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Cockroach brain functional anatomy
In insects like the cockroach the brain is distributed, i.e. some parts lie in the head and some in the abdominal cavity. Which part is responsible for controlling locomotion?

Technically speaking, locomotion is actually not produced by the brain in cockroaches; there are neurological controllers in the legs themselves which produce locomotion even when contact with centralized nervous system is severed.
I include this for reference, because it was not explicitly stated in your question.  However, I believe it was intended to be implied by the phrase "responsible for controlling."  In other words, from my understanding, you're more interested in what section of the brain actually controls those actions in a normal cockroach.
From Central Nervous Control of Cockroach Walking by Charles R. Froutner, you can see even just in the abstract that the movements became spontaneous when the connection with the segmental ganglion was broken, showing that this is very likely where the control is exerted.  (The segmental ganglion, for reference, is a part of the dorsal "brain" you made reference to.)

What is meant by "spontaneous movement"?

@AmitMaurya, from the article referenced: "rhythmic motor patterns, similar to those occurring during normal walking."

Ultimate control has to come from ganglion residing in head,  which receives sensory information from eyes and antennae about obstacles and terrain.

Shouldn't the locomotion after disconnection from segmental ganglion be in random direction?

Just to be clear, the brain is not distributed, it is the thoracic ganglia present in thorax that aid an arthropod for different tasks.
Arthropods have most of their sensory stimuli and motor actions controlled by Midline Brain Neurophils, called Central Complex (CC)
Quoting Journal of Experimental Biology >>

Previous studies have also linked the CC to motor actions. Huber
  showed that stimulation within the CC enhances locomotor activity
  (Huber, 1960). More recently, electrophysiology studies showed that
  the neural activity of some CC units is correlated with, and often
  precedes, changes in stepping frequency.


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The second law of thermodynamics and the cell (3 questions)?

How is that the cell maintains internal order, yet it discharges heat (disorder) to the surrounding?
If the cell is supplied with materials for metabolism and growth by the surroundings (disorderly environment), then how does that disorder generate order inside the cell?
When we zoom out from a single cell to a multi-cellular organism, will the net value of internal order of cells decrease disorder which would contradict the 2nd law of thermodynamics?
Note:I would appreciate serious informative answers. The questions are important for me no matter how silly they may look like for you.

I think you're neglecting an important point: the 2nd law applies to closed systems, and the cell (or multi-cellular bodies) is not a closed system.  It takes energy from outside to maintain its organization.  Place it in a closed box, and it will die when it has used up its internal reserves.

@jamesqf Alas, Schrödinger's cat was doomed from the beginning.

What research have you done yourself to answer this old chestnut? I entered "life and the second law of thermodynamics"  in my web browser and got a page full of links on this topic, including one that Google had highlighted.

First question: the answer is actually contained within the question.  The cell maintains order precisely by discharging heat.  The second law of thermodynamics states that the tendency of a closed system is to proceed from ordered to disordered.  Since thermal energy is (to our knowledge) the most disorderly form of energy that exists, in any given system where energy is involved, some energy will always be lost to heat.
For instance, if your cell performs the break down of ATP to drive some chemical need of the cell, some of the energy released in the breaking of the bonds in the ATP to form ADP will be lost as heat.  This means that the cell's heat is going up on average, and it must export heat to the environment.  If the heat was held inside the cell, the cell would rapidly become extremely disordered as proteins de-natured, non-enzymatic reactions sped up, and the cell basically self-destructed.
Second question:  I think you've slightly missed something.  Autotrophs (producer cells, such as plants) are the cells to actually "create order" in the biosystem.  They do this by capturing Carbon dioxide and water from the environment, and using light energy from the sun to bond them together and form complex biomolecules - usually carbohydrates.
These carbohydrates are then sent into the rest of the biosystem, where heterotrophs (consumers like me, you and the lion in the zoo) break them down to release their energy for tasks their cells need to do (cellular respiration, catabolism).  As time passes, all that energy is converted to heat and radiated from our bodies, and ultimately by the atmosphere off the Earth (barring excessive greenhouse gases.)
Third question: Not necessarily.  If the multi-cellular organism were a closed system, you are absolutely right.  The chemical energy would rapidly be all converted to thermal energy, and the order would disappear entirely.  However, bodies are not closed systems: they are continually radiating thermal energy and absorbing chemical energy, either from the sun through photosynthesis, or from autotrophs through ingestion and digestion.

A picture is worth 1,000 words:

(Image courtesy of stephsnature.com)

I would hope this picture is worth more than 1000 words, since that's only about 2 pages of single-spaced text. =P

Some pictures may be worth 1000 words, but imho this is completely meaningless, either on its own or in relation to a question on entropy. Doesn't even make good wallpaper.

@David, I thought the image was fairly self-explanatory, but maybe not, lol.  The point is that the energy coming into the system is in the form of light, the energy going out of the system is heat.  As I said in the post, heat is the energy form with the highest entropy.  Therefore, though the entropy in the system is not necessarily increasing, the energy outside the system necessarily is.  Please ping if you want more clarification.

source: Stack Exchange

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

sort: votes


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Characterising mechanisms responsible for generating structural variants
I have a high-quality set of structural variant breakpoints from tumour/normal WGS data, and I am interested in digging into the various mechanisms that might be involved in each event.
There are several mechanisms that are proposed to play a role in generating structural variants, including Non-allelic homologous recombination (NAHR), non-homologous end joining (NHEJ/MMEJ), alternative end joining (Alt-EJ) and several replicative mechanisms such as Fork Stalling and Template Switching (FoSTeS/MMBIR).
Each of these are distinct processes, that have occur at different time points in the cell cycle and have different potential for generating genomic rearrangements. However, I have not been able to find a consistent requirement for each mechanism.
I would like to know if anyone can think of a authoritative source for criteria I could use to form a working hypothesis as to the mechanism underlying each variant.
For example, if I have a 10 Kb deletion with 4 bases of microhomolgy at breakpoints I'm currently classifying it as an Alt-EJ event (largely based on the criteria I list below).
Several specific questions:
Microhomology at breakpoints is an essential requirement for several of these mechanisms (FoSTes/MMBIR). However, there appears to be no consensus as to whether this must occur exactly at the breakpoint, or whether it can be several bases away (for example here).
Secondly, according to this paper, the criterial used to classify structural variants is as follows (taken from the MeerKat manual):
NAHR: non-allellic homologous recombination, >100bp homology.
alt-EJ: alternative end joining, 3-100bp homology.
NHEJ: non-homologous end joining, 0-2bp homology or 1-10bp insertion at deletion break point.
FoSTeS: fork stalling and template switching, template switch, >10bp insertion at deletion break points.
However, almost every paper I read suggests different criteria, for example FoSTes events are normal associated with microhomologies at breakpoints rather than insertions.
Can anyone suggest a "consensus" of requirements for each mechanism?

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Why does the amount of adipose tissue contribute the most to the total body water amount in humans?
I don't quite get this concept. An obese individual will have a greater fat content in their body, and thus will have 45% water in their bodies (for example), versus a slim person that will have 75% of body water and a much lower fat level.
Is this because fat is made up of about 10% water, so the more fat you have in your body, the more water it "takes up" from the entire body water supply of your body?

Are you sure of your numbers? Can you name a source?

I am getting these numbers from my professor's notes, Dr. Melissa A. Vollrath, and she got them from the textbook Vander's Human Physiology: The Mechanisms of Body Function (14th edition)

Fat mass does not take up water.  It brings with it less water percentage than lean mass and so a person with more fat mass will have relatively less % body water.  Additional mass as fat contributed relatively less water than additional mass as lean tissue.
Consider a 50 kg individual who is extremely lean.  From your numbers, if this individual is 75% water (will will assume lean tissue is 75% water) that is 50 * .75 = 37.5kg water and 12.5kg nonwater body mass.
Now this 50 kg individual puts on 50 kg of fat.  The fat is 10% water (from your numbers) so an additional 10 kg of water.  This individual its now 47.5kg water and 52.5 nonwater; since this obese person weighs 100 kg now she has 47.5% water, similar to your example.
Suppose instead your 50kg person grew up into a 100 kg performance athlete.  Still no fat.  She is still 75% water because the lean tissue has 75% water.
It has to do with the % water each type of body mass brings with it.  This is with no special knowledge; using just the numbers in your example which is what your professor wants you to use.

Considering 100 kg fat or lean person - fat seems to substitute water? Water instead of fat?

@PeterBernhard - it is % water by weight of biological tissue.  Biological tissue lean or fat has some % water.  The % water is greater in lean tissue than in fat tissue.

no chatting: interesting you mention "athlete", as "obese" just put on more absolute kg weight than the lean ones (non athletics).

All living cells have water content. Fat tissue is made up of living cells, but fat cells have much more triglyceride and lipid content than water content. So fat tissue still has some water content even though it is mostly made of lipids.
An obese person should have more total body water because of this, and also he/she will usually have more muscle mass in the lower body as well.
The obese person will have a smaller percentage of water relative to their mass than a lean or muscular person would.

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Is there a taxon that "adaptively" radiates faster?
It seems that there are some taxa that have a greater potential to radiate through adaptations. Off my head, I can think of birds:

Darwin's finches
Hawaiian honeycreepers
House finches (Carpodacus mexicanus)
Manakin (or other passerine birds)

Also, there are some fish:

Cichlid fish (Lake Victoria in east Africa)
Threespine Stickelback

Plants:

Hawaiian silverswords
Erythranthe lewisii (Lewis' monkeyflower, great purple monkeyflower)

Lizard(s):

Anolis lizards

Insects:

Heliconius butterflies
Drosophila (Hawaiian Drosophila particularly)
Spider (Maybe peacock spider)
Leaf beetle

Generally:

Angiosperm plants
Dinosaurs
Marsupial mammals
etc.

So, is there a group of organisms (taxa could be any level: family, gender, species...) that is consistently radiating more than other?
By radiation I take the points that Grant defines here:

These examples have the following in common: (1) they comprise
  several to many species, (2) the species vary morphologically in
  conspicuous ways, and relatedly, (3) they occupy a diversity of
  ecological niches. Most of the species were (4) derived from a single
  ancestor in their current environment, and (5) most diverged
  relatively rapidly.

Threespine Stickelback and Brassica (and other domesticated species) are other examples.

Book recommendation: The Ecology of Adaptive Radiation by Schluter

Mammals have 2x times larger genomes than birds and lizards, and they radiate faster, which is why there are whales, moles, seals, bats. They have larger genomes partly because mammals have developed anucleated blood cells which are smaller and more flexible than birds, and if birds had very large genomes their blood cells would be less performent. Otherwise there could be burrowing and oceanic birds.

@com.prehens.ible I understand you did not write an answer but just a comment, but really I would need to see a reference stating that 'genome size is correlated with speciation rate and this correlation has to do with blood cells' to believe your comment.

@Remi.b do you think that domesticated species could be thought as adaptive radiation?

Beausoleil, Do you mean phenotype of breeds or species domestication? Remi,esesntially, birds have no choice about accumulating genes. they can't do it well because it clogs their capillaries: (iii) Estimates of speciation interval in mammals correlate positively with genome size. (iv) Genome reductions are inferred at the base of particular species radiations and genome expansions at the base of others. Not a single mammal has a smaller genome than a bird, i.e. a thimble sized vole's is larger than an emu's.

@M.Beausoleil Yes, sounds legitimate to me to not refuse the term to domesticated species. Franske et al. (2011) talk about adaptive radiation of cabbage.

@com.prehens.ible Oh.... sounds very interesting. Thank you. I managed to find a few reference on the subject (e.g. Kraaijeveld (2010)). I'll study this a little bit, sounds quite extraordinary. If you happen to have a reference for the idea that speciation rate is slow in brids than in mammals becuase of small genome size and genome size is smaller in birds than mammals because they have nucleated RBC, I'd be happy to have a look at it.

You are probably right Remi, We learned that there were many dormant genes that were shed if the genome became compact, except that was 20 years ago, today they talk mostly about gene repetitions. Anyways, birds could not radiate to whales because of the egg laying issues more than the chromosomes, else penguins perhaps could have made it to whale type ecologies.

The species from your list have some common traits:

Fast metabolism of themselves, food and fertilizers
sexual reproduction is more complex than crabs and coral
complex ecosystems and fast changing ecology
lots of ecological competition generally advanced compared to ferns, moss and crabs
More Possibility to travel through gene bottlenecks
recent in fossil history
prevalently small
possibility of population explosions
generalist and robust flexible habits and traits like tree nests, live birthing, flying, fangs, close inter-animal relations i.e. with bees,

If you study animals that have sedate speciation habits like platipus, they are limited in many of the common traits from that list.
The animal is therefore mostly dependent on it's ecosystem's stability, richness and opportunities, as well as the specie's own physical wealth, opportunism and stability. Those species have very complex and flexible ecology cycles working over them at a high rate. The rate of change of the ecology is also dictated by the other's organisms ability to radiate in record times, so today's species are in an arms race of the fastest rates of change in predator-prey-reproduction traits, with all the tools of the trade, i.e. fast movement, strong protection, freaky efficient cell-type mutations, locomotive, feeding, protective and spacial habits that by themselves can define the base of the most prevalent recent families.
Some species RNA is more susceptible to change and has to be be counterbalanced with different checks, it's to keep up with the arms race of competition in the complex ecology spaces of most of the planet.

You only need two things to radiate rapidly, fast reproduction and opportunity, many of the species mentioned changed rapidly becasue they had access to a wide open environment with little or no competition. They are also small quick reproducing, the faster you breed the faster you can change. A rodent can go through 60 generation in the time an elephant goes through one, that is 60 times as many changes that can occur. Small organisms tend to breed faster so in general small things evolve faster. This is believed to be part of the reason birds survived when other dinosaurs did not.
Another noted factor is generalists tend to survive change better than specialists which means they tend to get to radiate more, they are not necessarily radiating faster they just tend to survive whatever changes opens up niche space for more speciation. Specialists are more likely to go extinct, so generalists end up with more opportunity to radiate.
Now another important facet is preadaptations that can affect oppurtunity. For instance animals with hox genes have a big advantage in creating different body plans over ones without, like nematodes, but note this is only an advantage in this one facet of change, nematodes are arguable one of the most successful lineages ever, they just all have similar body plans. Some argue that having exons/introns helps by more dna to experiment with to get useful mutations, but right now this is just supposition.
Another example of a preadaptation is mammals could not radiate into large sizes until dinosaurs were not around, for instance it was easier for a large dinosaur to expand into large insectivore niche by changing diet than it was for insectivore mammals to evolve large size and all the adaptations to go with that. the dinosaur just had better preadaptations to fill the niche.


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Why does no one get vaccinated against plague in Europe?
I've read on Wikipedia that only people who work with Y. pestis and people in 3rd world countries get vaccinated against it:

Since human plague is rare in most parts of the world, routine vaccination is not needed other than for those at particularly high risk of exposure

But I know that it is easy for plague to conquer Europe. All your need is just some fleas and half of the continent dies, as proved in history.
So why does no one in Europe get vaccinated against plague?

Because it is not necessary. Living conditions have dramatically improved since the last time the black death got over Europe.

@Chris but why did improving living conditions affecting plague and not other diseases agains which we are getting vaccinated. My friend is an anti-vaxxer and I have to convince him, yet I am not a specialist.

Also, it's arguable that the people who survived the Black Death and other plague outbreaks had a degree of natural resistance, which they passed on to their descendants.  Consider how measles &c were able to kill off a large fraction of the population of the Americas after European contact.

I'm voting to close this question as off-topic because it is of low quality. "All you need is some fleas" indeed.

Ask yourself when was the last time that you went to a friend's home and had to worry about getting flea bites? Modern cities still have lots of rats, but modern construction, pesticides, and hygiene have greatly reduced the number of encounters between fleas and people. Contrast that with the early 18th century. When the young George Washington wrote an essay on civil behavior, he felt it worth while to include this item:

13th Kill no Vermin as Fleas, lice ticks in the Sight of Others, if
  you See any filth or thick Spittle put your foot Dexteriously upon it
  if it be upon the Cloths of your Companions, Put it off privately, and
  if it be upon your own Cloths return Thanks to him who puts it off.

Plague is almost exclusively transmitted to humans by fleas (the pneumonic form of the disease can be transmitted by aerosols but is rare). Few encounters with fleas, few cases of the Plague.
Mumps and measles (for example) are transmitted by human to human contact. No fleas needed. Modern life may have done away with flea bites, but it has only increased the number of persons we come in contact with each day. If you think about it, all the diseases we commonly get vaccinations for are ones spread by direct human to human contact: smallpox, polio, diphtheria, whooping cough, mumps, measles, flu. Tetanus vaccines are an exception, but that's a bacteria that is ubiquitous in the environment, and causes a very nasty disease.

https://news.nationalgeographic.com/2018/01/rats-plague-black-death-humans-lice-health-science/

Because antibiotics are relatively cheap and effective against Y. pestis. Also our easy access to high quality healthcare ensure that diseased individuals are rapidly isolated and threated. Therefore the benefits of the vaccine does not outweigh the riscs associated with it.
You can then argue from now till the end of time of whether other vaccines are worth using. Personally I trust doctors and other scientists to analyse the available data and make the best choice in each case.

my great gran said she didnt trust doctors and she lived till 99 and 10 months. never saw one! a bit of cynicism goes a long way.

Sure, but unless you have spent 5 years of your life studying medicine, life sciences, biology or chemistry, you have no basis on which to base your decision. Therefore you will be prone to make false assumptions based on wrong, partial or non-existent knowledge.

Plague infections are extremely rare outside of the third world. For the rare occasion that isolated cases of plague make their way into the developed world, plague bacteria overall haven't had much contact with antibiotics (few opportunities to develop resistance) and therefore are generally vulnerable to a standard antibiotic course.
Modern sanitation also helps a lot.


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Why cornstarch for athlete's feet?
It seems like a lot of foot (anti-odor or antifungal) powders are often based off of cornstarch (i.e., as the primary filler).
But wouldn't cornstarch (which, in some places, is also a common food additive) just feed the undesired microorganisms anyway? Or, perhaps, is its dessicating effect so powerful so as to nullify whatever nutritional value it might provide anyway?

athletes foot is not a carb specialized fungus, skin is higher in protein... its more likely to develop species unfavorable to athletes foot. put a cheese  in cornstarch, it may get marred... experiment time

Talcum powder was originally finely powdered talc, a rock, but talc is technically in the same mineral family as asbestos, it is completely harmless and not the same as the dangerous mineral used in insulation at all, (it is actually used as an additive in table salt). But some early talcum powder did contain actual asbestos, as does industrial talcum* today, this only made it more confusing. Manufacturers that used talc took a lot of flack during the asbestos scare (you tricked me into putting asbestos on my child), there were many lawsuits.  Corn starch is now used as a replacement for talcum powder in many many things labeled talcum powder, baby powder, or body powder.
The cornstarch is acting as a carrier/filler, so no its probably not the best thing because the fungus can metabolize it and it does not need to be there but the companies prefer using it to dealing with misinformed disgruntled buyers.
*talc and asbestos often occur in the same deposits.


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Speed of molecules in human cells?
What is the average speed of molecules in human cells?
Are there molecules moving much faster than others? What is it due to?

Speed? Are we talking about rate of diffusion, directional movement by energy expenditure or something else, please clarify.

And what kind of molecule?


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What is the difference between neurotransmitters acting as neurotransmitters and hormones?
My main confusion is what differentiates the action of a transmitter substance as a neurotransmitter and as a hormone. For example, when norepinephrine is being talked about as transmitter substance that modulates brain responsiveness and information processing, it's a neurotransmitter. But when norepinephrine is involved in the functions of the autonomic nervous system (ANS), does it work as a hormone or a neurotransmitter?
Quoting from Physiology of Behavior, by N. Carlson, 2013 edition:

"Neurons in the central nervous system contain a1- and a2-adrenergic
  receptors and b1- and b2-adrenergic receptors. All four kinds of
  receptors are also found in various organs of the body besides the
  brain and are responsible for the effects of epinephrine and
  norepinephrine when they act as hormones outside the central nervous
  system."

So does that mean that whenever norepinephrine works outside the CNS, it works as a hormone?

This figure from Campbell (2011), chapter 45, is very didactic and may clarify this nomenclature for you.
The processes of interest here are a, d and e:

The definition of hormone (in animals) is quite simple: a signaling molecule released in the bloodstream. That's the process a in the figure.
On the other hand, a neurotransmitter is released in the synapse, acting locally. That's the process d in the figure.
However, some nerve cells release their signaling molecule in the bloodstream (process e in the figure). Unlike the synaptic signaling, this molecule can act on a target cell at great distance.
So, despite the fact that we're talking about the very same molecule (norepinephrine in your example), in that last process this molecule is technically speaking a hormone, not a neurotransmitter anymore.

Source: Reece, J., Reece, J. and Campbell, N. (2011). Campbell biology. Boston: Pearson Learning Solutions.

Right.  It's nomenclature to differentiate actions and release in the CNS (neuronal) versus outside (endocrine in this case). A neurotransmitter will act locally to it's release site typically from a neuronal synapse, while hormones tend to be released into the bloodstream and can act much further away as well as at a different time scale.
Source from textbook: Principles of Neural Science (Fourth Edition), Kandel et al. 2000, McGraw-Hill Medical ISBN 10: 0071120009


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Infra/Ultra sound exposure
What risks are associated with ultrasound/infrasound listening via bone conduction?
Would you risk yourself serious physical harm doing this?
What levels for these frequencies are safe to the human body?


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What kind of spider is this from Sydney, Australia?
I was cleaning the pool when this guy crawled on my foot. I hit him away and noticed a bite mark. I managed to snap a photo of him.

I went to the doctor because I was worried it was a funnel web and she told me to just keep an eye on it, ice it and take anti histamines if it itches.
I have a tiny bit of tenderness in my foot.

Good news is that this is definitely not a funnel web spider (Atracinae), which, by the way, is not that dangerous✻.
The image doesn't have a good resolution, but that seems to be a spider from the Family Lycosidae, known as wolf spiders, more specifically Venatrix pictiventris.
Here is an image for comparisson:

Source: http://www.findaspider.org.au/find/spiders/497.htm
This is the distribution of Venatrix pictiventris in Australia, going from Tasmania to Queensland, with most observations in New South Wales:

✻ I advocate for the protection of sharks, spiders, snakes, bats etc. So, whenever I can, I try to demystify arachnophobia. People love saying that the funnel web is deadly and so on, but for you to have a better idea, moths (e.g. Lonomia) kill more people than spiders.

Thanks! The photo you provided looks very similar to the guy that got me.


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Behaviour of chromosomes and genes
I recently read a comparison between behaviour of chromosomes and genes - which had two statements understated -

Independent pairs segregate independently of each other
One pair segregates independently of another pair

I further found that the first one indicates segregation pattern of gene and the second accounts for chromosome.
But that bothers me, I am unable to compare chromosome and gene on this basis. I feel the two statements really confusing and it appears to me that both the statements apply both to chromosomes and genes.
Though, law of segregation for genes includes one pair of genes that segregate independently of each other but independent pairs too segregate independently of other pairs. As genes are present on chromosomes, what then defines their segregation differently.
Also, what does segregation of chromosomes imply? Does it include separation of sister chromatids in anaphase of meiosis as well as mitosis or separation of bivalents also during meiosis?
Is the question biased on independent assortment more than segregation pattern, please do correct me.
Those doubts appear absurd to me, but I hope that someone would help me, please.

Direct quote, please!
Please, when you are referring to something you've read, always add a link and attempt to offer direct quote. From your question it is a little hard to understand what is the original claim about. I suspect the following will help you though.
First, definitions
First, you might want to make sure, you know the definitions of

allele
locus

Segregation and recombination
There are two concepts you shall examine. Segregation and Recombination
Segregation
Segregation is the process by which hommologous chromosomes are independently separated into different cells during meiosis. The concept of segregation was first discovered by Mendel and expressed in his law of segregation

The Law of Segregation states that every individual organism contains two alleles for each trait, and that these alleles segregate (separate) during meiosis such that each gamete contains only one of the alleles.

Note that this law is partially (or mainly) wrong as it assumes that each phenotypic trait is affected only by a single locus with two alleles which is actually very rare.
Recombination
I am here describing recombination by its effects and by relating it to segregation. Recombination is the process that causes genes phyiscally linked on the same chromosome to not segregate entirely together. Recombination is caused by chromosomal cross-over, which are "recombination" between the "content" of the two homologous chromosomes. When chromosome segregate, it is actually the recombined chromosomes that segregate (in terms of the molecular machinery both process of segregation and recombination happen very much at the same time actually).
The concept of recombination has been discovered by Morgan with his fruit flies experiments. The Morgan is actually used today as a unit of recombination distance between two loci.
Source of information
You can have a look at any intro course to genetic such as these courses by Khan Academy for example.

Sorry for not providing link. I would try adding link next times.

@VidhiGupta No worries. We all go through the phase of learning to ask very good questions.

Definitely. This one is just the second question I have asked on this site and I am actually happy about it. Hope I would get an answer to my queries or maybe some more queries...

The difference is:

Different chromosomes always segregate independently
Different genes may or may not segregate independently

There are different mechanisms at work. The chromosomal segregation mechanism always separate chromosomes randomly (independently), as whole chromosomes are moved as a unit.
A different mechanism causes segregation of genes that reside on the same chromosome. It sends only large pieces of the chromosome to different daughter cells.  Each piece contains many genes, so within a piece, the genes don't separate at all, so do do not segregate independently.
When two genes are on different chromosomes, they segregate independently because their chromosomes segregate independently.  When two genes are on the same chromosome, they do not segregate independently since they may end up on the same segregating piece of their chromosome.

what about chromatid separation? Don't they segregate independently from each other.


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What is a set of chromosome and what is a pair of chromosome
What is the definition of set of chromosomes? Does it differ from pair of chromosomes?

Yes those two expressions refer to different things.
Set of chromosome
The term "set of chromosome" refers to ploidy number. A haploid has one set of chromosome, a diploid has two sets of chromosomes, an hexaploid has six sets of chromosomes.
In humans, each set of chromosome is made of 23 chromosomes (22 autosomes and 1 sex chromosome).
Pair of chromosome
A pair of chromosome refers to the two homologous chromosomes in a diploid individual (one chromosome from each set for a given chromosome number).
Source of information
If the above is unclear, then you should have a look at any intro course to genetic such as these courses by Khan Academy for example.

Plz clarify this a bit more. 1- Does each set of chromosome come from mother and father in a PAIR of chromosome?  2- Chromatid - a single chromosome in a newly copied pair - Do Two Chromatid contain the Identical DNA  sequence ?

Yes, although most of the time, we don't know which chromosome of a pair comes from which parent (we don't know which chromosome of a pair belong to which set). 2) Yes. There are many related posts to this second question of yours. E.g. see What are homologous chromosomes? or Chromosome and chromatid numbers during cell cycle phases. Feel free to open a new post if you've got more questions.


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What animal is this (snake/slug/worm)?
I found this guy in my driveway this morning. I live in Northern Florida, near Jacksonville.
I initially thought that it was a baby snake (note the black on brown lengthwise stripes), but it moves very slowly and methodically, like a slug, perhaps. Never saw a slug so long and skinny.
He's about 3.5 inches (90mm) long, and can hold his head up high to look around, raising up almost a third of his total body length.
Maybe some kind of worm?
The "hammerhead" style head is what is making me scratch mine.

Look up (Google Images) "hammerhead worm". You'll see your pretty little guy.

They are also likely to be invasive to North America, so feel free to squash if you prefer. .

Or catch it and see if it will eat an earthworm.


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A stem cell method for creating artificial wombs?
1) Grow the endometrium using stem cells (It has already been done (Cambridge, 2017))
2) Attach the embryo to it and allow the placenta to grow.
In 2003, there was a
researcher at Columbia  who did something like this, but there was no technology  to create endometrium tissue. She used some donated infertile tissues, but the rat embryos did attach to it and grow, although the growth itself was retarded. That's understandable since the endometrium has some special secretory functions.  So what could be the issues with the method I have suggested?
A lot of the new approaches seem to involve artificial placentas , which are probably not very easy to create. The don't seem to be the most obvious approach either. I think a large part of the issue is that you won't get funding if you say you want to create an artificial womb, because of the ethical issues involved. So you have to show some connection to neonatal stuff and hence the easiest approach is neglected. Am I right in this assessment?

Links to the papers you are referring to would be much appreciated.

@alec_djinn I have included popular science articles.

personally I think that artificial wombs grown by robots are the only way that advanced speciecs such as humans can be reborn on a star system 100 or 1000 light yeaers away. i like the technology.  ... Your question didn't specify In Vivo or Vitro artificial wombs. you need heart/blood/lymph etc.

In the paper you have (indirectly) linked, the authors describe cultures of organoids. Despite their fancy name and the catchy title of some news article about them, organoids are very far from being mini organs. They are a bunch of cells that grow in a 3D structure and they may resemble an organ in term of cell type and some cell-to-cell communication, but that's pretty much all. Mind that an organ is vascularized, organoids are not. The vascularization allows for organ-to-organ communication, like the delivery of brain-made hormones, for example. Such communication is extremely important during the embryo development, it's not only the endometrium missing here. I am not saying that is impossible to make artificial wombs, but organoids alone will not be sufficient.

Well, as far as I understand, the womb requires just one tissue effectively, the endometrium. The other tissues in the womb (smooth muscle, stem cells) are not necessary if you just want gestation. So it doesn't seem like an entire organ with all the signalling is required. The hormonal levels in the blood itself can be mimicked I guess, as long as those hormones can be received and understood by the endometrium.


text:
How is Glyceraldehyde 3-phosphate converted into glucose?
In the light-independent reaction of photosynthesis, one of the products is glyceraldehyde 3-phosphate, and the Wikipedia page on the light-independent reactions states that 6 of these can be used to form glucose.  However, the Wikipedia article on gluconeogenesis does not mention this, and the Wikibooks article on gluconeogenesis only mentions the molecule glycerinaldehyde 3-phosphate (which I'm not sure if it's a typo, because I can't find any information on glycerinaldehyde).
So how does G3P actually become glucose (and is there a good reason this information is not available on those Wikipedia pages, plus the page on G3P)?

Advice to students of biochemistry
This site is concerned with biology, not with biological entries in Wikipedia. Wikipedia is a voluntary effort to which anyone may contribute, and is full of errors and omissions. It’s structure means that it is focussed on individual small topics, rather than presenting an integrated account of various areas of science. The student who wishes a balanced integrated account of a topic that has been subjected to editorial review should consult a text book. Those whose resources do not permit this should try searching on NCBI Bookshelf, which provides free on-line search-only access to old editions of texts. For biochemistry, Berg et al. is recommended.
The generation of glucose from triose produced in the dark reaction is well understood
The answer to the question can be found in e.g. Berg et al. 20.1.3:

The 3-phosphoglycerate product of rubisco is next converted into three forms of hexose phosphate: glucose 1-phosphate, glucose 6-phosphate, and fructose 6-phosphate... The steps in this conversion (Figure 20.9) are like those of the gluconeogenic pathway (Section 16.3.1), except that glyceraldehyde 3-phosphate dehydrogenase in chloroplasts, which generates glyceraldehyde 3-phosphate (GAP), is specific for NADPH rather than NADH. Alternatively, the glyceraldehyde 3-phosphate can be transported to the cytosol for glucose synthesis.

Berg et al. Fig. 20.9
The Section 16.3.1 referred to is a general treatment of gluconeogenesis, which is the same in all organisms or cells that possess the enzymes to catalyse its unique steps. (Some cells may not have — or need to have — the initial steps from pyruvate. In fact, Fig. 20.9 shows the steps to G 6-P — the only step missing is the phosphatase step that generates glucose.) There is therefore no reason to expect an account specific for plants.

Nice!  That paragraph from Berg was exactly what I was looking for. +1

Glucose is made from the trioses (3-carbon sugars) in plants according to the usual gluconeogenesis pathway.  That is, glyceraldehyde phosphate is converted to fructose-1,6-diphosphate by triose phosphate isomerase and aldolase, and then dephosphorylated to obtain hexose phosphates. Free glucose is not usually the end product in plants though; instead, glucose is coupled to ADP for use in synthesis of starch.
I'm afraid I did not find any good open-access references on plant gluconeogenesis, but it should be covered in most biochemistry textbooks.

The tricky part of gluconeogenesis is going from pyruvate to phosphoenolpyruvate. If you're starting with glyceraldehyde 3-phosphate, going backwards to glucose is easy. It's just the normal (reversible) glycolysis enzymes, used in reverse. (So if you're looking for references, look for those which say that that part of glycolysis is reversible.) -- This probably explains why it's not mentioned explicitly. People intimately familiar with central metabolism would think it "obvious" that it can run backwards.

@R.M.   Actually, glycolysis "above" glyceraldehyde phosphate is in fact not reversible, due to the phosphofructokinase step, which must be bypassed by fructose bisphophatase to be energetically favorable.

@RM — The ”tricky step“ is hardly relevant to this question as we are starting from glyceraldehyde 3-phosphate, not pyruvate. Remember that cells such as fat cells that use the pentose shunt to generate NADPH can return G 3-P to glucose via the latter half of the gluconeogenic pathway but do not possess the enzymes for using pyruvate as a gluconeogenic substrate.


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Population where most of the newborns die soon?
Is there an ecological name to describe a population of organisms where most of the newborns die after birth without reproducing? The population as a whole keeps growing, however, because there are enough individuals that manage to reproduce.

Yes, we talk about r/K selection theory:

In ecology, r/K selection theory relates to the selection of combinations of traits in an organism that trade off between quantity and quality of offspring. The focus upon either increased quantity of offspring at the expense of individual parental investment of r-strategists, or reduced quantity of offspring with a corresponding increased parental investment of K-strategists, varies widely, seemingly to promote success in particular environments.

The type of species you describe are the r type.
Please note the following potential confusions:
A species can vary its strategy through time and space
Species can change from K to r (and vice-versa) depending on the environment and number of individuals. Consider humans as an example.
The expression r/K selection theory can be misleading
The term "selection" in "r/K selection theory" can be a bit misleading as it refers more to a demographic reality (which has come to be due to selection pressures) but not to the selection process behind it.
Alternative meaning of 'r/K selection theory'
The terms r and K are sometimes used to mean whether a species has reached carrying capacity (K) or whether they are growing in number (r) which is not exactly the same as the interpretation of whether there is much parental investment in the species presented in the wikipedia article.
This second interpretation is actually closer to the origin of the terms r and K. The most common (and one of the simplest) equation of population growth through time is the logistic equation (see here for an easy explanation and also wiki > Population ecology )
$$\frac{dN}{dt} = rN \left( 1 - \frac{K}{N}\right) $$

, where $N$ is the population size, $t$ is time in generation, $r$ is the maximal growth rate and $K$ is the carrying capacity. On the graph above, $r$ represent the maximal slope (that is the maximal growth rate).
r selected species are those that have a growth rate as indicated at the center of the graph. K selected species are those that have a growth rate of 1 (no increase in $N$) as the ones that are at carrying capacity $K$.

Thanks, very good answer. That's the term I was looking for. On the other hand, is there a synonymous name for it, that is just a word, in use, instead of this name that involves an $r$ from an equation?

You can just talk about an r-selected (or r-strategy) species. I don't think there is another term. If it is not intuitive enough when you talk to lay people, you can talk about species that favour quantity over quality of offspring.

Remi is right the closest you get to a term is r-strategist or K-strategist. Also keep in mind these are ends of spectrum not discrete categories.

@becko They are also said to have a fast life history as described in life history theory which is a theory built upon r/K-selection theory.

@Eff Thanks. Can you point to some references?

@becko I would simply start with the wikipedia article on life history theory. I may be able to find some good references later (I'm not with my computer at the moment). Remember that both r/K-selection and Life history theory are concerned with many traits other than number of surviving offspring. In fact, a whole suite of life history traits are correlated: maturation time, lifespan, number of offspring, size of offspring, amount of parental investment, etc. Fast life history is roughly equal to r-selected, and slow is K-selected.


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Why is GTP, rather than ATP, used in nuclear transport?
Why is GTP used for nuclear transport and not ATP, given that ATP hydrolysis is used to drive most cellular energonic reactions?

Welcome to Biology SE! This appears to be a homework question. Homework questions are off-topic on our site unless you have shown your attempt at an answer. For more information see our homework policy.

Would be very interesting to know, if there was some systems-biology reason (that would extend beyond a superficial answer such as the most prominent nuclear transport proteins using using GTP). (note: ATP can be required for some aspects of nuclear transport, in particular for RNA)

@vkehayas  I think this is an open question in biochemistry, and as such not likely homework (or else a very tricky assignment :)  To my knowledge at least, it is not understood why different nucleotides are preferred as energy source by different systems -- if indeed there is any advantage to this scheme at all.  Protein synthesis and gluconeogenesis (PEPCK) also uses GTP, btw.

@Roland I am aware that this is not a resolved issue. I was attempting to nudge the OP to give us some background on why this question is interesting to them and what research they have done already.

I have edited the question slightly and removed the homework tag as I don't think it relevant. (I have gone on to provide an answer of sorts.)

Disclaimer
Although this question appears to be either unclear or unanswerable (or both), and shows no evidence of research on the poster’s part, I have chosen to address one aspect of it to emphasize a general concept. This, despite the fact that my knowledge of nuclear transport processes is minimal.
Brief Answer
GTP, rather than ATP, is used for nuclear–cytoplasmic transport via importins and exportins, because this process involves one of a large family of ‘G proteins’ that — as their name implies — operate through the use of GTP. Whereas ATP is generally used to drive endergonic molecular reactions, the hydrolysis of GTP in G-protein cycles can be thought as a device to terminate a molecular process. Whether G proteins adopted GTP rather than ATP merely by chance or for a biological reason is a matter of speculation.
NTP hydrolysis — for fun or profit?
It would appear that the question relates to protein-transporting ‘importins and exportins’, which I learn from the Wikipedia article on nuclear transport are regulated by the small G protein, Ran. When complexed to GTP, Ran facilitates the export of proteins by exportins, a process that is terminated by hydrolysis of GTP to GDP. The GDP-bound form facilitates the import of proteins by importins, a process that is terminated by GTP displacing the GDP.
So if we consider the role of the hydrolysis of the nucleotide triphosphate — here GTP — it is clearly not to supply thermodynamic energy for an endergonic process such as muscle contraction, light generation or a chemical reaction with a +ve ΔG:

Rather, it is to produce a conformational change in a protein which allows the termination of a process. This termination is generally through the GDP-bound form of the G protein (grey) interacting with some other protein (black):

This diagram is deliberately simplistic so that the general features of G-protein action can be seen. However, I think it illustrates the same point made in Berg et al. Section 15.6. Other examples are signal transduction of hormone action via cyclic AMP and binding of aminoacyl-tRNA to the ribosome.
Why do G proteins use GTP?
This ‘choice’ of GTP in the original ancestral G protein could have been mere chance, that was subsequently reflected in other G proteins that arose through gene duplication and divergence. That would imply that, at least, it was not disadvantageous. Or as the oldest G proteins are perhaps those involved in protein biosynthesis — a process still catalysed by a ribozyme — the choice of GTP might have reflected an RNA base-pairing interaction in the ‘RNA world’.
Alternatively one might suggest a biological rationale for separating two types of energy-requiring processes — perhaps by regulation of the enzyme that catalyses the conversion of ATP to GTP, dinucleoside-phosphate kinase. However I am not aware of any evidence to support this idea.
Hydrolysis of GTP in other contexts
As mentioned in a comment by @Roland, there are instances where GTP is used to drive endergonic reactions (phosphoenolpyruvate carboxykinase) in a manner analogous to the use of ATP, but this is quite different from hydrolysis of GTP in G proteins. I do not believe that any convincing rationale for this has been propounded, nor for the similar exceptional use of UTP in glycogen synthesis and CTP in phospholipid synthesis. This question has been discussed in another post.


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How do we call a "burst of evolution"?
I have in mind that evolution is not a constant / continuous process and that there are bursts of evolution.
Are there terms to refer to the concepts of fast vs slow evolution rates?

FYI, I was motivated to ask this question to address this question by @HarryWeasley in a comment.

Thanks a lot! It was indeed  'punctuated equilibrium' which I was referring to when I said 'bursts of evolution'! Thanks again, it's rare for someone to post a new question based on just a comment of mine!+1 for both your question and answer! :)

They talk about a cambrian explosion, but that's more an explosion of life. it's a form of genesis in unscientific terms, genesis, so it's an apex/ peak/ of species genesis.

There are indeed periods of fast evolution and period of evolutionary stasis. The term "burst of evolution" is never used in the literature but below are three common terms when discussing these concepts.
First we have to realize that the term 'speed of evolution' does not mean much. We can be talking about change in phenotype through time (See Punctuated Equilibrium and Evolution and Ecology time scales) or speciation rate (See Adaptive Radiation and Mass Extinction). Also, we have to realize that we can talk about such speed of evolution on a given taxon or for the entire life on earth.
Punctuated Equilibrium
We often refer to the fact that there are periods of evolutionary stasis and periods of rapid evolution as punctuated equilibrium

Punctuated equilibrium (also called punctuated equilibria) is a theory in evolutionary biology which proposes that once species appear in the fossil record they will become stable, showing little evolutionary change for most of their geological history. This state is called stasis.

Here is a representation (from the above wikipedia link) of phenotypic divergence following an extremely gradual view of evolution and an extremely "punctuated" view of evolution

Evolution and Ecology time scales
Since the 2000s, there has been increased recognition that evolutionary processes even matter on a ecological/demographics scale. That is ecological/demographics processes and evolutionary dynamics influence each other dynamically and the old view that evolutionary processes are much slower than ecological/demographics processes is sometimes wrong.
See the post History: Do evolutionary and ecological processes occur at the same timescales?
Adaptive Radiation / rapid diversification
The speciation rate also varies through time. There are "burst in speciation rate" if you like the term. A sudden burst in speciation rate is called an adaptive radiation

In evolutionary biology, adaptive radiation is a process in which organisms diversify rapidly from an ancestral species into a multitude of new forms, particularly when a change in the environment makes new resources available, creates new challenges, or opens new environmental niches. Starting with a recent single ancestor, this process results in the speciation and phenotypic adaptation of an array of species exhibiting different morphological and physiological traits. An example of adaptive radiation would be the avian species of the Hawaiian honeycreepers. Via natural selection, these birds adapted rapidly and converged based on the different environments of the Hawaiian islands

You can find a list of classical examples of adaptive radiation on the above wikipedia link or at the post Is there a taxa that radiates faster?. If you don't want to be too extreme, you can as well just use the expression rapid diversification.
Mass Extinction
There are essentially two differences between an adaptive radiation and a mass extinction. 1) one is about an increase in speciation rate while the other is an increase in extinction rate. One is about a single taxon, the other one concern most of life on earth.
Because, a mass extinction sounds quite apocalyptic and because we seem to be at the start of a new mass extinction, most people are familiar with this term.

An extinction event (also known as a mass extinction or biotic crisis) is a widespread and rapid decrease in the biodiversity on Earth. Such an event is identified by a sharp change in the diversity and abundance of multicellular organisms. It occurs when the rate of extinction increases with respect to the rate of speciation. Because most diversity and biomass on Earth is microbial, and thus difficult to measure, recorded extinction events affect the easily observed, biologically complex component of the biosphere rather than the total diversity and abundance of life.

I want to highlight that when thinking of a mass extinction, many people think of a single event clearing up the surface of the earth in a day but the reality is very different. In fact, a mass extinction can well last thousands of years.

Great answer! Almost accepted it before I realized I hadn't posted the question! (+1)!

well to start evolution is continuous but not a constant rate. The rate is controlled by population size and the extremity of the selective pressure. Strong pressures in small populations tends to result in more rapid changes than weak pressures in large populations.
As for what to call rapid evolution it depends on what form of evolution is being seen.

For instance a single large change in a single generation (often becoming a speciation event) is called saltation and is extremely rare, especially in animals, requiring a perfect storm of conditions.
A founder effect induced rapid change is called a Genetic Revolution, although you will see it referred to as just a founder effect more often, and is caused by drastically decreasing the population which causes changes to spread much faster.
Technically extinction might also qualify as a rapid evolutionary change.
Quantum evolution is a hypothetical change in which new higher taxa arrise, but it is both poorly defined and there is absolutely no evidence it has ever occurred, indeed it appears to be mostly an artifact of how classification is determined, so I would hesitate to use it.
Macromutation is the term for large single mutational changes, things like  cold shock gene duplication would fall under this category. Tissue morphogenesis would be related to this, as it is a large developmental change which may or may not be the result of a large genetic change. A frame shift mutation could result in this.
A rapid change in multiple species in the same place and/or time are referred to as adaptive radiation events, rapid diversification, if it is large and  sudden enough it may even be referred to as explosive radiation.

Part of the issue is saying something is "fast" is a more qualitative assessment so it does not have a term in and of itself, the closest you see is things referred to as "rapid" so you might see rapid speciation or rapid extinction, rapid X or Y.

I think the OP is referring to geological periods where lots of different lineages arose suddenly, like the Cambrian explosion. If so, I think “rapid diversification” is exactly right.

A few comments. 1) Strong pressures in small populations result in more rapid changes than weak pressures in large populations is true or false depending on the details of the model and what statistic you are considering to measure speed of evolution. I would advice against using this kind of general statement. 2) I think the term 'genetic revolution' is very rarely used in the evolution literature (see e.g. this google scholar search).

An adaptive radiation is not just [a] rapid change in multiple species. It is a sudden very high rate of speciation. 4)  a single large change in a single generation (often becoming a speciation event) is called saltation and is extremely rate. It depends what you mean by rare. Typically ploidy change mediated speciation and hybrid species are sudden events leading to speciation and not so uncommon in some lineages (Rieseberg et al. 2003). Otherwise, I think the answer is good.

Sudden is a fine qualifier I will add it. Yeah speciation kinda weird in plants to begin with, In runs back to the problems in defining species. And by rare I mean rare compared to other forms of speciation across all of life, for a general question I was trying to keep myself to a general answer.

@remi I'll clean it up and add some qualifiers, tell me what you think.


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Could humans breathe if the average methane content of the atmosphere increased to 1%?
Below is a table of atmospheric composition. Could humans breathe if the average methane content of the atmosphere increased to 1%?

Table 7a-1: Current Average composition of the atmosphere up to an altitude of 25 km.

Gas Name          Chemical Formula    Percent Volume

Nitrogen          N2                  78.08%
Oxygen            O2                  20.95%
*Water            H2O                 0 to 4%
Argon             Ar                  0.93%
*Carbon Dioxide   CO2                 0.0360%
Neon              Ne                  0.0018%
Helium            He                  0.0005%
*Methane          CH4                 0.00017%
Hydrogen          H2                  0.00005%
*Nitrous Oxide    N2O                 0.00003%
*Ozone            O3                  0.000004%

* variable gases

Could you provide a link for the table?

1.0 what?  Percent, ppm, or?

Not sure what you had in mind, but if the atmosphere was 1% methane there would be a massive contribution to global warming. I don't know if anyone has run a model with that much methane but it could very well be an unsurvivable level for human's time on the planet, regardless of direct biological effects.

See http://www.sciencedirect.com/science/article/pii/S1871174X16300488

Methane is biologically inert and can only act as an asphyxiant at high concentrations by displacing oxygen. An environmental exposure limit has been set at 5,000 ppm, though 10,000 ppm (1%) had no effect:

It is obvious that an exposure limit that presents an explosion hazard cannot be recommended, even if it is well below a concentration that would produce toxicity; thus, exposure limits should not exceed 5% by volume in air.
Animals exposed to methane at 10,000 ppm showed no toxic [effects]; an uncertainty factor of 2 is suggested to derive an EEL—5,000 ppm. There is no evidence that duration of exposure is important in methane toxicity.

Source: Methane in Emergency and Continuous Exposure Limits for Selected Airborne Contaminants Volume 1 (1984)


text:
How do you sequence a tree genome?
I'm writing a grant proposal, and part of the research will involve sequencing and comparing DNA from trees in America and Japan. How does one analyze the genome of a tree and compare it to a conspecific?

how is that different from sequencing animal genome?

I don’t know. Is it different?

Are you trying to sequence the entire genome or just portions of it? This review paper may help you get started, specifically the portion titled "how do we sequence" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1456863/

it seems like you haven't done studying on your own, which is the first step usually. Genome sequencing is pretty common these days, and a lot of information is available. Maybe start with simple googling "how to sequence genome". Also, as grant writing goes, if you include work that you don't know how to do maybe you should seek collaboration with genomics people

I agree with aaaaaa - if for a grant, the level of this question indicates you need to do way more reading of the literature than you apparently have been. (Otherwise you're just wasting the grant committee's time.) For example, a quick search finds a list of sequenced plant genomes - you can start from the references there to see how they did it. -- That said, you're probably looking for "genotyping" rather than "whole genome sequencing". Doing a web search for "genotyping trees" pops up a number of papers you can start from.

In journal articles, they are doing many studies every year describing the state of the art tools and procedures for sequencing plant genomes.
by researching 5 minutes you have results of this kind:
http://www.pnas.org/content/95/16/9693.full

Protocols involved commercially available kits (e.g., Qiagen’s RNeasy Plant Minikit), non-commercial RNA extraction lab protocols (e.g., CTAB, acid phenol) and hybrid methods that combined components of both commercial kits and lab protocols. The detailed protocols used for all isolations are available online in Appendix S1.
  http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0050226
Tissue and organ samples for Northern blot analysis of gene expression patterns were taken during the growing season and frozen in liquid nitrogen, then stored at −80°C. Shoot-tip samples are the terminal 1–2 cm of succulent stem tissue from elongating branches and terminal leaders. Immature xylem was harvested with a vegetable peeler from the surface of woody stems after removal of the bark, and includes cells with primary cell walls derived from the cambial zone through the zone of radial cell expansion. Compression wood and side wood immature xylem RNAs were those used for preparation of the libraries, whereas vertical immature xylem denotes samples taken from stems of control trees growing vertically. The tissue described as “phloem” was collected from the inner surface of the bark of vertical stems and actually includes periderm and other tissues as well as active phloem. Planings were collected from the surface of vertical woody stems with a wood plane after immature xylem was harvested and includes cells that have formed secondary cell walls strong enough to resist harvesting by the vegetable peeler. Needle samples were partially expanded juvenile needles.

here are some more texts for you to check
http://www.pnas.org/content/106/31/12794.full
https://bmcevolbiol.biomedcentral.com/articles/10.1186/1471-2148-7-214
From_field_to_film_Rapid_sequencing_methods_for_field-collected_plant_species
It took me 5 minutes to find these informations by searching articles for

plant sequencing methods


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What is it called when there is natural truncation selection?
Truncation selection is when a breeder selects for animals that exhibit a value for a trait that is above a certain threshold.  What is it called when nature selects for a value of a trait that is above a certain threshold?  I want to say natural truncation selection, but I don't see any mention of that.  To clarify, what I mean is, what is it called when, as a result of natural selection, all perish but those with a value for a particular trait that exceeds a particular threshold.

The term that comes to my mind is directional selection, but I'm not sure that's what you're asking about?

Truncation selection
The term  truncation selection has been used a lot in theory papers because it is a simple model and because it is of interest to breeders. Truncation selection is most likely more common in a breeding setting than in nature and from wikipedia,  truncation selection is defined as specific to breeding

In animal and plant breeding, truncation selection is a standard method in selective breeding in selecting animals to be bred for the next generation

However, as much as the definition fail to repeat animal or plant instead of just animal, IMO it fails to recognize that such notion could as well exist in nature. I would personally not be shock to read a paper talking about  truncation selection in wild populations.
Threshold model
If you really want to avoid talking about truncation selection, then you can eventually picture the phenotypic trait as a liability factor (as it is done in sex determination literature, see Perrin and Beukeboom's book) and selection acting as a threshold on this factor. Note that the concept of threshold and threshold model is very common and everyone will understand what you mean.

"If you really want to avoid talking about truncation selection, then you can eventually picture the phenotypic trait as a liability factor (and it is done in sex determination literature, see Perrin and Beukeboom's book) and selection acting as a threshold on this factor." Can you expound on what you mean by this?

In the sex determination literature, sex is often considered as a threshold trait on some liability factor. For example in humans, SRY create TDF and TDF is the liability factor. If TDF is at a high enough concentration, it will be a male, otherwise a female. Similarly, you can picture fitness as a threshold trait where your continuous phenotype of interest (heigh or whatever) is the liability factor.

Would you define "liability factor" please?

I won't be able to cite you a nice neat definition, but I mainly encountered this term in the sex determination literature and it is some factor (protein concentration typically) which depending on its value will affect a phenotypic trait based on a threshold model. I am not sure the term is always used like this though. Sorry, I can't give you more info on that. If interested you might want to have a look at this book.


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What impact do genetic engineering techniques have on seed breeders?
In research of seed breeding, I'm trying to understand the impact of genetic engineering techniques like CRISPR (This is the main one as I understand) on traditional seed breeders. Through searching on the internet, I believe to have found the following two types of impact:

research: increased speed of detection which genes make for which vegetable trait. This is supposed to be used already by many breeders.
Growing: Reducing the breeding cycles by up to a factor 2, by early selection which plants are the good ones in the breeding process (I don't really understand how this would work)

So the main total impact of new breeding technologies would be the shortening of breeding cycles, putting increased pressure on fast innovation.
Am I missing any type of impact? Is CRISPR going to change seed breeding in a dramatic way? For instance, is there a way to take someone else his/her seed, then using crisper (in some way?) to immediately know which genes make up for the desired vegatable traits? Or some increased speed in which one could copy traits of other seeds? Also I'd like to know how the second point works: using CRISPR to reduce the breeding cycles for seeds.


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Are trees still carrying their leaves more likely to be felled by an autumn storm?
Is there evidence that trees still carrying their leaves are more likely to be felled by an autumn storm than trees already having lost their leaves?
At first sight this seems plausible (and might be easily verified statistically), but at second sight it seems mysterious, considering a) the weak forces that keep leaves attached to their branches (at least in autumn times), b) the flexibility of the branches, and c) the chaotic way in which they are shaken by a gust.
Anyway, after storm Xavier which passed Germany and Poland on the 5th and 6th of October, this was spread ("kolportiert") by the media and in private communication:

Is there a thorough biomechanical model which explains whether or why this is true or false, resp. to which extent?
I would suspect that in this model a) eigenfrequencies (of branches, limbs and stem) and b) resonance will play a role.
(This model would give an interesting analogy to the sudden generation of action potentials in neurons (corresponding to the breaking of a limb or stem) by spatio-temporarilly integrating the synaptic inputs (corresponding to the shaken leaves) on the dendritic tree [sic!]. Addendum: There's a great book that brings botanical and neuronal trees together: Giorgio A. Ascoli, Trees of the Brain, Roots of the Mind.)
(Note, that one short gust almost never will fell a tree. It must be a rather long gust, or an appropriately long and/or timed sequence of shorter gusts.)

Addendum: The way how fluttering ion channels (on a very short time scale - grey dots below) give rise to a rhythmic and possibly resonant temporal pattern (on a much longer time scale - red or blue line above) may be compared to the oscillations of the tree as a whole, whose "rhythm" (red) cannot be detected when looking at single leaves fluttering (grey):

See also here.

Most certainly, yes. Especially if that storm brings heavy winds (hurricanes, tornadoes) or ice/snow


text:
Do Black Hair Fuzzy Caterpillars bite?
I saw a caterpillar in my bathroom. It's about 2 inches long and 3/4 inches in diameter. It has long (about 1 inches) long hair on his body.
I live in eastern India, Asia. I don't know if it was alive, as I didn't see any remarkable movement.
Are they dangerous? Do they bite? How to get rid of them?

It would be better if you would post some pictures of them

I can nearly guarantee that there are nearly zero species of caterpillar that have a nasty bite. Some caterpillars like the pine processionary cause skin rashes. some caterpillars can Kill you, better check it on this list: https://www.ranker.com/list/caterpillars-that-can-kill-you/eric-vega

I saw, it has long (about 1 inches) long hair on his body.

The hairs you refer to may be urticating hairs, which can cause extreme itching & irritation. Without a picture of the caterpillar, I can't say for sure though; out of extra precaution, let's just assume they are (until an image is provided).

Are they dangerous?

As long as you don't let the caterpillar hair come into contact with your bare skin/body, there should be no risk of harm. That being said, be mindful of indirect contact; i.e., perhaps picking the caterpillar up with your shirt sleeve, the hairs now being on the sleeve, then you wiping your face with your shirt sleeve later in the day. See here for more information, including treatment, should said exposure ever occur.

Do they bite?

Caterpillars do have the ability to bite, however, their bite isn't strong enough to pierce human skin. Nothing to worry about here..

How to get rid of them?

To "get rid" of the caterpillar, I recommend getting a hard, thin surface - such as a piece of cardboard - ushering the caterpillar onto the surface, and then placing the caterpillar somewhere safe outside. If the caterpillar is in the process of molting, relocation can easily kill it, so please be diligent when attempting to relocate.


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How do sporozoites travel into the human host when the mosquito is sucking blood?
I mean how are the sporozoites able to swim in the reverse direction of blood flow through the proboscis of the mosquito into the human body?

Nice question!  Basically, the mosquito does not only suck; it also injects some saliva into the host with its saliva glands.  From National Geographic:

The mosquito starts salivating as soon as it probes the [host]’s skin, releasing substances that prevent blood vessels from constricting, stop blood from clotting, and prevent inflammation. Sometimes, Choumet could see the saliva as small bubbles that hung around the tips of the mouthparts. And even after the mosquito stops feeding, pockets of saliva linger in the lower layers of the skin.

And from cdc.gov:

After 10-18 days, the parasites are found (as "sporozoites") in the mosquito's salivary glands. When the Anopheles mosquito takes a blood meal on another human, the sporozoites are injected with the mosquito's saliva and start another human infection when they parasitize the liver cells.

The probiscus is actually equipped to inject saliva as well as to suck blood.  And once the saliva has entered the victim, it can spread to the whole body since the blood is constantly moving.  From mosquitnoband.com:

Mosquitoes also have special hematophagous arthropod saliva in their proboscis. Hematophagous arthropod saliva is a scientific way of saying “spit from a blood-sucking creature with an exoskeleton.” This specific type of saliva has chemicals and proteins in it that prevents blood from clotting. So what do mosquitoes do with their hematophagous arthropod saliva? They inject it into their victim before they start sucking its blood to prevent any clotting while they slurp.

Hope this helps!


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Protein food eating tendency
As I understand human love fatty food as they taste good because it has more energy which was good when we were primitive and food was scarce and unreliable,
Is there same urge for protein food too? it doesn't give much energy.

Proteins are actually pretty calorific but indeed much less than fat. From wiki > food Energy

However, we crave for proteins for other reasons. We digest proteins to get their building blocks, the amino acids. With these amino acids we can rebuilt our own proteins. Proteins are at the very center of our metabolic activity. From wikipedia > protein

Proteins perform a vast array of functions within organisms, including catalysing metabolic reactions, DNA replication, responding to stimuli, and transporting molecules from one location to another.

Many of our DNA sequence are called protein-coding-sequence (often just called gene although definition of what a gene is vary quite a bit). Those sequences are transcribed into mRNA and then translated into protein in order to have some effect on our body. A protein could be an enzyme for example.
For more information on the role of proteins in living organisms, have a look at an intro course to Biology such as for example those of Khan Academy. Khan Academy > macromolecules > protein and Khan Academy > Central Dogma.


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What are the chemical characteristics of cofactors that functionally differentiate them from the side chains of amino acids?
Cofactors are essential for the function of many enzymes, such as NAD+ in the glycolytic pathway - I was wondering how the chemical properties of these cofactors allow them to fulfil their function and/or what it is about the chemical properties of amino acid side chains that limits their utility in the kind of reactions that require cofactors.

Are you interested in all cofactors, or only organic ones? (see also: https://biology.stackexchange.com/questions/19896/where-can-i-find-a-list-of-common-enzyme-cofactors-and-or-co-enzymes)


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Could AI be applied to protein folding?
Two years later, there is a follow up question to the one asked here: How do we know if the folding@home project results are right?
Since we are quite sure F@H is working right and following this article's statement:

Similar techniques could be applied to protein folding, reducing energy consumption, or searching for revolutionary new drugs and materials.

...I would like to ask if AI stuff, like deep learning, neural networks and the rest of today's buzz words could be applied to molecular dynamics, especially in the protein folding field?

Yes, and no :-)
In the meantime many protein structures can be predicted quite accurately - even those for which no reference fold had been known before.
In this case the important buzz word is "big data": co-mutations (of charged amino acids) that can be found when sequencing many independent genomes. (... which indirectly bypasses the emphasis on dynamics for protein folding)
Editorial: 2017, Science: http://www.sciencemag.org/news/2017/01/hundreds-elusive-protein-structures-pinned-down-genome-data
Perspective: Soding et al. , 2017, Science ( http://science.sciencemag.org/content/355/6322/248 )
Research article: Ovchinnikov et al. 2017, Science ( https://www.bakerlab.org/wp-content/uploads/2017/01/ovchinnikov_science_2017.pdf )


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Can yeast survive without mitochondria?
Some yeast cells have very low mitochondria copy number (see number of mitochondria in non budding cell, you can count mtDNA). This makes them susceptible to fluctuations, and one can conceive that some yeast cells might arise entirely without mitochondria. Would they survive? Could they reproduce?
Please, assume they have all the nutrients required, in particular excess glucose to ferment, so mitochondrial energy output is dispensable.
If you could point me to some references that would be awesome.

Basic answer: Yes, they can survive, but only if they do not need to undergo cellular respiration.  I quote from Microbiological Research, Volume 169, Issue 2-3, p. 185-195:

Mitochondrial DNA (mtDNA) is a compulsory genetic component for encoding essential respiratory enzymes in all eukaryotic cells.

In other words, for cellular respiration to occur, the yeast must have the mtDNA.  However, the article goes on to explain,

However, some yeast species (called rho positive) could survive without mtDNA under conditions of fermentation (a metabolic pathway alternative to respiration). In these species, partial or complete losses of mtDNA (spontaneous or induced by mutagenic factors) is associated with the formation of respiratory deficient mutants (rho− type or rho0 type) characterised by slow growth on fermentable carbon sources (e.g. glucose) and inability to grow on non-fermentable sources, such as glycerol or ethanol.

In other words, yeast can survive in the presence of correct conditions for fermentation to occur.  In the absence of those conditions, the yeast must have the mitochondrial DNA, because in order for it to survive, it must perform cellular respiration.

No, yeast cannot survive without mitochondria.  Petite positive yeast can survive on fermentable carbon sources without mitochondrial DNA, but they must have a mitochondrial compartment.  Mitochondrial respiration can even be lost in human tissue culture cells, but they too must have mitochondrial compartments.  Mitochondrial compartments are where Fe-S cluster assembly and other essential biochemical pathways occur, thus they are required for eucaryotic cells to either live for a long time or reproduce.

Can you add a reference?


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How much electrical energy is required for intracellular stimulation of a neuron?
How much electrical energy is required for intracellular stimulation (firing) of a human neuron? Electrical energy is measured in joules, and equal to voltage multiplied by current. If you don't know energy,  you may specify voltage applied and current. Just for example, to capture heart, a pacemaker must discharge 0.1 microjoule of electrical energy.
There might be more parameters involved like pulse width,  phase etc.  Energy combines all the parameters in one single value. In case you don't know energy level,  please specify the defining parameters as well.

I think this question is somewhat ill-posed, but I'll try to answer it:
None.
All you have to do is to short the inside of the cell to the outside/ground. Of course in reality this means expending some energy somewhere, but at that point it's an engineering problem, not one of biology, and it has nothing to do with the neuron itself.
Action potential firing is a completely passive process. The only part that requires energy (besides protein synthesis) is for the sodium-potassium ATPase that maintains sodium and potassium gradients.

I agree that this is an ill-posed question. (OP is probably trying to ask the engineering question...) Na/K-pump spends enormous amount of energy to ready that state though. Each AP does have an associated energy cost that way.

Yeah, that cost is necessarily driven by things like the size of the neuron, how branched the axons are, myelination, etc, and the cost is still a fraction compared to the cost of synaptic transmission in most cells: action potentials are really incredibly efficient. Synaptic transmission is really only costly because you have excitation and inhibition that cancel each other out in terms of voltages but create large currents that require pumping. All that said, I read the OP's post to be mostly about triggering, rather than propagating an AP.


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Can a shark stall?
Today in marine biology I learned that, like airplanes, sharks use their pectoral fins to generate lift.  The question that neither me or my Professor know is if a shark can or cannot stall.
A stall occurs when the angle of attack of the wing (in aircraft) is exceeded, creating stalls of wind behind the wing.  This kills the lift and the aircraft begins to dive towards the earth.  Even though water is a more viscous liquid (than air), could a shark suffer the same effect?

As it turns out, yes- they can. First few hints in favour would be- 1) A stall is a fluid dynamics concept; and 2) Sharks have streamlined bodies.
The source for this answer is a researchgate article: https://www.researchgate.net/publication/331145186_Hydrodynamic_analysis_of_shark_body_hydrofoil_using_CFD_methods
The study uses a real-scale  image of  a Tope Shark (Galeorhinus  galeus). Below, you can see the hydrofoil production*.
(*A foil is a solid object with a shape such that when placed in a moving fluid at a suitable angle of attack the lift (force generated perpendicular to the fluid flow) is substantially larger than the drag (force generated parallel to the fluid flow). If the fluid is water the foil is called a hydrofoil.)
The pressure and velocity contours are there plotted for various angles of attack ($\alpha$), which can help determine the stall angle. The following is the velocity contour:

(Re stands for Reynolds number, which is predict flow patterns in different fluid flow situations. At low Reynolds numbers, flows tend to be dominated by laminar (sheet-like) flow, while at high Reynolds numbers flows tend to be turbulent.)

The velocity contour plot (Figure 11) shows that for α=0˚ the water speeds around both upper and lower  surfaces are close to each other and the lift force at the smaller angles of attack is relatively low due to nearly symmetrical geometry. The velocity at the boundary layer of the wall is observed to be approximating to zero (blue region) at each case due to the viscous effects around the wall. Increasing  α expands  the high  speed zone  (red color)  above  the  boundary  layer  of  upper surface,  also extends the  flow separation zone which is shown as blue.  It is observed that, the hydrofoil is at the condition of stall at α=10˚ due to the flow separation.

The simulations at both Re  numbers reveals a stall angle  around 7-8 degrees which is also verified by JavaFoil results. Beyond the 8 degree  stall  angle, the lift  performance  is  deteriorating and the drag  coefficient increases exponentially. This result shows that the variations in TSH swimming speed do not affect the performance behavior of Tope Shark; demonstrating the body shape of the tope shark is appropriate for a wide range of swimming velocities and is suitable for both cruising velocities and burst of speed.

Although I dont know about the shark diving using pectoral fins, i do know about sharks somewhat "stalling". They slow down movement to attack seals and whatnot. This article may help you : https://www.earth.com/news/slow-moving-sharks-strike/#:~:text=A%20new%20study%20from%20the,to%20pounce%20on%20their%20prey.&text=This%20behavior%20suggests%20that%20the,the%20best%20seal%20to%20attack.

Welcome and thanks for your answer. Answers should, in principle, be stand-alone. Referencing is great, even mandatory here on our site, but every answer should elaborate to a certain extent, such that the reader knows what the answer is. In this case, we don't even know whether the phenomenon you describe has anything to with the pectoral fins in the first place. If not, the answer is irrelevant to the question, as the animal may simply stop propelling itself forward or something.

oh sorry! im still a bit new, anything else i should know?

Yep - that we expect users to adapt their posts after receiving feedback :)


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Did radial symmetry evolve twice?
In the history of animal evolution, both the Cnidarians and the Echinoderms have radial symmetry, according to this cladogram:

Source: http://www.cpalms.org/Public/PreviewResourceLesson/Preview/45851
Do both groups having this feature mean radial symmetry evolved twice?

Can you please add the source of where you got this image from?

Thank you for mentioning, @Remi.b. The source is in updated post.

Good question! I had never really though about it, so thank you!
Echinodermata have a pentaradial symmetry
Echinodermata actually don't have a radial symmetry like jellyfish do. They have a pentaradial symmetry as they systematically have 5 arms.
Parsimony
Even if Echinodermata were radially symmetric, then it would actually be unlikely that bilateral symmetry evolved, was then lost and evolved again. It is much more parsimonious that bilateral symmetry evolved once and was later lost in the echinodermata lineage.
Developmental and Genetics of pentaradial symmetry
As one would expect modifications of hox genes are involved into the evolution of this peculiar body plan. From Lowe and Wray 1997

Here we report the expression domains in echinoderms of three important developmental regulatory genes ( distal-less, engrailed and orthodenticle ), all of which encode transcription factors that contain a homeodomain. Our findings show that the reorganization of body architecture involved extensive changes in the deployment and roles of homeobox genes. These changes include modifications in the symmetry of expression domains and the evolution of several new developmental roles, as well as the loss of roles conserved between arthropods and chordates. Some of these modifications seem to have evolved very early in the history of echinoderms, whereas others probably evolved during the subsequent diversification of adult and larval morphology.

Here is the whole abstract of Mooi and David 2008

The strangeness of echinoderm pentaradiality results from superposition of radial symmetry onto ancestral deuterostome bilaterality. The Extraxial-Axial Theory shows that echinoderms also have an anterior/posterior (A/P) axis developed independently and ontogenetically before radiality. The A/P axis is first established via coelomic stacking in the extraxial region, with ensuing development of the pentamerous hydrocoel in the axial region. This is strongly correlated with a variety of gene expression patterns. The echinoid Hox cluster is disordered into two different sets of genes. During embryogenesis, members of the posterior class demonstrate temporal, spatial, and genetic colinearity within the extraxial region. We suggest that displacement of genes from the more anterior Hox classes toward the 5′ end of the chromosome leads to control of the later-developing, radially symmetric axial region. Genetic disorder is therefore another way of using colinearity to build the unique echinoderm symmetry.

As insinuated above, note that (in most echinodermata species at least) only adults have a radial symmetry. Larvea have a bilateral symmetry. Here are a bunch of picturesand schema.
Larvea

Adults

It is actually hypothesized that radial symmetry did evolve again, but there are homologies between the echinoderm symmetry and bilateral animals:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2176165/


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How do I go about traveling with DNA extract samples?
I am traveling from Fairbanks, Alaska to Vienna, Austria in six weeks and need to bring 10 very small (~50 ul) samples of extracted arctic ground squirrel DNA with me.
I need to travel with these on dry ice in a little carry-on cooler.
Has anyone flown with DNA samples? Any advice on how to go about it? Questions to ask customs?

I think it could also be asked at Travel.SE for a better answer.

Dry ice is classified as "dangerous goods" in most countries, probably because it can explode! It depends on the airline how much or if you can carry it with you. As an example, Swiss Air allows up to 2.5 kg per person with prior registration. See this question for carrying DNA. As these regulations vary by country and airline, you'd probably be better off if you contact your airline before going to the airport.


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Why does HIV chooses the Macrophage cells to infect first?
Upon entering our body HIV directs the macrophage cells to manufacture more virus particles. It injects the Viral RNA into the Macrophages. With the help of the enzyme reverse transcriptase the Viral RNA converts into viral DNA that embeds into the DNA of macrophage cells. In this process the macrophages remain alive.
Just Curious-
Since Macrophage cells have phagocytic activity, why does HIV chooses them to be their Virus producing factory and not some other cell like RBCs which are apparently much more abundant and have no phagocytic activity at all.
In other words what facilitates the macrophages to be HIV's manufacturing plant?

Your title and final question are not the same question.

I think they are just the two different ways in which this problem can be represented

Short answer
HIV infects macrophages because macrophages display the CD4 cell surface receptor needed for initial HIV attachment, and also display the co-receptors CCR5 and/or CXCR4 that are also needed for virus entry into the cell.
Cells that aren't good hosts for HIV don't have these receptors.
Addressing some confusion
You ask why HIV chooses macrophages as a virus producing factory. Be careful that you don't excessively anthropomorphise viruses - viruses 'choose' which host cell to infect in the same way that you 'choose' to feel pain when you stub your toe. It is a product of evolution, and not the result of a logical thought process by the HIV virus.
Other viruses happen to infect epithelial cells, or liver cells, or plant cells. HIV infects CD4+ cells. There is no 'best' option that viruses will somehow 'choose'. Anything that allows for successful reproduction and transmission is a viable option, and the rest is down to random mutations and evolution.
Red blood cells as virus factories?
Finally, you ask about red blood cells as a better host for viruses. In fact, red blood cells make very poor host cells for viruses, as they lack the cellular machinery required for DNA replication and protein production. It is this cellular machinery that is usually hijacked by viruses in order to replicate. Red blood cells lose their nucleus early in development, and it is only more complex organisms (such as the Plasmodium species that cause malaria) that can effectively hijack a red blood cell. These Plasmodium parasites have their own nucleus for protein production and DNA replication.

Thank you very much! I think I asked kind of a silly question


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Irradiation instead of pasteurization?
Can we just replace pasteurization with simple irradiation for most (if not all) foods? (For example, such as milk, to sterilize and preserve flavors)

I don't know about "replace", but it is used.

@arboviral It still doesn't answer the question. I know what pasteurization and food irradiation is, thank you ; )

Both pasteurisation and irradiation work by killing micro- (and macro-) organisms in food. The two processes are broadly similar and in both cases the objective is to reduce the number of bacteria or other microorganisms in the food rather than completely sterilise it. Due to this and other similarities food irradiation is sometimes called cold pasteurisation (for example in this paper).
Food sterilisation has some advantages over pasteurisation: for instance, it can be used on (most) solid foodstuffs, including fruits, vegetables, grain foods, spices and meats (such as chicken), while pasteurisation can only be used on liquids. However, irradiation cannot be used on dairy products or eggs as it results in changes in flavour and texture (source).
There are other reasons why irradiation is not used as widely as it might be. One is that some markets were already saturated with pasteurisation, which is an older technology. Another is that public acceptance of irradiation is lower, with (for example) concerns about safety of the products, although these are not rational concerns and Crawford and Ruff note that similar concerns affected acceptance of pasteurisation when it was introduced. This may also partially explain why irradiation is sometimes called cold pasteurisation, although by international agreement irradiated unprocessed food sold in stores (not in restaurants, or processed foods) is labelled with the Radura symbol anyway.

I also have a suspicion that the startup costs associated with food irradiation plants are relatively high, but couldn't find a reference for this yet.
Some further reading
Lester M.Crawford, Eric H.Ruff (1996) "A review of the safety of cold pasteurization through irradiation" Food Control Volume 7, Issue 2, April 1996, Pages 87-97
"Advantages and disadvantages of the use of irradiation for food preservation" Journal of Agricultural and Environmental Ethics March 1991, Volume 4, Issue 1, pp 14–30
"Food irradiation", Better Health programme, Victoria State Government website (accessed 2017-10-24)


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Query regarding calculation of survival analysis
According to this tutorial, for table to find the survival estimates, the square root of the 6th column is multiplied with the 4th column, which is Survival probability. The value that should come for the 7th column for the 2nd row is 0.052((square root of 0.003)*0.950=0.052) but in the tutorial it is given 0.049. Am I making any mistake with the calculation?
Many of the values in the table does not match with the calculations given.

"0.003" is rounded up; the exact value is 1/380, which is 0.00263157894... (and some more decimal places).
If you calculate the table entries to a few more decimal places, you get 0.04873397172 (and so on), which rounds up to 0.049.


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What does synapses hold together?
From three answers to the same question at Quora I've learned of three forces that keep synapses together:

They are held together by cell adhesion molecules (e.g. neurexin and neuroligin).
They are surrounded by support cells (glia?) that hold them together.
They are packed densely together (and just couldn't move, even without specialized support cells).

I'm sure all of these ways of holding synapses together play a role.

But are there others?

In any case it may make sense to ask

which of these "forces" is the strongest, and how strong is it?

For example: If axonal tension is supposed to be a driving force of gyrification, the "weakest link in the chain" is probably the synapse. So the forces holding the synapse together must be strong enough to counteract the forces that drives the neurons in different areas of the cortex apart (whatever these may be). For "axonal tension" or "axonal tethering", see also here.


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Can we detect the origin of a 1000 year old dead body after grave excavation?
I recently read an article saying DNA analysis has shown some of the people buried in Viking graves in Scandinavia originated from places like Persia and it is talking about something around 1000 years ago.
How accurate could this analysis be based on our DNA and the fact that we have 99.9%  DNA similarity?

Vikings travelled through the mediterranian and all rivers for trade, there are museums with roman jewellery and persian silk artefacts found in sweden. The analysis is FORENSICALLY precise... your mother has blue eyes, you have blue eyes. persians have type A1 protein, swedish have A2... they only have a 50 percent complete DNA to find a collection of A1,B1,C1 genes, to know that the human was almost entirely from zone 1.

Adding to comprehensible's answer, 99.9% similar DNA still leaves 0.1% of different DNA. Within this 0.1% would be enough differences to be able to find the differences that comprehensible mentioned. This is also how the ancestry tests that are so popular these days work.
Additionally, for that type of place-of-origin analysis, my impression is they commonly look at isotopes of chemicals found in the bones, and matching it to profiles found in other regions.
For example, let's say that an area we're interested in has high levels of isotope X but low levels of isotope Y in the water and food, which we discovered from examining the archeological record. If we find someone in that area whose bones have low levels of isotope X and high levels of isotope Y, we can conclude that this person traveled here later.

Note that 0.1% of the human genome leaves four million differences. Four million is plenty of room for identification