
  with n copies of itself. Then the median of L' is the N50 of L. For
  example: If L = {2, 2, 2, 3, 3, 4, 8, 8}, then L' consists of six 2's,
  six 3's, four 4's, and sixteen 8's; the N50 of L is the median of L' ,
  which is 6.

In simple words:

scaffold N50 is the median contig size of your genomic assembly. It's
  a metric that you can use to evaluate the quality of your assembly,
  since an overly small N50 suggests that you were unable to generate
  many contigs of biologically meaningful size (i.e. you probably have a
  lot of bogus little contigs in your assembly). You can increase your
  N50 by eliminating sequences which are bound to cause you problems,
  e.g. short repetitive stretches.
note that this metric only applies when doing de novo assembly. If you
  are aligning to a reference (i.e. for variant discovery applications)
  this metric doesn't apply

For a sample workout on an arbitrary small dataset:
http://www.r-bloggers.com/calculating-an-n50-from-velvet-output/
This answer was compiled from multiple sources:
http://www.researchgate.net/post/What_is_N50_Scaffold_in_Genome_sequencing_Technique
http://seqanswers.com/forums/showthread.php?t=2332
https://www.broad.harvard.edu/crd/wiki/index.php/N50


text:
How fast the brain recover itself at sleep? What can be done to accelerate this process?
In Computer Science we have "Big O Notation" to describe how efficient is an algorithm at processing some task. Those can be linear, time constant, exponential among others.
Using that analogy, How much time the brain needs at sleep to recover itself from an intensive day at work/over stimulation/training/learning/etc?
After it reach it's "specific time", I know that we dream, and that can take very few minutes. Last night I've dreamt of hardest college exams, even done my last one in 2011. So, dreaming time is a period where the brain clean itself from toxins? I've waked up early, so I should have "dreamed a litle bit more" to recover, or the dream it's just the output imaging of the brain recovery process?
What can I do to recover faster? Things like dimmer and silent ambient help better than the total time slept? How they affect and interrelate? If you can provide technical and scientific papers, it will help a lot!
Thanks a lot for your time and patience!
Edit: "Typed Bio O instead of Big O".

You should see some talks from TED about deep sleep.
One researcher summarized that adults generally need 8 hours every night to be at optimum strength. What is most important though is the Delta-wave sleep that occurs during very deep sleep.  To accelerate the process: It's pretty fringe research, what he said is early days... Alledgedly, playing a certain kind of noise triggered near the delta wave phase promotes Delta wave activity in the brain as measured with electrodes. it's essentially slow delta-synchronised seashore kinds of of grey noise played in sleep at the right moment. He said they were working on a device for it.

here's the talk.
https://www.ted.com/talks/dan_gartenberg_the_brain_benefits_of_deep_sleep_and_how_to_get_more_of_it
My own method to have amazing sleep is lots of nights at my girlfriends and to change mattress every few days mat my house, because my unconscious breathing is forced to exercise different muscles of the chest based on whether I am on a swimming pool matress, a futon, a cozy matress, covers similar to sleeping on a lawn. Physiology and muscles benefit from varied exercise, including the 8 hours of chest muscles during sleep. another matress for example I feel all the breathing in the lower belly. I just got out a pool matress for the last 2 nights on boards and rugs, and I dreamed that I was flying around the mountains and cities for about 3 hours and that other people were flying too, which is always nice. I swear I was sleeping a bit rough 3 days earlier on a normal mattres. other factor for me optimum warmth and lots of water for me:) i'm weird though because I had liver damage from a pesticide and following doctor care when I was 18 and I need drink more and sleep hot in order to sleep well.


text:
Why is cancer more lethal than (hypothetical)infections?
I am a computer science student and I'm interested in algorithmic aspects of cancer! Once I heard that there exist more bacteria in human body than our own cells, I wondered that why bacteria, which divide faster than cell bodies, do not cause something like cancer in body? Isn't it evolutionary more probable for bacteria to gain aggressive properties and invade human tissues? Or maybe is it the case that bacteria really produce some lethal colonies like cancers in the body?
One difficulty with cancers is that cancer is a very complex disease  because of it's intra-tumor and inter-tumor heterogeneity. Isn't it more probable for bacteria to cause extremely heterogenous infections with regard to existing simple evolutionary models which are used to describe cancer?

Most of the bacteria you refer to live in the gut, and have evolved to coexist, not invade. Pathogenic bacteria are aggressive, and have evolved to invade human tissues, but our immune systems keep them in check. You would not call them "cancers" though.

@KarlKjer shouldn't it be that the pathogenic bacteria have not yet evolved to coexist with humans?

@Polisetty it's a common misconception that pathogens evolve toward "coexistence". Pathogens are selected for transmission, and while low virulence can sometimes help transmission, so can high virulence. So saying "not yet" implies an inevitability that isn't real.

@KarlKjer you are right but normal cells are evolved to help the whole organism but accidentally they become invasive! I think that bacteria according to their numbers and their higher rate of mutations are more prone to show such aggressive behaviors!

It's meaningless to suggest a bacterial tumor; tumors are by definition from the same organism as the host. If you have an overgrowth of bacteria you would just call that an infection, there's no need to reuse the term tumor in that context because an entire separate vocabulary exists to describe infections.

@BryanKrause you are completely correct! But the main point is why cancers are more lethal than infections? Cancer is very complex because of  it's intra-tumor and inter-tumor heterogeneity. Isn't it more probable for bacteria to cause extremely heterogenous infections in existing simple evolutionary models which are used to describe cancer?

@CharlesE.Grant You are right but the question is really that what is inherently different? Why something like anti-bacterial drugs do not exist for cancer! As far as I know one of the popular answers to this question is tumor heterogeneity and that cancer is not a single disease! The question is  why it is not the case in the bacteria scenario!

@Dandelion That's pretty similar.  Anti-bacterial drugs also kill good bacteria.  Likewise, there are drugs that kill cancer cells but also kill good cells.  Cancer cells, like bacteria, can be said to "evolve resistance" to drugs.

Cancer is not inherently more lethal than bacterial infections. That's simply an artifact of the time we live in. Broad spectrum anti-bacterial drugs we invented in the 1st half of the twentieth century. Before that, most folks died of infections. Cancer was relatively rare because most folks didn't live long enough for cancers to become apparent.
Why do we have generic drugs for bacteria and not for cancer?  Largely because bacteria are not eukaryotes and we are. The biology of bacteria and human cells are so different that it's relatively easy to find drugs that dramatically affect bacteria, but not people. I say relatively easy, but still took several thousand years of human history to figure it out.
Because cancer cells are just variations on our normal cells, it's very hard to find something that kills the cancer cells, but not the rest of us. That's why chemotherapy makes folks so sick: the chemotherapy agent is killing, or significantly impairing, fast growing healthy cells along with the cancer cells. The most successful cancer drugs have identified rare metabolic pathways that are important to specific types of cancer, but not so important to healthy cells.

Thank you but I think that extremely huge number of bacteria living in our body still seems unbelievably harmless! Almost all infections -as far as I know and of course I know just very little molecular biology and almost nothing else in the field of biology and bacteriology- have external sources!!!

All the bacteria in our bodies, not just the infections, come from external sources. You start collecting them as you path through the birth canal and never stop. As to being "unbelievably harmless":  there are lots of bacteria that are perfectly harmless when they are living in your gut, but potentially lethal if they start growing in your blood, your lungs, or your urinary tract. It's worth keeping in mind though that cooperation (symbiosis) can be a powerful evolutionary strategy.

Charle's E. Grant's answer, that bacteria are typically different from us and hence easier to kill, is most of the answer. Remember that this applies not only to drugs but to our immune system, which can have difficulty detecting cancers (while catching most of them) but is excellent at detecting foreign organisms like viruses or bacteria.
You do still ask a valid question however - shouldn't the enormous number of replicating cells in our gut mean that some bacteria occasionally arise which break the co-operation between bacterium and host, and cause problems (albeit problems mainly limited to the gut) ?
The answer seems to be - yes. We're only beginning to understand how people's microbiomes work, but it seems likely that they can be dysfunctional and this causes health problems. Sometimes this involves a single strain of bacterium overwhelming all others - this is in some ways analogous to a tumor.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315779/

Cancer cells are technically human cells and programming the immune system to recognize them can cause autoimmune problems. Some cancer mutations also fail to manifest on cell surfaces, making the cancer cells near impossible to medicate (without widespread friendly-fire on healthy cells) or immune-target.
Bacteria are plenty different enough that the immune system can target them with abandon and almost no risk of autoimmune problems. If they aren't resistant, you can shut them down with antibiotics (specifically designed against prokaryotes). A common approach includes interfering with bacterial ribosomes (which are fortunately different enough that the treatment doesn't significantly interfere with human ribosomes). If the antibiotic ever stops working, throw in some bacteriophages.


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How does the brain’s limbic system work together to form a working memory, short-term memory, and long-term memory?
In the past few days, I was reading about the limbic system and how its components (hippocampus, hypothalamus, thalamus, etc.) cooperate.
Among papers and forum posts I read about how those components interact and how each of them plays a vital role in the memory formation.
But, is there someone who can give me an abstract view of how the limbic system components form the cycle that results in the formation of memory?
Something like:

The sensory signal comes through the Temporal lobe.
Goes to Thalamus where it is classified as new, existing or similar to already existing memory.( maybe somewhere between this or maybe after the next step the working and short-term memory should be involved?)
Goes to Hypothalamus to be classified as good or bad experience.
Goes to Hippocampus so it can be saved the neocortex at some point (while sleeping for example).

and so on...
Thanks!


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How can individual strands of coat hair have only a single color when considering codominance?
I understand how codominance works. We have two (or more) alleles for one gene, neither having dominance over the other. They are both expressed independently, which means that different phenotypes are visible simultaneously. However, I'm not sure how it really works when we take, say, coat color. If both alleles are active, assuming each one produces a different pigment for each color, that means there are both pigments in a cell. What I see explained is that, if you look closely, each hair has a different color, and when you see it from far away, it gives the impression that the coat is made of one single color. But how can one hair have the same color all throughout? How can the different pigments be aggregated like this? As in, how is it that they do aggregate like this?

Why do some cells produce hair, and others fingernails, or insulin?  FTM, why do some animals have spots or stripes?

This paper may help get you started, how spots and stripes form . https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4380182/, how simple rules/interactions can create complex patterns is quite interesting.

@jamesqf, why does a strand of hair have one color only if every one of the cells it's made of produces both pigments? That's what I mean. I was looking for something in broad terms, but it seems to be impossible to generalize.

The point I was trying to make is that (AFAIK - I'm not a biologist) each cell does not produce both pigments.  Indeed, hairs are not produced by single cells, but by rather complex organs called follicles.  At some point in their development, they've differentiated to produce different colors and types of hair.  So you get coat patterns in animals, differences between head & body hair in humans, &c.

Right! That's closer to what I was looking for. So there's a kind of centralization and differentiation at work here. I'm only in 12th grade and was curious about the details of how this works. The book we use doesn't go into any length about this, and I'm pretty sure asking my teacher would be pointless.

@ixjf: I'd start by just doing a Google search on "hair follicle development" - that's what I did, to reinforce what I thought I remembered from past reading.

The terms dominance/recessivity, additivity, co-dominance, incomplete dominance, etc... express a relationship between genotypes and phenotypes but the mechanism behind this relationship is not being defined by these terms.
There might be a large number of mechanisms associating genotypes at a given locus with phenotypes. There is, in general, no reason to expect a mechanism of relationship of dominance at a given locus to be similar to that at another locus. In other words, there is no general mechanism leading to dominance/recessivity, additivity, co-dominance, incomplete dominance, etc...
On top of that, the actual mechanism in specific cases leading to particular genotypes - phenotype association are often unknown and I don't think we have good knowledge about what mechanisms could be more common or even how to categorize such mechanisms.
You might want to have a look at the posts

Why are some genes dominant over others? What is the mechanism behind it?
Evolution of dominance

or some papers such as

Llaurens et al. (2009)

In general, it appears suggested that one needs to know the specifics of the biological pathway to be able to predict dominance relationships and gene interaction network (see Llaurens et al. (2009)).

I do realize there isn't a general mechanism for this. That's why I asked the question specifically for coat hair (need not even be generalized, just a light), hoping that would narrow it down. The question still intrigues me. I was hoping something that I would think is a given would have been understood by now!

You will need to be even more specific than coat color. For example, in female cats, X inactivation (dosage compensation) has an important role in determining coat colour. In human, 378 markers affecting skin color have been identified! You might want to narrow the question to a very specific study system.

I would recommend cherry picking your system of interest so that you have best chance that an answer exists. Consider the Mc1r gene in mice (Hoekstra et al. 2006) for example. Also, as the current post has already received an answer, I would recommend asking this new (narrowed down) question on a new post.

The gene isn't specified here, but the general idea expressed is variegation.  There are individual hairs (it could be larger regions) that are controlled by one of the two genes, but there is some randomization of which one.
An easy system to picture this in would be the X chromosome.  One X chromosome is inactivated in the female, and the other is not.  If the gene is on the X chromosome, each allele controls specific hairs.
Position effect variegation is well known to affect coat color.  If one allele is dominant but silenced randomly in some cells, an effect akin to codominance could be seen, though it seems dubious to say it really is codominance.


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Change in synthesis rate of a molecule changes equilibrium concentration
I was reading the topic of 'The concentration of the molecule can be adjusted quickly only if the lifetime of a molecule is short' from Molecular Biology of the Cell by Alberts.
At the end of pg-837 (this part can also be found here), the author says -

"In fact, after a molecule's synthesis rate has been either increased
  or decreased abruptly, the time required for the molecule to shift
  halfway from its old to its new equilibrium concentration is equal to
  its normal half-life—that is, equal to the time that would be required
  for its concentration to fall by half if all synthesis were stopped."

What do they exactly mean by 'shift halfway'? I am not able to understand quite clearly what the above sentence means. I hope some of you may be able to help me. Thanks.

Note: The term equilibrium is different from steady-state w.r.t chemical reactions. Steady state is the right term for the above example. Equilibrium is used in the sense of forward and reverse reactions in a single reversible reaction. The above example considers two irreversible reactions — production and degradation.

... ... the time required for the molecule to shift halfway from its old to its new equilibrium concentration is equal to its normal half-life

This is not true if the degradation reaction is zeroth order or if these reactions are nonlinear. But for a linear production degradation set of reactions ($X$ is a biomolecule formed at a constant rate $\alpha$ and degraded at a first order rate  $\beta$ ), the reaction rate can be represented by the following equation.
$$\frac{d[X]}{dt}\bigg|_1=\alpha _1 - \beta [X]$$
At steady state $\frac{d[X]}{dt}=0$, which means $[X_{ss_1}]=\Large\frac{\alpha _1}{\beta}$
Half life as defined, by setting $\alpha$=0 and solving the differential equation = ${\Large \frac{log(2)}{\beta}}$
When the formation rate is changed to a new value:
$$\frac{d[X]}{dt}\bigg|_2=\alpha _2 - \beta [X]$$
and $[X_{ss_2}]=\Large\frac{\alpha _2}{\beta}$
From the above equation following equation can be deduced (by integrating the differential equation):
$$-\frac{1}{\beta}.log(\alpha _2 - \beta [X]){\large|}_{X_{initial}} ^{X_{final}}= t_{\frac{1}{2}} $$
when you substitute $X_{initial}=X_{ss_1}=\frac{\alpha _1}{\beta}$ and $X_{final}=\Large\frac{\frac{\alpha _2}{\beta} - \frac{\alpha _1}{\beta}}{2}$ (halfway between new steady state and old steady state)
you would obtain: $$t_{\frac{1}{2}}= -\frac{1}{\beta}log\left(\frac{\alpha _2 -\beta\frac{\alpha _1}{\beta}}{\alpha _2 - \beta \frac{\frac{\alpha _2}{\beta} - \frac{\alpha _1}{\beta}}{2}}\right) = \frac{log(2)}{\beta} $$


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Purifying a linear plasmid after restriction digest?
I expressed a yeast vector in E.coli and purified about 13µg of it. I then linearized it using a restriction enzyme, and attempted to gel purify it. I attempted this twice. The gel showed a clear bright band at the right spot, but after gel purification I end up with only 0.7µg of linear plasmid. I doubt I made the same mistake twice. What is the best way to purify a linear plasmid after digest?
Edit:
The plasmid is about 3.5 kb. I incubate an overnight culture of E. coli, miniprep the following morning, elute into water. I end up with 13µg of DNA in 200µl of H2O. I add the PmeI (10µl) and the CutSmart buffer (23µl) from NEB, incubate overnight. The following day, I run the 230µl through a 1% gel and get a single band around 3.5 kb. I excise the band, and perform a gel purification using the Biobasic kit, add denaturant (probably guanidine hydrochloride), wait for 10 minutes for the gel to dissolve, run through column, wash 2X with wash buffer with ethanol added, elute in water.
Thanks,
Max

Could you share the size of your bands with us and give a bit more details about your current purification method!

The plasmid is about 3,500 kb. I incubate an overnight culture of E. coli, miniprep the following morning, elute into water. I end up with 13 ug of DNA in 200 uL of H2O. I add the Pme I (10uL) and the CutSmart buffer (23 uL) from NEB, incubate overnight. The following day, I run the 230 uL through a 1% gel and get a single band around 3,500. I excise the band, and perform a gel purification using the Biobasic kit, add denaturant (probably guanidine hydrochloride), wait for 10 minutes for the gel to dissolve, run through column, wash 2X with wash buffer with ethanol added, elute in water.

230uL of solution seems like a lot to put on a gel. Are you using multiple lanes and therefore putting a lot of gel through the gel extraction kit? I know they can only handle so much gel at once.

Could you please make this as an edit to your question! Why do a gel purification? you can just use a kit similar to QIAGEN gel extraction kit and do a non gel based plasmid purification and elution, using the buffers used as usual! PCR DNA clean up kits will do as well!

Good idea. I will attempt to purify using PCR cleanup. Thanks Bez!

What is the loading capacity of the columns you used for the purification?

Which kit did you use exactly?

@Max if that has answered your question please let me know so that I can post the response as an answer.

Yes, please do!

I have a quick question: How are you growing your culture? Is it a liquid culture? The reason I am asking is that you DNA concentrations sound very low before you cut the DNA. I regularly grow E. coli in a 4mL LB in H2O for subsequent DNA purification using the QIAGEN plasmid mini-prep kit (3mL protocol) and I get nearly 120ug/uL of DNA with A60/A280 of ~1.9.

Hello gravityassist,
I grow about 20 ml overnight in low-salt LB with Zeocin (25 mg/ml). I do 4 minipreps and end up with 200 uL of 65 ng/uL. We tend to get 50ul of between 50 - 120 ng/ul for our low-copy plasmids.

3500kb???!!!.. Are you sure? I think it must be 3500bp=3.5kb.

3,500 bp. My bad.

Can't exactly say what problem you are facing but you can follow these steps for efficient restriction digestion and elution.

Never set up a digestion reaction with more than 1µg DNA per 20µl; if you require more digested DNA, then set up multiple 20µl reactions with maximum of 1µg DNA in each (500-700ng is ideal).
10µl enzyme for a 230µl reaction: bad idea. Set up 10×20µl reactions with not more than 0.5µl enzyme per reaction tube.
Avoid overnight incubations; 4 hours should be sufficient (NEB PmeI is 10 units/µl and 1 unit is the amount required to cleave 1µg DNA in 1h in a 50µl reaction. You are adding 5 units in 20µl. Overnight incubation is too much)
Deactivate the enzyme after the reaction.
Just run a little bit of sample from one tube in the gel to see if digestion has happened. After confirming digestion simply use the PCR purification kit. You can pool your tubes.
Optional: Elute in Tris-Cl pH 7.5 instead of water or use warm (60⁰C) water.

Additional: Check the maximum DNA capacity of the columns used. If you overload them, you will drastically loose yield.

@Chris That is an important and nonintuitive problem, I once wasted a whole gigaprep kit because the protocol a former lab member gave me said to use twice as much DNA as the column could hold, then my advisor thought I could fix the low yield by loading even more DNA.

@user137 I have run into this problem as well, this is why I mention it.

@user137 note that a column can be reused. So you can use it for multiple rounds of elution for same plasmid.

@WYSIWYG How should I clean up the column to reuse it? Gigaprep kit are expensive and we only produce 1 plasmid on that scale so reusing a column should be ok for us.

@user137 well you can add a little bit of tris-Cl pH 7.5, spin it for 2min at 12000rpm for 2 min to remove residual stuff and then reuse.

@WYSIWYG We may be confusing gigaprep and miniprep, the Qiagen gigaprep column looks about 6 inches long with diameter of about 2 inches and works by gravity. Even if it can survive centrifugation I don't have a rotor that large.

@user137 ahh.. then you would probably need vacuum pumps.. Nonetheless for the same plasmid type it is not an issue. you can reuse it without much worry. just use vacuum before reuse to ensure that nothing stays in the column.

Why do a gel purification? you can just use a kit similar to QIAGEN gel extraction kit and do a non gel based plasmid purification and elution, using the buffers used as usual! PCR DNA clean up kits will do as well!


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Does anyone know what this purple plant is? (picture taken in Turkey)
Is anyone familiar with this plant species, picture taken in the Dalaman region of Turkey. It has large purple leaves.

This shrub is called Tradescantia pallida. You can read more about this shrub on this website https://florafaunaweb.nparks.gov.sg/Special-Pages/plant-detail.aspx?id=2521
I hope this helps you


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How long can Legionella survive at 60°C?
I'm coding some stuff for water heaters and one of the functions is anti-Legionella.
Anyway, I've read on wikipedia that 90% Legionella dies in first two minutes if the water temperature is 60°C, but I'm interested in how long should the temperature be 60°C for 99.99999% of Legionella to die? (I guess I can never get to 100%)
Follow-up question: On what intervals should this be done so that the water isn't contained? Should it be one week, two weeks, several days?
Final question: If the water in a water heater has 60°C for 30 minutes every 2 weeks, would the water be safe?

If the water can be repeatedly contaminated, you would probably need to continuously keep its temperature at the disinfection level to limit the risk of contamination to 0.00001%.

Usually cell death would follow first order kinetics.
$$X=X_0e^{-kt}$$
where $X$ is the number of cells at time $t$, $X_0$ is the initial number of cells and $k$ is the death rate constant. You can get the constant by solving for 90% reduction in 2 minutes. Then just substitute and get the time required for 99.99999% reduction — 10 minutes.
For your follow up questions, see the same wikipedia article.

Moist heat sterilization (superheating to 140 °F (60 °C) and flushing)
  is a nonchemical treatment that typically must be repeated every 3–5
  weeks.

It also depends on how much is the bacterial load in the input.
Other sources (Farhat et al. 2012; Whiley et al., 2017) suggest 70°C treatment for 30 minutes.
However, Legionella has been shown to survive heat treatment of 70°C/30min (reviewed by Whiley et al., 2017). Legionella can also be "protected" by other micro-organisms such as certain types of Amoeba, in the water.
So, probably multiple levels of disinfection is needed.

Ok, great, this is just what I needed


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Why is glycerol supplied/used as 87% solution?
While preparing glycerol stocks of my transformed bacterial cells (DH5alpha) the protocol I had to follow was that I would make one 50% glycerol stock (500µl culture, 500µl glycerol 50%) and another 87% glycerol stock (850µl bacterial culture, 150µl glycerol 87%). 87 seems to be a very specific number. Any particular reason why 87% glycerol concentration is used?

In which protocol/reference did you find the 87% glycerol?

I think my lab protocol follows sambrook russel's molecular cloning.

Yes I will try to provide a proper reference.

Glycerol is typically sold at 87%, which just pushes back the question one step. Many years ago I was told that this is because of glycerol's hygroscopic nature, such that a higher concentration would tend to absorb water from the atmosphere and dilute itself anyway. Does this stop at 87%? Figure 1 from Glycerine: an overview suggests that 50% relative humidity might lead to a glycerol concentration that is in the ballpark of 87%, but 40 or 45% relative humidity looks closer.  Not definitive, so I'll leave this as a comment.

Typically, a glycerol stock will have a final concentration of 10-20% of glycerol. Glycerol is highly viscous. Pipetting higher concentrations of glycerol is difficult (especially for smaller volumes). Therefore a lower concentration such as a 50% solution (works for me) is convenient: add 300µl to 700µl of bacterial culture.
Regarding 87%: some vendors provide 87% glycerol along with anhydrous (>99%) glycerol. The reason is probably the same: it is easier to pipette 87%.
From a vendor's website:

Glycerol is a component of several buffers, media or reagents in
  biological research. It is supplied as glycerol anhydrous or 87 %, the
  latter containing 13 % water. Both glycerols are from the same
  quality, the 87 % glycerol has the advantage of a lower viscosity.
  Anhydrous glycerol can be pipetted with difficulty only, especially at
  low temperatures.

But the question is why 87% and not 90 or 80? See Michal et al. (2017)  for a relationship between viscosity and concentration of glycerol-water mixtures.

Another graph plotted from the data given in the document mentioned by iayork in the comments. Different coloured lines denote data at different temperatures (in °C). Original data from: The properties of ordinary water substance. Compiled by N. E. Dorsey, New York (Reinhold), 1940.

So I am guessing that 87% must have been optimal beyond which the viscosity just shoots up rapidly with a small increase in concentration. I wish to reiterate that this is just my guess. I could not find a authoritative (in fact any) reasoning on why precisely 87% glycerol is (or was historically) supplied.

Thanks so much for such an well reasoned and knowledgeable reply. That ought to be the reason for using 87% glycerol stock.

I think this is more plausible than the hygroscopicity I was told was the reason, since 87% doesn't show an obvious connection with anything on the hygroscopic chart whereas it's a better match with viscosity. The vendor's comment you quote also strongly supports this. Upvoted!


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What is "contigs" in Picard's ReorderSAM?
I've used BWA to map my NGS reads against the hg38 genome, and I have a BAM file. I'm not doing genome assembly, and my reference genome file has the human chromosomes. Thus, I shouldn't have "contigs". But...

https://broadinstitute.github.io/picard/command-line-overview.html#ReorderSam

and quote:

ReorderSam reorders reads in a SAM/BAM file to match the contig ordering in a provided reference file, as determined by exact name matching of contigs

Q: What does contig ordering mean, for my whole-genome-sequencing experiment? In particular, what does matching the contig against a reference file mean?

I'm not familiar with picard and their reorderSam function, but as far as I know/understand from their documentation they mean this:
The ordering of the contigs while using a reference sequence.
Like this:

 Figure 5: Anatomy of
  whole-genome assembly. In whole-genome assembly, the BAC fragments
  (red line segments) and the reads from five individuals (black line
  segments) are combined to produce a contig and a consensus sequence
  (green line). The contigs are connected into scaffolds, shown in red,
  by pairing end sequences, which are also called mates. If there is a
  gap between consecutive contigs, it has a known size. Next, the
  scaffolds are mapped to the genome (gray line) using sequence tagged
  site (STS) information, represented by blue stars. © 2001 American
  Association for the Advancement of Science Venter, C. et al. The
  sequence of the human genome. Science 291, 1304–1351 (2001). All
  rights reserved. (source)

ReorderSAM (Picard)
So in Picard you have your INPUT (File), the reads in this file are then mapped on the REFERENCE (File). This can also be seen in their code:
// write the reads in contig order
109
            for (final SAMSequenceRecord contig : refDict.getSequences() ) {
110
                final SAMRecordIterator it = in.query(contig.getSequenceName(), 0, 0, false);
111
                writeReads(out, it, newOrder, contig.getSequenceName());
112
            }

(code source)

ReorderSam reorders reads in a SAM/BAM file to match the contig
  ordering in a provided reference file

Some more background
There are two main approches two obtain a genome sequence:

there are two "main" approches for this:  g. Second-generation
  sequencing technologies produce millions of short(a few hundred bp)
  strings of nucleotides (reads), which is ideal for resequencing when
  reads are mapped to a reference genome (reference-based assembly). De
  novo genome assembly based on second-generation sequencing is
  challenging due to difficulties with GC- or AT-rich and homonucleotide
  DNA stretches, which are under-represented in the sequencing output (source)

The characteristics of these are:
de novo

no bias towards a reference genome
no template to adapt to
the    assembly is normally more fragmented
it normally works better for large-scale/median scale differences (source)

reference mapping

less contigs
in most methods the reads that don't map are not used in the final sequence (this is also the case with reorderSAM: Reads mapped to contigs absent in the new reference are dropped
you look what is similar to your reference genome
SNPs and very small veriations are more easily positioned and compared among groups (source)

I would highly recommend to watch this short animation to differentiate between these two and understand what reference genome mapping is.


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Why DMSO is used as a control?
Coming from a non-biology background, I've realised many academic papers on experiments use DMSO as like a control. This is an example:

KN-93, a specific inhibitor of CaMKII inhibits human hepatic stellate cell proliferation in vitro

What make DMSO so special that so many scientists use it for their experiment and report their results? Why do we need it in the first place?

Its likely used as a control when its also being used as a solvent, not everything can be done in water

@zacdav Make your comment an answer, because that's the answer to the question.

Note that this is often described as a vehicle control. Essentially you are controlling for the effect of the solvent (ie the vehicle) used to introduce the compound of interest.

DMSO can be used as a solvent for a range of experiments. In these cases it makes sense to use the solvent as the control.


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Why telomere shortening slowing down cancer?
I am reading Alternative Lengthening of Telomeres in Mammalian Cells, about how telomeres linked to human cancers.

Due to the end-replication problem,5,6 the ends of linear chromosomes
  shorten with each round of DNA replication.7 In human somatic cells,
  the progressive telomere shortening that occurs with continued
  proliferation eventually results in the triggering of a replicative
  checkpoint. Telomere shortening and the structural changes that it
  presumably causes, leads to a DNA-damage checkpoint response at the
  telomere and induction of a permanent p53- and Rb-dependent growth
  arrest (i.e., replicative senescence).8-10 Because this limits the
  proliferative capacity of somatic cells, including those that have
  accumulated oncogenic mutations, telomere shortening and replicative
  senescence are a potent tumor suppressor mechanism.

The paragraph states a shorter telomere is a potential suppressor to cancers. Why is that? Why exactly a somatic cell proliferate slower with a shorter telomere DNA sequence?
Conversely, why a longer minority leads to human cancers?

Think about the 24 different linear chromosomes in a diploid human XY cell.  In the absence of active telomerase enzyme to repair the chromosome ends following one round of cell division, then every time that cell divides each end of each chromosome will get a little bit shorter.
If the cell keeps dividing indefinitely, like a tumor cell, the chromosomes are effectively shrinking.  Eventually this chromosome shortening will result in deleting actual genes (at first, 24 chromosomes x 2 chromosome ends = 48 genes).   Not all of those genes are essential for cell viability; and the distance, or length, of DNA between the telomere and the first gene on that end will be variable.  But as soon as the chromosome shortening removes part of an essential gene, then that cell will quickly die.
It would be like erasing the words at both ends of a sentence, one letter at a time.  In the beginning, someone else would still be able to make sense out of your sentence, but eventually they would not be able to fully understand what information you were trying to convey.
Most of the terminally differentiated cells in an adult human are no longer actively dividing, so it is not a problem, they don’t need active telomerase.  However, cancer is a condition of unregulated cell division, and so all cancer cells have to have some mechanism of repairing the ends of their chromosomes.  Reactivation of TERT (Telomerase Reverse Transcriptase, the protein component of the telomerase enzyme) gene expression is extremely common in cancer cells.


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Plot coverage per base for BAM file
I have a BAM file and a BED file for my own chromosome. I would like to get coverage per base and ideally construct a histogram of coverage across each gene.
The motivation is to visualise the coverage across each gene. If my experiment is good, I should expect uniform coverage. It's also important to compare the coverage near the boundary of the genes.
A R (bioconductor) solution is ideal, because I can directly visualise.
How to do it?

From your bam-file, you can generate a BED(-graph) of per base coverage with bedtools genomecov (use the -ibam, -d and if you want a BEDgraph also the -bg flags).
There are multiple R packages for bioconductor which read and visualise these, including sushi.

skymningen's suggestion of genomecov is absolutely correct. The command I use is:
bedtools genomecov -bg -ibam sorted.bam > sorted.wgx

This generates a BedGraph file.
Unfortunately, the R package sushi had a bug that it didn't generate anything if the interval I wanted is too small. I preferred IGV.


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How to interpret this cuffcompare result? Sensitivity over 100?
I run a cuffcompare:
cuffcompare -r transcripts.gtf TransStandard_1.0.gtf

I got the following result:
#= Summary for dataset: /home/tedwon/Sources/QA/data/trans/TransStandard_1.0.gtf :
#     Query mRNAs :     165 in      78 loci  (157 multi-exon transcripts)
#            (69 multi-transcript loci, ~2.1 transcripts per locus)
# Reference mRNAs :     165 in      78 loci  (157 multi-exon)
# Super-loci w/ reference transcripts:       77
#--------------------|   Sn   |  Sp   |  fSn |  fSp
    Base level:     100.0   100.0     -       -
    Exon level:     110.6   110.6   100.0   100.0
  Intron level:      99.6    99.6    99.6    99.6
Intron chain level:     100.0   100.0   100.0   100.0
  Transcript level:     100.0   100.0    99.4    99.4
       Locus level:     100.0   100.0   100.0   100.0

 Matching intron chains:     157
          Matching loci:      78

      Missed exons:       0/872 (  0.0%)
       Novel exons:       0/872 (  0.0%)
    Missed introns:       3/756 (  0.4%)
     Novel introns:       0/756 (  0.0%)
       Missed loci:       0/78  (  0.0%)
        Novel loci:       0/78  (  0.0%)

 Total union super-loci across all input datasets: 78

What I don't understand is that why the sensitivity and specificity for the exon level are over 100? The values in this example are both 110.6. Shouldn't it be from 0% to 100%? The website doesn't address it.

Can you please format the output properly (adjust the tabs so that the lines are aligned)

I don't know if this is still needed but I went through the source code of cuffcompare to see if this phenomenon is indicative of the false positive rate or an issue with the tool (and to provide a more thorough answer). It seems like it may be a bug in the code for cuffcompare (which is a massive amount of code). If you look at line ~1518 in the source code at this URL:
https://github.com/cole-trapnell-lab/cufflinks/blob/master/src/cuffcompare.cpp

There are several statements that suggest Sn values > 100% would be possible and should be reassigned to 100%. These results may occur from keeping "redundant" transcripts if they start with the same 5' intron. How do your "fuzzy" Sn and Sp compare to this result? are they are similar?
The developers are no longer maintaining this software in favor their new faster version, Hisat/Stringtie. However I find the output to be more complete from Tophat and Cufflinks. To get a better understanding of the output, you could compare the number of potentially novel features in your cuffcmp.combined.gtf to the total number of features in your new cuffcmp.combined.gtf using overlapping and contained features as a proxy for false positive rate. Comparing these values with the total number of lines in your reference annotation may provide you with another Sn estimate without performing qPCR.
# to count the number of potentially novel
grep -c "\"j\"" cuffcmp.combined.gtf

# to count the overlapping and contained features
grep -c "\"[c,o]\"" cuffcmp.combined.gtf

# to count the number of exact matches
grep -c "\"=\"" cuffcmp.combined.gtf

# To count how many features are identified for each gene
cut -f4  -d ";" cuffcmp.combined.gtf |   uniq -c

# To count how many known genes gene were identified
cut -f4  -d ";" cuffcmp.combined.gtf |   uniq -c | wc -l

# To count number of features in the reference gtf
wc -l reference_annotation.gtf

or if you prefer to use Bioconductor packages like rtracklayer in an R environment, you could read the cuffcmp.combined.gtf file and analyze the data further
library(rtracklayer) # if you have the package installed
rtracklayer::readGFF("~/full/path/to/cuffcmp.combined.gtf")

is that science direct an open access article? if not, some users may not have access. Also, you may want to check out the how to best answer a question in the help center http://biology.stackexchange.com/help/how-to-answer it would definitely improve your answer if you added some background and links to other users to follow along - thanks for your efforts!

@Drew The Evaluation of Gene Structure Prediction Programs paper does give the definitions but nowhere it define how sensitivity can be over 100%.

@Drew I believe this is a bug as sensitivity over 100% is totally unacceptable. This is like probability over 1.

I thought that this might be the result of including novel features in the cuffcmp.stats output which are added to the numerator but not to the denominator of the Sn and Sp calculations.  However, given that your output lacks novel features and produces greater than 1 Sn and Sp calculations, that assumption is incorrect.   It  may be a small enough task to modify the source code on your local workstation.

https://github.com/cole-trapnell-lab/cufflinks/blob/master/src/cuffcompare.cpp


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Book/source for learning bioinformatics, focused on genomics?
Does anyone know of sources for learning bioinformatics, focused on genomics? I would like to learn a lot of skills I could apply potently in the workforce if I ever became adept at the fields. My computer science knowledge is weak, and my biology knowledge is mediocre, but I find the topics to be interesting.
I have read "The dynamic Genome, A Darwinian Approach", by Fontdevila, and it was a bit rough for me. I have also read some of a introduction to genomics textbook, by Arthur M Lesk, and found it to be very "academic".

Hi, There are some bioinformatics introductory courses on "coursera" ..cud be useful to u...

Unix and Perl to the Rescue by Keith Bradnam and Ian Korf is an excellent introductory book and guide for bioinformatics (Linux and Perl) in genomics. It includes exercises and starts with the very fundamentals. You will still need some basic understanding of genetics and biology though.

Beginning Perl for Bioinformatics by Jim Tisdall http://shop.oreilly.com is quite good, in my opinion, and his sequel, Mastering Perl for Bioinformatics is also great. The focus is largely, but not exclusively genomics.

Elementary Sequence Analysis by Brian Golding and Dick Morton is a good starter. Online resources can be found here:http://helix.biology.mcmaster.ca/courses.html
Here's a great online tutorial for sequencing techniques, with introduction, examples and everything.
http://bioinf.comav.upv.es/courses/sequence_analysis/sequencing_technologies.html

While not a book per se, the edX Lifesciences course has been really useful for me, it does a great job of covering the entire pipeline of genome analysis that one would need to use. The link containing all 8 classes is here, scroll down a bit and you can see links to all of the classes in this module:
https://courses.edx.org/courses/HarvardX/PH525.3x/1T2015/dffde833663e4f71ab64246ebe5598d1/

A Primer for Computational Biology is a great open-access book with intros to Unix, R, and Python. As the title says, it's focus is computational biology (e.g., applying a variety of methods and analyses) rather than strictly bioinformatics (the development of novel methods and analyses), but I've found very valuable both for myself and for teaching others.

This is a book being worked on by some people at biostars.  It's being constantly updated
https://www.biostars.org/p/225812/
Perl is a good place to start if you don't know any coding, but when you want to use already written libraries, you'll want to know R or python, if not both.

I strongly suggest you to take a free course on courseraThere are many valid courses focused on bioinformatics for beginners and they offers slides, notes and everything is necessary to start. If you are looking for a nice book to get started, then I suggest you this one


text:
Does caffeine increase the speed at which sperm travels?
I'm not even sure if this claim is true, but...
This source states that

Caffeine gives both types of sperm a boost, but the Y-sperm would get a little more of a boost.

This article reinforces the quote. In fact, this "tip" can be seen all over the internet to preferentially conceive a male rather than a female.
My question is how. What is happening at the molecular to increase the overall mobility of sperm? It clearly wouldn't work as a neurotransmitter (as it "normally" works).

I also realize that this question could be formatted for Skeptics.SE. Feel free to edit the question so that it's more suited for this site.

This answer suggests that the "extra boost" could be due to all Y sperm being lighter and therefore perhaps faster than X sperm - regardless of caffeine consumption.

@RoryM I'm familiar with that, as the comments to this answer also suggest: http://biology.stackexchange.com/questions/1062/x-chromosome-weight

I'm more interested in the "boost" itself rather than the differential boost.

Ah it was that question I was trying to find earlier xD

The cell response for caffeine, is at the molecular level of RyR (Ryanodine receptor), and the main effect could be a temporal rise in Ca+2 cytosolic concentration, so it can change the electrical behavior for the whole cell, and then affect their mobility. But the main area for RyR research is at spermatogenesis, there are a lot of papers like this one, for that topic


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What happens when cells in your body run out of telomeres?
In my biology book I read about an experiment where the genes encoding telomerase were 'knocked out', but they could still live a normal life and no adverse effects were noticed until the 6th generation of offspring (although it did not say what the effects were).
I have often often heard how longer telomeres indicate longer life potential, but what happens when you run out of them? Would rapidly proliferating cells be affected before others? Do the cells then just stop dividing or would they continue to divide? If they continue to divide what would the effects be?

do you have a link to the study that 'knocks out' the telomeres and finds the cells to not have any adverse affects? As I understood it the cells either enter a state of permanent cell-cycle arrest (senescence) or apoptose (programmed cell death) when they reach their Hayflick limit (i.e. when their telomeres run out).

A figure in the book taken from 6th generation telomerase deficient mice was taken from: Cell, Blasco, M. A., ‘Telomere shortening and tumor formation by mouse cells lacking telomerase RNA’, 91, pp. 25–34

@Taleah Please don't "hijack" questions to ask your own question, especially not if they are a year old. Your can ask this as an own question, tag it with "homework" and specify what you tried to answer the question.

During mitosis the genetic material in the cell is replicated to produce a copy of the genome for each resulting daughter cell. Due to the nature of the process, the ends of the chromosomes are not completely replicated, resulting in a slightly shorter copy of each chromosome after each round of replication.
Telomeres are extensions to the end of chromosomes that prevent damage or loss of genetic information during cell division. Telomeres are not replaced (in 'normal'/somatic cells), which gives rise to a replicative lifespan; the number of times a cell can divide before permenantly leaving the cell cycle (known as cellular senescence).

This is generally viewed as an anti-cancer mechanism to protect against errors creeping in to the genome through many cell divisions. In order to become cancerous, a cell must first overcome its replicative lifespan [ref.]. This is achieved by activating the (normally inactive) telomerase enzyme that extends the telomeres - embryonic stem cells are one of the few cell types that normally express this enzyme, so they have unlimited replicative potential - a very important trait for stem cells.
So a rapidly proliferating cell would indeed 'use up' it's telomeres before a different cell type. The cell would then either enter a state of senscence (permenant cell-cycle arrest), or apoptose. There are a lot of factors governing which outcome is realized, but the senscent cell population increases with age, and is proposed to contribute to many aging phenotypes (there is a recent fascinating study published in Nature where the authors remove all the senscent cells from aging mice, and the mice actually get healthier! Can't wait for studies that relate to human aging and senescent cell clearance (ref.)).

I have elaborated on the function of telomeres in the context of organismal aging in my answer to this question.


text:
Why doesn't mitochondrial DNA accumulate damage over successive generations?
From what I recall, mitochondrial DNA is very susceptible to damage from oxidative stress because it is a site where free radicals are generated and their DNA isn't packed into chromatin like nucleic DNA is. How then is it possible that mitochondria can stay in-tact when it is repeatedly passed on to offspring?
I would have thought that an accumulation of errors would cause them to malfunction over time.

If it was the case that we were inheriting damaged mtDNA, we would be inheriting ageing from our parents which in itself is not advantageous in terms of evolution.Considering that the germline mitochondria is purely maternal, nature has evolved a way to switch off the mitochondria of oocytes, and keep it in a simple state, mainly to serve as a template. This template is essentially error free, as the levels of ROS generated, is very low.

Mutations in DNA (mitochondrial or nuclear) in most cells in the body can be harmful to the health of the individual, but will have no influence on the next generation. The genes which we pass onto the next generation are separated off during early development into special ‘germ line’ cells which form sperm and eggs. Great care is taken to minimise the risk of mutation to these genes – genes in germline cells act as a blue print for the next generation. This is essentially why aging is not heritable, and it is a system that works pretty well.
Research has uncovered a rather elegant solution to this problem – those mitochondria that will be passed to the next generation are maintained in an inactive state.Mitochondria are only inherited through the maternal line – every mitochondria in your body came from your mother, and this is true for most animal species. The mitochondria in sperm are generally discarded at some point prior to fertilisation.
Membrane electrical potential, a measure of the activity of the electron transport chain, was reduced in oocytes compared to both sperm and the surrounding tissue. Further, ROS production was 50- and 100-fold lower in the eggs of fruit flies and zebrafish respectively. Finally, they confirmed that oocyte mitochodria in both species exhibit a simpler structure, indicative of reduced activity. So, it seems that in both fish and flies, the mitochondria in egg cells represent little more than a blueprint, ready to be passed on to the next generation error-free. By deactivating ovarian mitochondria, the fidelity of information is ensured across generations, and aging is not heritable.

Taken from: http://blogs.ucl.ac.uk/gee-research/2013/11/11/damage-and-fidelity-the-role-of-the-female-germline-in-mtdna-inheritance/
You can read the article here: de Paula, Wilson BM, et al. "Female and male gamete mitochondria are distinct and complementary in transcription, structure, and genome function." Genome biology and evolution 5.10 (2013): 1969-1977.


text:
By selecting sex cells after meiosis, would it be possible to create two offspring with inverse parental DNA of one another?
Would it theoretically be possible to select two sex cells after a male meiosis (filtering out the two where crossover had taken place) and combine each with two sex from a female meiosis (imagining they were all egg cells, even though only one would be) to create offspring with inverse inherited parental DNA of one another?
For example: If the mother's DNA is AB and father's is CD then the offspring could have AC and BD - inherited from both parents but completely different from one another.

Theoretically? Yes. Very theoretically possible.
In practice? It's difficult to isolate the exact daughter cells (sperm) from the same meiotic event, have these cells complete maturation, and only then have them fertilize an egg. Normally you need quite a lot of sperm cells even with in vitro fertilization, but also in principle all you need would be a single sperm cell to make a zygote!
To address some misconception: when you say "inherited from both parents but completely different", that applies also for regular sex cells and fertilized eggs. You don't need to fish for the precise 2 daughter cells following meiosis to get this outcome. Mitosis produces 2 genetic copies, while meiosis in humans produces 4 unique daughter cells. All individuals, as diploid as we are as humans, are products of genomes that have been very well shuffled (recombined).
Reality: the real-life reasons to perform such a procedure would be taken as very dubious, so I don't think realistically anyone would perform this. But in the designer baby era of the future, who knows!

Sure it would be bery dubious. Was just a silly idea i had. I did have a misconception about crossover where i thought only 2 daughter cells would recombine, when it seems they all do. Still, it seems the resulting children would have mutually exclusive DNA besides that which is shared by both parents. Would i be right in thinking that one child would recive an X chromosome and the other Y from the sperm making the children opposite sex too?

Correct! The ratio of Y and X chromosomes in the haploid sex cells (spermatozoa) is 50:50 as a result of meiotic distribution, and this originates from the X and Y chromosomes being separated between two daughter cells during meiosis.

Here there be monsters
The biggest problem with your scenario as presented is that the complementary genes in the female do not go into the "secondary oocyte" but into the "first polar body" ("2" below).

The first polar body remains in the perivitelline space beside the oocyte, but it is a tiny thing, generally considered too small to potentially make a zygote.  It is emitted as a diploid during the first division of meiosis, and divides again afterward.  I think the one below has already divided.
Now, because it's impossible, we should naturally expect to find such a case, and I will not disappoint:  Bieber, 1981.  In that case the polar body had not divided yet, and the resulting twin, within the chorion, was a triploid and severely deformed "acardiac monster".  A 2015 review mentions polar body twinning without describing the possibility of diploids, so I'll assume this hasn't actually been demonstrated.  I know the first polar body is a bit half-hearted about its division.

It should be relatively straightforward to obtain immature sperm while they are still linked by cytoplasmic bridges as illustrated above, do in vitro sperm maturation to obtain complementary sperm, and attempt some sort of fertilization of egg and a daughter of the first polar body.  The resulting twins would share a chorion but monochorionic and diamniotic.  Such a procedure would still be very likely to produce a malformed embryo due to the development of a very tiny zygote.  I was concerned about epigenetic differences, but after a helpful comment, I did find a reference that the methylome is similar to that of the secondary oocyte, and a paper reporting that it is possible to transfer polar body nuclei to oocytes with 42% viability.  Given remaining uncertainty and a lack of apparent medical necessity, it might still be more advisable to stick to routine human cloning with germline genetic modification. :)

I knew there'd be a problem with female meiosis producing only one egg, but I guessed maybe DNA could maybe be transplanted from a polar body into another egg. I hadn't considered that epigenetic information could make this infeasible, so thanks for the additional information.

You are right!  I'd seen one thing about epigenetic changes and polar body extrusion which I may have misinterpreted, given other sources I found.  I'll update the answer accordingly.


text:
How fast do stomata respond to environmental changes?
How fast does stomatal resistance respond to environmental changes? Correct me if I'm wrong, but I assume that atmospheric humidity would be the fastest changing factor (e.g. rain storm on a dry day, or a warm change coming through). If the relative humidity changes from say 50% to 100%, how quickly will stomata open? And how fast in the opposite direction?

Stomatal speed varies depending on a lot of factors, especially anatomy even within species, but especially between species.

Evidence from several studies has also suggested that smaller stomata respond faster than larger stomata

The paper I just cited from (first link below) includes is a long review of the what is currently known and also original research into the process. It includes a really detailed, lengthy chapter on the stomatal speed, but which is mostly lacking in easily citable numbers except for closing times:

Stomatal aperture responds more slowly, typically with half-times of 10 to 20 min, reaching a new stable, (near) closed state after 45 to 60 min

A few more clear numbers come from the second paper I link to below, however this is in response to changes in light, not humidity.
It includes a table (table 1) on mean stomatal closing and opening time delays in four plant groups and plants adapted to two climate conditions. In most groups, closing happens slower, taking about 50 percent longer, with mean times varying between 6 and 18 minutes. Opening is faster in every group but one and takes between 4 and 30 minutes. In plants adapted to dry climate conditions stomata respond faster.
Sources:
Stomatal Size, Speed, and Responsiveness Impact on Photosynthesis and Water Use Efficiency
Effects of stomatal delays on the economics of leaf gas exchange under intermittent light regimes


text:
What is the need for lobules in (human) testicles?
While I was studying the reproductive system, the question popped up in my mind. Each testicle has lobules formed out of the tunica albuginea, in which there exist seminiferous tubules. Why is the testicle divided in these lobules? What's the point? Why isn't it one single big cavity?

No. Each testicle has lobules formed out of the tunica albuginea, in which there exist seminiferous tubules. My question is why the testicle is divided in these lobules, rather than just being one big cavity. I'll update the question to include this explanation.

The structure of the testes as with many other organs in living things has all to do with form, function, and efficiency. The testes are extremely efficient sperm producers, with on average 1,500 sperm cells being produced per minute in the average human male. If the testes were just an open space of fluid with free-floating sperm producing germ cells, it would not be as nearly an efficient design, not to mention the waste caused by an inability to sort through sperm producing cells and the cells they produced.
According to this site, each lobule in the testes contains about 1-4 seminiferous tubules, each an average of 50 cm in length. Like many structures in the human body, intestinal walls, nephrons in kidneys, etc, the complex structures and organization of the cells that have a specialized function involves increasing access to the inputs and outputs of their function and increased surface area to increase that function.
This site has a helpful graphic showing the structure of the seminiferous tubules that are wrapped up in each lobule. The germ cells which split and create sperm cells are lined along the wall and when the new sperm cell they produce have developed enough, the sperm cell is released to be moved through the tubule where it can be prepared and developed further. This complex structure allows for uniform, controlled, and efficient production of sperm, essentially, a sperm factory running with an assembly line, and is a design that nature has kept and improved upon for millions of years.

Thank you for your answer. However, most of it is offtopic and doesn't really answer what I was asking. Can you back the idea that lobules make for a more efficient design? I can't find anything on the internet.


text:
DNA denaturation and Renaturation
If we denature dsDNA by heating it and then rapidly cooling it then what would happen?
I read this question, where it was written that if we were given dsDNA sample which was completely denatured and then if we rapidly cool it. What would the result be? Would it anneal rapidly too or the annealing will be slow?

If we see PCR the annealing time varies but is around 45 sec min with temperature range from 55-65 °C ( depending on Tm value). So my first doubt is that is it called rapid cooling?
In case of preserving the RNA or DNA- cooling on ice pack preserves its structure and prevents any further changes in structure also.
I tried to read papers and I read somewhere thatif we completely denature it then it anneals slowly. That takes place in two steps- first, it will try to find its completely match by collision process. Second, it will zipper up. That takes around 55 mins. So that states that it will be rapid annealing.

“I read this question” Where? Is it some sort of homework or test question. Are you sure this has anything to do with PCR? Could it be a basic question that has been used for the last 50 years and merely relates to the effect of temperature — low, medium and high on the hybridization interactions?

How long of a DNA molecule are we considering? For short fragments like in routine PCR, the collision process and annealing will occur much quicker than 55 min. What temperature is it annealing at? Think of it like molecule kinematics....

It really depends on a variety of factors. (1) the nature of the dsDNA, is it a plasmid or chromosomal DNA? Plasmids more easily renature than chromosomes, so rapid cooling and heating my not affect renaturing of plasmids, but affect DNA.
Cooling it slowly in some PCR-based experiment may be done if you want to annealing DNA fragments but are not sure about the optimal annealing temperature. Commonly done if you want to anneal two primers together for example. You need to be more specific so we can help you out.

I have edited my question. Can you check again?

To denature something can have different meanings:
In context of dsDNA it means separation of the 2 stands, while the individual strands themselves are fragmented.
I assume your question addresses PCR. In this context, rapid cooling to very low temperatures would prevent annealing of the two separated strands.
Other than that I want to point out a common misconception, that rapid cooling somehow has 'destructive' effects, which is not true. The more rapid something is frozen, the better it's structure is preserved.

But in PCR the primers are of short length, that means it would anneal rapidly as, annealing in that case is primer attachment. If I consider a complete ds DNA which would again anneal. That might be a long strand, so that would probably take more time?

A long strand takes more time. Also lower temperatures don't automatically mean faster annealing. There is an optimal temperature around 50C, where far below that the reduced molecular movement actually reduces the annealing speed.