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Is Active Transport Required For Life?
Is active transport required for all living cells to function?
I was under the impression that if a cell doesn't have active transport, it either would lose molecules through the membrane and not be able to maintain a proper gradient, or molecules would be trapped inside the membrane (waste) or outside the membrane (food).

For an organism (think single-celled) living in just the right kind of environment, it might just be possible to survive using only facilitated diffusion, at least as far as small molecules are concerned. This kind of organism would have to maintain exactly the right concentration of the molecules it wants to keep or get rid of, based on the external concentration of those molecules.
For example, if an organism was living in a glucose-rich environment, it might be able to fulfill its glucose requirements by (1) making the membrane itself tightly impermeable to glucose and (2) tightly controlling the number of passive glucose transporters.
It would be nigh-impossible to achieve this for every solute in the environment, especially those that are able to permeate the membrane.
If there were such a thing, it might be found in organisms that live in very low energy aquatic regimes such as anaerobic methane oxidizers, where the solute concentration in the environment doesn't really change in small time scales.
Even in such environments, the number of small ions in the environment is likely to be high enough that some active transport would be required to maintain the osmotic balance within the cell.

So, as far as you know, active transport is universal characteristic of cellular life?

As far as I know, yes. However, as I said, theoretically, life without active transport might not be a total impossibility under exactly the right circumstances.


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What does "rapamycin-sensitive oncogenic transformation" mean?
Can someone explain exactly what "rapamycin-sensitive oncogenic transformation" is? I get that it's a drug that suppresses the immune system but what does it have to do with oncogenic transformation?
Here's the article where they talk about it:
http://www.pnas.org/content/104/13/5569.full

i am not particularly sure but it could be related to dysregulation of the mTOR pathway.. mTOR pathway is involved in survival in stress..

The mammalian target of rapamycin (mTOR) is a Ser/Thr protein kinase that functions as an ATP and amino acid sensor to balance nutrient availability and cell growth. When sufficient nutrients are available, mTOR responds to a phosphatidic acid-mediated signal to transmit a positive signal to p70 S6 kinase and participate in the inactivation of the eIF4E inhibitor, 4E-BP1. These events result in the translation of specific mRNA subpopulations. mTOR is phosphorylated via the PI3 kinase/Akt signaling pathway and also autophosphorylates under translationally repressive conditions. mTOR plays a key role in cell growth and homeostasis and may be abnormally regulated in tumors. It is currently under investigation as a potential target for anti-cancer therapy.
The mTOR signaling pathway shows how mTOR is involved in numerous cell processes that can be dysregulated in cancer, including cell growth, proliferation, angiogenesis, autophagy, and various kinds of metabolism. "Rapamycin-sensitive oncogenic transformation" therefore means that the transformed cells still have intact "wild-type" mTOR complexes that can be down-regulated by the tumor-specific administration of rapamycin analogues, hence inhibiting the above-mentioned processes and arresting or killing the cells.

source: Stack Exchange

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What is this marmot-like animal (Tigray, Ethiopia)?
I was searching what are the animals I frequently saw in the north of Ethiopia. I took some bad quality pictures.
For me it looked like a large squirrel, local people called it a rat, and on the internet I find rock hyraxes are quite frequent in the region, but they appear not to have a long tail like the animals I saw, and they don't have the white lateral line

It's definitely not a rock hyrax, it looks a lot like a ground squirrel.

This looks like some sort of ground squirrel. Especially in the second picture, the posture is  very characteristic of squirrels in general. The tail also looks very squirrel-like to my eyes. My best guess, without better pictures, is the Striped Ground Squirrel (Xerus erythropus).
See the images at:
http://www.flickriver.com/photos/8834404@N02/2902284598/
http://www.flickriver.com/photos/kpzaremba/5094580855/

The Wikipedia picture isn't particularly good, but searching for Xerus erythropus on Google Images gives some results that look a whole lot like your squirrel.

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First genomic survey of human skin fungal diversity
"The researchers found that a single type of fungus, belonging to the genus Malassezia, is predominant on the head and trunk. Hands, which harbor a great diversity of bacteria, are home for relatively few types of fungi. In contrast, feet, including toenails, heels and toe webs contain tremendous diversity.
"Applying DNA sequencing to a study of the skin's fungi is the natural progression in understanding microbial life that co-exists on our bodies," said NHGRI Scientific Director Daniel Kastner, M.D., Ph.D. "Along with recent genome sequencing to define bacterial diversity, this analysis of fungal diversity provides a more complete human microbiome picture."
"Fungal communities occupy complex niches, even on the human body," said Heidi Kong, M.D., co-senior author and an investigator in the dermatology branch of NCI's Center for Cancer Research. "By gaining a more complete awareness of the fungal and bacterial ecosystems, we can better address associated skin diseases, including skin conditions which can be related to cancer treatments.""
Source
Is there another reference for this research please?

The link is given at bottom of the article that you linked to. It's a Nature paper so you need to have access rights.

Just a tip, links of the form http://dx.doi.org/whatever tend to link to academic articles.

@ChinmayKanchi I can't access that link.

The doi-based link looks like this: http://dx.doi.org/doi:10.1038/nature12171

Hi @AlanBoyd, how are you doing? thanks for your reference.


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Ill effects of urea and NH₃ on metabolism
What exactly does urea do that harms our body? Does it interfere with our cellular processes or disturbs the colloidal onchotic pressure of our blood?
I have heard that NH3 damages the brain. What does it actually do?

Urea and ammonia are two very different molecules, except for the fact that urea is a metabolite of ammonia, they have almost nothing in common in a chemical sense. I would suggest that you restrict your question to one of those molecules, and maybe add some more detail about what exactly you are interested in.

The denaturing effect of Urea is mostly at very high concentrations.   (~Molar levels)!
Physiologically, urea, a product of the breakdown of retired amino acids, will build up rather quickly if it weren't secreted in the urine. Looking into this, it doesn't seem as there is a clear understanding of why this causes a disease, though the buildup of a waste product definitely is a unifying concept.
Uremia - kidney failure - causes a build up of urea in the blood as the kidney eliminates urea from the blood into the bladder.  The specific effects of Urea on cell metabolism are probably numerous as the symptoms:  anorexia and lethargy, and late symptoms can include decreased mental acuity and coma. Other symptoms include fatigue, nausea, vomiting, cold, bone pain, itch, shortness of breath, and seizures.
Being a metabolic waste product, it certainly would interfere with and inhibit any enzyme that produced urea - the Urea cycle in particular.  Its clear that uremia is ultimately associated with cell death, oxidative stress, some cell signalling and proliferation.
I'm just googling around here, but I don't think there is any one single answer as to what goes wrong when the cells are exposed to too much urea.

@SatwikPasani you may be interested in this answer in relation to one of your questions.


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How do pet gecko lizards pose a health risk?
Does having gecko lizards living in your house pose any health risk?

If you're referring to keeping geckos as pets, like all reptiles, amphibians and birds, they come with a small but finite risk of contracting salmonellosis. Having said this, the infection is easy to avoid if you maintain basic hygiene.
On a personal note, I know dozens (perhaps hundreds) of people who keep or have kept reptiles as pets and have yet to meet anyone who contracted salmonellosis. Basically, if you wash your hands after touching the gecko, keep it away from food preparation areas and don't put the lizard in your mouth, you should be fine.
If you're talking about geckos living free in your home, as is common in many tropical places, I have never heard of any health risks associated with them. If anything, I would think that the geckos would reduce health risks by eating insects such as cockroaches and mosquitoes that are prominent disease carriers.

I have geckos in my home too! They get rid of cockroaches, mosquitoes and flies. Plus, I love watching them, they have great personalities!

I especially love watching young geckos try to use stealth.


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Do cockroaches eat their shells after moulting?
I recently witnessed a cockroach eat its shell after it moulted. Do cockroaches always do this?

I have read that spiders eat their webs to re-spin them somewhere else. Eating a shell Might be some form of recycling

Yes, it's fairly common for insects to eat their egg casings, shed skin etc. where possible. In a similar vein, as Alex Stone mentions, spiders often eat their webs too. There's generally plenty of valuable protein and nutrients tied up in there, so why not recycle?

Thank you for the link! I thought along the line of recycling but I wasn't sure.


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Hardy-Weinberg applied to three alleles and stimation of allele frequencies
I have this equation:
Corresponds to HW in equilibria with three alleles:
$(p+q+r)^2=1$
Expanding the square results:
$p^2+2pq+r^2+2pr+q^2+2qr = 1$
I need to separate homozygous and heterozygous, that means:
$2pq+2pr+2qr=1-p^2-q^2-r^2$
How I can use a equivalence similar to $(p=1-q) or (q=1-p)$ in two alleles to resolve the last equation?

in this case it will be r=1-p-q and similarly for others

Why do you need to separate homozygotes from heterozygotes?

I'm with jkadlubowska - what's the purpose of separating hetero and homozygotes?

To calculate the proportion of the alleles (p, q and r), if the homozygotes are three times than heterozygotes.

So you omitted some data of this question? The thing is, you can substitute whatever you want, e.g. 1-p=q+r or p=1-q-r, but that leads you nowhere if you don't have any more data. Something like p^2+q^2+r^2=3pq+3pr+3rq is crucial to solving this problem. Anyway - these are two equasions, you still need a third to ba able to assign specific numbers to p, q and r.

i think WYSIWYG has answered this question.  can't do much more unless you have a further answer you are looking for

I agree with jkadlubowska that some information is missing.  If you want numerical values, the number of equations must be equal to the number of variables.  Otherwise, the best you can do is solve for two variables in terms of the other. Did you want to do that?

Everybody said it already, but there is none.  The original HWE equation ($(p+q)^2=1$) works because you've got two variables and two equations ($p+q=1$) to work with (in reality, these are just one equation and one variable, since $q=1-p$ so $p+(1-p))^2=1$).  Now you have three variables and still only the one equation ($p+q+r=1$) which is, mathematically, impossible.
You need go out and measure some frequencies.  In particular, you need to measure two of them - I'd choose two of the homozygous types for convenience's sake.
This basically summarizes everything nicely for ya: http://www.bio.miami.edu/dana/dox/trinomial.html

mathematically impossible -> mathematically insolvable.  Its quite possible.


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Amino acid characteristics that determine their chemical properties?
What chemical aspect of amino acids results in their having different properties such that the chemical and physical properties of polypeptides vary with both amino acid content and amino acid order?

Sounds like a homework question to me.

What differences do the amino acids have from one another?  There is your answer.

Look up amino acid R groups.

Sounds seriously like your homework, so it'd be better if you researched. However as a starting point amino acids can be polar and non-polar. These properties cause varying forces of attraction between amino acids and their surrounding environment. The location changes the way they can interact. Ask if you are unsure about something :)


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In vitro enzyme production
I need to express a protein in vitro but I don't know where to start.  I will likely do a  T7 transcription protocol but for translation I am not sure what to do.  Are there any good kits?

there are in-vitro protein synthesis kits.. but you may try expressing the enzyme in bacteria and purify..

There are kits: Google "in vitro expression" and you will find that all of the major companies do one. I have no experience with any of them.

Don't take me wrong, but if you don't know where to start, kits are probably the worst starting point. It is not by mixing unknown solution A with proprietary buffer B that you will understand in vitro enzyme production. Once you master and troubleshoot the technique, using kits as pipetting shortcuts is fine.

@GianpaoloR what is your recommendation to use besides kits?  Should I use T7 RNA polymerase to create mRNA from my gene of interest, purify the mRNA, and then use a lysate for translation?

yes, rabbit reticulocyte, wheat germs or Hela extracts. There are detailed steps on Current Protocols.

New England Biolabs, which has an excellent reputation for well-tested, well-documented, and robust products, has a line of protein expression and purification products that I'd definitely take a look at. I've used the pMAL system for expression of fusion proteins in E. coli, and the PURExpress system looks just like what you're looking for. I have a personal (but not financial) connection with them, and I can vouch for their quality and technical support.
Pierce/Thermo is generally a good place to look when dealing with protein stuff. I've had good results with lots of their stuff, but I haven't done in vitro expression in ages, so I can't remember what I used. (BTW, I have no connection with them, I just tend to like their products.)
As Alan Boyd mentioned, lots of companies like Life Technologies, Promega, Qiagen, and Sigma have in vitro expression kits. Which one you pick will ultimately be influenced by what exactly you need your protein to do, the desired scale of expression, the type of tag(s) you want to put on it, what equipment and expertise you have in your lab, and how much time and money you want to invest.


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Reason behind formation of different shapes of cell
I have always wondered how cells are modified to give them a specific shape. On what specific part of a cell does gene regulation act  for giving the shape ?

Are you interested in the specific mechanisms of cytoskeletal remodelling or simply asking what portions of the cell give a cell its shape?

Cell shape is dictated by the cytoskeletal arrangement. There are both intrinsic and extrinsic factors that control cell shape.
Extrinsic factors consist of environmental factors such as extracellular matrix. Rho-GTPases relay the environmental signal to the cells to cause cytoskeletal rearrangement.
Intrinsic factors are basically the stable transcriptomic identity (a gene regulatory programme) which determine a cell shape. I personally don't have an idea about what genes give an intrinsic cell shape. For e.g. why does hela cell look different from HEK cell in the same type of cell culture plate under same conditions (even at low densities where there is no neighbor effect).

What is the meaning of Rho-GTPase , hela and HEK cell ?

Rho-GTPase is a protein which relays extracellular cues to the cell and causes cytoskeletal rearrangement. HeLa and HEK are commonly used animal cell lines (check wikipedia enries on these)


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Do male marsupials have a pouch?
Do male marsupials have a pouch, or is it a female organ only (like the womb)?

In most marsupials, only the females have a pouch. However, males of the water opossum and the extinct tasmanian tiger (or thylacine) also have a pouch.  The males of both the thylacine and water opposum used/use their pouch to keep their genitalia from getting entangled in vegetation.

...evolution can even make underwear!

Not all male thylacines had it, but yes, some did.


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Experimental evidence for the selfish gene vs. the selfish individual
In the Selfish Gene, Dawkins makes the argument that a better  view of evolution (i.e. more in accordance with experiment) is obtained if you view the basic unit of evolution to be the gene rather than the group. Having read the book, I am convinced (inasmuch as a layperson can be convinced) that group selection comes up with incorrect predictions about evolution, so is a fallacious interpretation of evolution (is this a correct interpretation of the book and is this conclusion common opinion among biologists?).
I have heard that historically, his book was part of a backlash against the then prevalent viw of group selection.
TL;DR
However, is there an experimental way to prove whether the gene-selection or individual-selection interpretation of evolution is more correct?
I hope my question is not ill-defined whilst leaving 'unit of evolution' vaguely defined.

Today, most evolutionary based studies are molecular.  Take a look at the neutral theory of molecular evolution

Selfish gene/selfish individual are not mutually incompatible. Old-style group-selection on the other hand is incompatible with the gene-centric (selfish gene) approach. Good question, BTW. I'll take a stab at it once I organise my thoughts on the matter, it's been a long time since I read The Selfish Gene.

I agree with @ChinmayKanchi but its often said here that this is all proven.  I haven't really found that myself - publications in reputable journals including Nature continue to appear.   But maybe someone can post their full argument? @RichardSmith?

Answering this question properly would require me to at least skim a dozen papers to refresh my memory. But essentially @shigeta is right, the gene-centric view is held by the majority of biologists, but it's not a done deal. And there's little direct evidence either way. Personally, I think the answer is probably that selection acts at multiple  levels.

My understanding of this is that the complete reference for molecular centralized evolution is The Selfish Gene itself.  I'm going to cite Alan Grafen's essay here,
Richard Dawkins, proposes that the logical, fundamental unit of evolution is the replicator.
The replicator is the fundamental unit of reproduction - whether these replicators survive or do not defines the properties of the biological system they reside in.  These words were chosen carefully because DNA sequences themselves are not replicators exactly - many individual copies make up the animals in a gene pool and the replication of one copy or another doesn't matter.  The distinction between a physical strand of DNA and the replicator is the bulk of more than one of Dawkins book.  It shows why the life of an individual means nothing to biology or evolution, how the boundaries of genes as transcriptional elements do not define the replicon (commonly misunderstood by molecular biologists).  The replicon (a genetic unit of replication) manifests a behavior or phenotype in the organism that helps it reproduce and is reproduced.  This can be cooperation with other members of your species or egg rolling or killing other sperm and is usually the result of many individual mRNA transcripts working in concert.  A given gene as defined by mRNA transcription commonly participates in multiple replicon type behaviors.
But DNA is in the mind of the molecular biology camp highly intertwined as a replicator because it is the physical medium through which the replicator is passed from one generation to another.  Without DNA, meiosis and the rest there are no replicons.  The earliest replicators were possibly simple transcripts which self replicated and not much more, but over time they have become a network of intertwined molecules working in a system.
To my understanding this is axiom more than proof.  It does not need to be proven because the physical transmission of DNA replication over time is the minimal necessary scenario to picture biology and evolution as we understand it.  The selection amongst groups of genes or groups of cells or groups of individual multicellular animals seem unnecessary given the physical framework of DNA replication.
Certainly that these connections have been shown.  The inspiration for The Selfish Gene is the confirmation of Robert Triver's Selfish Gene hypothesis with the discovery of t a terribly selfish gene which takes up the better part of chromosome in drosophila and increases its chances of showing up in the next generation by showing up in sperm more than half the time.  There are lots of other examples in the Selfish Gene and the Extended Phenotype, which answers many of the common questions about this thesis.  The literature since has been pretty productive. That being understood, its one thing to prove that something is true in biology, and another thing to prove that all other similar mechanisms are simply not true.
Yet even in Dawkins essays we see that the replicator is a bit of an abstraction some practically indefinable group of genes. Even as they each compete against each other, they create phenotypes collectively and the replicon becomes abstracted from the fundamental mechanism of replication.  The most popular example of replication Dawkins creates - the meme - has no relationship to DNA at all - a sticky idea that spreads socially and replicates in the minds of individuals.
When we look at terribly complicated but obviously advantageous behaviors, the connection between the replicator and the competition of individual genes gets muddy.  EO Wilson, having discovered pheromones and started ecology and sociobiology as disciplines still publishes group selection arguments.  Having studied social behavior in insects over his career and co-authored one of the most complete compendiums on the subject, he has put forth consistant arguments since the 70s that group selection still has a place in evolution. Unlike others, Wilson has I think always kept the conversation scientific and isn't jumping off any ideological cliffs (though responses say differently, the whole conversation is still published).
I don't see how an unbiased forum can ignore the fact that the editors of Nature still call this an open discussion.  Some may object, but calling the subject closed is overreaching I feel. There are others besides Wilson; I'm not familiar enough with the whole discussion to go into David Sloane Wilson and the rest, though they publish in reputable places.
I've started in this post since the question has been sitting around for a while. I expect others will post their corrections/objections/views - please do!  Whenever group selection is mentioned it often happens that someone will pop up and say 'this is not appropriate for a scientific discussion of biology here' but never any justification of disqualifying questions - I think that's not really scientific.  The fundamental attraction to academic thought to me is that minority voices that have legitimate observations are tolerated and often result in scientific revolutions, after which they are venerated for their persistence.
Here's a good place to tell us why some questions are beneath discussion in biology.  I personally do not agree; even if a position is intertwined by politics and religion, its the scientific value that should be judged, not by the company it keeps - lest science become just another intolerant clot, not driven by logic, observation and facts.  I ask you, why bother then?

This is a superb answer!

Agree with Chinmay, but I'll give time for your call for corrections/objections/views.

That's a good thought @Alyosha - this sort of question probably needs a conversation not a single answer.


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Does brain activity generate heat gradients in the brain?
I'm reading this article on guiding axon growth using temperature gradient, and it mentions that the trajectory of growth of neuron connections can be influenced by temperature gradients as little as 0.1C.
This got me thinking - does thinking generate heat or increases blood flow enough to create heat gradients within the brain? If so, this may explain how the brain rewires itself.

It is well-known that brain activity locally rises blood flow and temperature, and so there is a temperature gradient from the brain tissue (source) to the vascular tissue (sink). But this isn't what you're anticipating, probably.

I've re-read the article and it actually mentions that heat repels the axon growth(text under the photo). This is indeed not an answer I was anticipating.

Possible duplicate of How does the brain's energy consumption depend on mental activity?


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What is in the space between neurons in a brain?
When neuron animations are displayed, there are frequently seen neurons, axons arranged in a lattice with a lot of empty space between. I'm interested if there is indeed empty space in the brain, or if it is filled with some sort of fluid? I've checked an article on cerebrospinal fluid but am not sure that it is present all throughout the brain.
The reason I'm asking is that I'm thinking of neurotransmitters- they are released in synapses, but I'm not sure how they stay there - are they suspended in some liquid as well?

Not so empty, actually.
The human brain has a mass of ~1.5kg, and volume ~1200cc (a little bigger for men, a little smaller for women). So is heavier than water by a good margin.
While it has Cerebrospinal fluid, that only occupies the subarachnoid space (the space below the skull and above the cortex, contained between two layers: pia matter and arachnoid membrane) and the ventricular system (several spaces inside the brain, remnants of the embryological development of the brain).
Neuron density may vary widely, depending mainly on the particular characteristics of neuron cell types and their interconnections. But besides neurons, there's a lot of infrastructure inside the brain. For example:

Astroglia: They are a type of glial cells which participate in the formation of the blood-brain barrier (supporting the endothelial cells), nourishing of neurons, maintenance of ion and neurotransmitter concentrations, among others. They also keep in place most of the tissue.
Microglia: Small cells with immune (phagocitic) functions inside the brain.
Radial glia: A more specialized precursor cell, that also participates in neuronal migration in the brain.
Oligodendrocites: Cells responsible for the insulation (myelination) of axons.
Neuroepithelial cells: The stem cells in the brain.

Neuroglia, which includes the first four cell types above, accounts for ~90% of tissue in human brain (http://classes.biology.ucsd.edu/bipn140.WI13/documents/Gliamorethanjustbrainglue.pdf).
Also, when you collect some billions of axons, they can be quite representative in terms of mass and volume. The ratio between white matter and gray matter is close to one for humans, but lower for smaller mammals (http://www.pnas.org/content/97/10/5621.full.pdf).
About the last part of your question, the synaptic cleft (the space between pre-synaptic and post-synaptic neurons) is a salty solution: water with high concentration of sodium and chloride ions (and also calcium ions, neurotransmitters and a lot more). These ion concentrations are fundamental to the generation of action potentials, neural signaling, and the general dynamics of the brain.

To get an idea of how crowded the brain is, play around with the eyewire project (https://eyewire.org). I always thought the brain was mostly space, like it is in diagrams. But it's more like densely packed spaghetti than a fishing net.

I really wonder which of these special cells (or anything else) is responsible for getting nutritions to the neurons for creating electrical potencial. Or are the ions just freely released into the brain?

The answer here again is water. Please see my answer to the main question. Electrical gradients IN the water is what drives the work done in cells.

Apologies for just referencing Wikipedia, but this is a very old bit of science.
The neuron gap junction - the point where the axon touches the next cell over - is 4 nanometers.
This is actually a controlled channel where the neuro transmitter molecules are transferred from one cell interior to another - its a controlled cellular - cellular channel so they really are as close to touching as they could be.

The reality is a variety of very dense arrangements of axons and neurons:

This image is from the cremi challenge website, where you can find some varieties of neuron maps from different regions.
Here's a video explanation of the process for building the neural images:
https://youtu.be/OoU_GF4fc6w?t=659
There are some efforts to map the neuron circuits of mice and drosophile fruit flies, to be able to add them into computerized physical versions of the animals. It's still many years away for even a fruit fly.
There's a good video of nanometer slices here https://www.simonsfoundation.org/2021/03/22/the-connected-connectome-part-2-beyond-the-fly/#
This pic answers the title of the question, here we see 10 micron wide cell bodies of neurons, the cell bodies are distanced by 15-35 in that region.

The question is what's BETWEEN neurons. Most of these answers don't actually even answer. They just say "it's not very empty". Yes, the gaps between neurites are quite small, but not compared to a water molecule. In the images that I took below, it may appear that there is no spacing, but this is misleading as the tissue and areas shrink quite a bit as a result of the processing required for imaging. If you use cryo-fixation however, you can see the gaps more clearly. These gap sizes are not trivial. While they may only span anywhere from a few nanometers to a few hundred, SOMETHING occupies this space. The answer is water. Water molecules are about 1/4 of a nanometer. If you do an Xray analysis in these spaces (as I have done), you will find that its overwhelmingly filled with oxygen and hydrogen, aka water. I could go on, but that is all the question asks of and I hope I have demonstrated sufficiently that water is indeed the most prevalent substance occupying the space in between neurons.

It's mostly filled with water. But not ordinary water, it's like a fluid liquid crystal, 4th phase water. It's quite dense and the carrier of cellular components. 99% of the molecules are water and the distance between subcellular surfaces is usually only a few nanometers and water occupies those gaps in its sticky viscous state

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Can sexual reproduction create new genetic information?
Is there a small chance that in sexual reproduction a new allele forms in the off-spring that was not present in either of the parents, or are the alleles in the offspring always from at least one of the parents?
Is new genetic information ever created during sexual reproduction, or only through mutations during an organisms life time?

Only gamete genes can be passed on from the organism, they are transient. it is estimated that 2/3rd of the mouse genome has been completely rewritten since 65mn years. mice only have 1/3rd of their original genome since that time. https://www.wired.com/story/shrinking-bat-genomes-spark-a-new-model-of-evolution/ gene variants only occur during transcription, i.e. the gametogenesis.

Homologous Recombination not only shuffles different mutations together, but similar sequences near each other from gene duplication events and from regions with highly repetitive sequences can recombine and cause gross changes in the sequence of the genome in hot spots.

That'd be any different in mitosis? I'd like to get a hold on what is specific to crossing over - what kind of mutations are specific to maiotic crossing (over)?

mitosis pretty much just duplicates the chromosomes in the cell.  (some changes do happen but not on the scale of meiosis).  In Meiosis the two chromosomes mix and mutations on the different copies of the two chromosomes can end up in the same chromosome.  the ends of genes can be changed to kill or activate the gene. lots more can happen than mitosis

Many mutations occur during DNA replication (or when a mutagen is around, but that also largely affects replication).
Mutations occurring "during sexual reproduction" might occur during gametogenesis, when the eggs and sperm are developing in the parents. If a mutation were to occur during these processes, it could be that the alleles in the offspring are different from that of both parents.  Alternatively, an intragenic crossover during synapsis might produce new alleles (if the parent is heterozygous).

"Alternatively, an intragenic crossover during synapsis might produce new alleles (if the parent is heterozygous)"  - There seems to be some concept of allele that encompasses the exchange of parts thereof. I mean, allele can be shifted, but can parts of alleles be shifted, too? That, indeed, would be different from creation of new alleles by mutation and transcription, the latter I read of as being excluded from "allelic variation".

I know of some discussion about "what is a gene?". - What is in a gene that might be exchanged means, what is a gene, in an allelic approach.

An interesting question! During homologous recombinations many mutations are actually fixed (here meaning that those that have accumulated over time can be restored) as both chromosomes are condensed and can be compared by the DNA repair enzymes. However additionally mutations can occur and be passed on. As gametocytes primarily do not have to do much more than housekeeping (energy metabolism, basic cellular processes etc) genes they do not rely on can mutate and become dysfunctional. This frequently causes miscarriages, if you check the chromosomes there can be massive errors due to deletions or translocations in miscarried fetuses. Specifically the ova, as these are made before the female is born and then are "revived" as needed they carry the burden of mutations throughout life and this causes the increased rate of genetic diseases (particularly Down's syndrome) observed in later pregnancies.
tl;dr
Mutations can continue if they're not deleterious. Those that are particularly common that lie in "functional" genes are the ones that lie in HLA. These genes are involved in the immune system, and differences across generations are frequently observed. This is because there are many and if one fails, another can take its place. Mutations that are neutral occur the most frequently (i.e. don't affect offspring at all). But new alleles can most definitely be generated, and is the whole basis of evolution.

Biological information has several hierarchies is ambiguous between syntactic information in a hierarchical modular system, and functional information, without a particular context[1].
Out of necessity the DNA is sequence is generally highly conserved, but small changes can easily lead to gross changes in folding, function and the minimum energy states of the protein. (Proteins are ultimately dynamic systems, with many constantly sampling their minimum energy conformation structures - the static pictures on magazine and book covers are misleading)
Additionally an allele, by definition, is a gene variant that occurs in at least 1% of the population - by consensus (and and sufficient statistical power). As such the term is part of population genetics. For instance, for a 400AA long protein, that would mean that a particular homologous recombination event has to occur very frequently and be favored by at least one of many (known) mechanisms.
Is new genetic information ever created during sexual reproduction, or only through mutations during an organisms life time?
Yes. Recombination has several mechanisms, is not a perfect event, and shows different efficiencies depending on the type of mechanism and "helpers"/helper-types as well as helper concentrations involved, - notwithstanding cofactor-concentrations.
[1]John Collier, Hierarchical Dynamical Information Systems With a Focus on
Biology, Entropy 2003, 5, pg. 100-124


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How does hair grow and is it similar to how grass grows?
If I recall correctly, nails (finger nails or toe nails) grow by adding matter at its base. So for instance, if you would draw a dot at the very bottom of your nail, it would end at the top in a couple of weeks.
I was wondering how this works with hair. Is new hair added at the bottom and the old hair 'pushed' away? Or does hair consist of layers that always try to get further and further (that would mean longer hair is thicker than shorter hair). And is this wayof growth similar to how grass grows?

In hair and nail growth new cells are added to the bottom. These cells are produced at the follicle. There are three stages called:

Anagen : active growth
Catagen : end of active growth
Telogen : total stop of follicular growth

I don't know what you mean by like grass but both nails and hair have a first in first out order.
Feathers present a contrasting case: the outermost portion is the most recent. Feather growth is relatively more complex. This article is a nice read on feathers.

Well, does grass grow in a similar manner? First in, first out?

plants grow differently.. the tips grow.. its opposite to hair growth

And all hair cells are all dead cells...


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What are centromeres *really*?
I've gathered that a centromere is a a region*  where the DNA is bundles up even tighter (around protein different to Histone) and chromatids are 'joined'. However I'm still mostly in the dark regarding its physical structure and functioning.
At what point during DNA replication is the centromere created, and how is it created? How does it hold the chromatids together (what are its components)?
Specifically:
When it is being created (presumably during cell division) how is the positioning  of the centromere controlled? Which flags are used by the enzymes in the process of making the centromere to tell them that it is the right spot: a section of DNA that 'says' "Right part of centromere, to be attached to left part"?
Secondly, after their condensation into chromosomes (e.g. during prophase), are the sister chromatids physically intertwined around each other** for the purpose of joining, or are they simply adjacent?

Is there a 'loop' in the centromere slung over the adjacent chromatids to join them?
If they are intertwined, how is this achieved during DNA replication, whilst the non-centromere parts of the sister chromatids are not intertwined?

How does the centromere break down to allow the chromatids to separate (e.g. during meoisis 2 and anaphase)?
On a somewhat unrelated note, what in the centromeres do the spindle fibres attach to, and how do the tips of the growing fibres notice it to head it its general direction?

*(i.e. there is not a separate physical object dubbed 'the centromere', rather it is a collection of objects in a region)
**(That is, considering no other molecules than the chromatids, if you were to pinch the top and bottom ends of the left and right chromatids and pull them apart, could you separate them without them locking together (basically, do they intersect knot-theoretically)?)

There are many questions in your question. I'll try to answer each question pointwise.

Which flags are used by the enzymes in the process of making the
  centromere to tell them that it is the right spot

There are some centromere associated repeats in the DNA which mark the site for centromere assembly. There is no particular consensus sequence of this repeat. However, this study says that in certain cases stable chromosomes are formed in the absence of centromeric repeats.

are the sister chromatids physically intertwined around each other for
  the purpose of joining, or are they simply adjacent?

They are joined by proteins called cohesins. Cohesins looks like rings which form around the sister chromatids. During anaphase, the anaphase promoting complex (APC) activates an enzyme called separase, which in turn degrades cohesin.

what in the centromeres do the spindle fibres attach to, and how do
  the tips of the growing fibres notice it to head it its general
  direction?

Centromeres serve as a site for the assembly of kinetochore. Kinetochore is a multi-protein complex which forms contact with the spindle fibres (specifically, K-fibres. Refer this previous post). An essential component of kinetochore is the motor protein dynein which makes the kitetochore to crawl along the spindle fibres, towards the pole. The wikipedia article on kinetochore is quite descriptive and you can refer that for details.

Thanks you. I put many questions in one place for continuity.

Supplemental

When it is being created (presumably during cell division) how is the
  positioning of the centromere controlled?

The marks of "centromere" is added the G1 (CENPA) and S phase (all other members of the CCAN) of the cell cycle. As for how the positioning is controlled... the answer is unknown. But it does appear that when a centromere sequence is replicated, the proteins from the original centromere are divided between the two new copies of the centromere DNA sequence . So a DNA sequence is a centromere because it was a centromere. But how did it get to become a centromere in the first place is currently unknown.


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What beetle is this?
I've found it in my kitchen. It seems to be that he flew through the window from the street.
The country is Russia.

What size was this specimen?

This is Mealworm beetle, Tenebrio molitor, a species of darkling beetle.
http://en.wikipedia.org/wiki/Mealworm

Thank you @terdon for help!

I am not an entomologist, I just happen to have worked on the genome of the red flour beetle, Tribolium castaneum and this looks very similar. A quick wikipedia search turned up the amusingly named "confused flour beetle", Tribolium confusa, which looks almost exactly like what you have photographed:

So, I would guess (I stress that I don't really know) that this is some sort of Tribolium species and, by now, is thoroughly confused even if it was not to begin with.

Thank you very much for the answer. I've just read about this on Wikipedia and found that this is a Mealworm —  http://en.wikipedia.org/wiki/Mealworm — a bigger version of a Tribolium.

@SunnyRebornPony well done! Could you please post that as an answer and accept it? The species name is mealworm beetle, Tenebrio molitor, mealworms are the larval (apparently edible!) stage.


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Would a spinal injury decrease human height?
A woman I know has been losing height at a rate of few cm a year following a severe spinal injury. How is this possible? What kind of injury could cause such progressive loss of height? Could this be a genetic defect? Are there any disorders that cause this type of shrinking?
In case it could be relevant, her brothers are very tall.

i asked this question as well on fitness.stackexchange.com and on http://skeptics.stackexchange.com, they think here is a better place, so they downvoted my question, i hope you don't downvote me too, I just want to know what's wrong with this woman before she dies, that's all. I searched all around the web for disorders, couldn't find any! i just want an explanation

please see http://www.healthboards.com/boards/bone-disorders/609860-shrinking-young-age.html

I dont have a definite answer for this but this is what I speculate: spinal injury can cause paralysis which leads to atrophy (wasting away) of skeletal muscles. This may be the cause of the observed reduction in height.

atrophy happens because of prolonged disuse

Her height is that of a small bottle of cola? You expect us to believe you know a human being who is ~20cm tall?

@terdon i'm talking about this bottle

That bottle has a height of 18 cm, are you saying you know someone who is less than 20cm tall? I am sorry if this is a failure to communicate but it sounds like your question is a joke. The shortest person in the world had a height of 50.8cm, more than twice what you describe. It would take a hell of a lot more than a spinal injury to shrink someone to that size, and I really doubt that the human body would continue to function. If this is just an exaggeration, please remove it from your question.

@terdon lets not argue about the height, you wont believe me and we'll not get any answer, my question is "is there any disorder (or spinal injury) that would cause you to keep shrinking for the rest of your life?" we know that the brain tells the body to grow, would a shock or something make the brain tell your body to shrink instead of growing? i don't care about her height, i care about the problem she has

Fair enough, and I'm sorry, I thought this was a joke. If you don't mind I will edit your question to remove the bottle reference so others don't make the same assumption.

@terdon that's fine, i also made a mistake by mentioning that

@Fischer.. did you consider muscular atrophy as a possibility.. i dont know if bone atrophy is also triggered by continuous disuse..

As @WYSIWYG pointed, muscular atrophy is the main cause for height decrease.
A spine injury leads to neural impairment and paresis / paralysis. This affects directly muscular trophism. It also limits physical activity, this being another favoring factor for muscular atrophy and overweight issues [1]. Association of bone degenerative processes (osteoporosis, osteopathy, osteolysis) is also a factor and it is dangerous because it promotes spinal cord injuries if vertebral height reduction amount is notable [2].
Focusing on muscular atrophy, here is how it can decrease height: by increasing vertebral column curvatures mostly on the upper region with articulating vertebrae. The vertebral column tends to gain a spring-like, spiral shape, associating accentuated cervical lordosis, accentuated thoracic  kyphosis and thoracic scoliosis.

Image source: Scoliosis Treatment Alternatives. Chiropractic for Scoliosis Treatment Review (2014). Accessed 21.07.2014
While reading the comments to the question I found something interesting:

we know that the brain tells the body to grow, would a shock or something make the brain tell your body to shrink instead of growing?

Yes, the brain (hypotalamus) initiates a neuroendocrine response that leads to growth hormone secretion. The secretion is about 700 micrograms/day in a young adolescent, while in a healthy adult it is about 400 micrograms/day [3]. The deficiency in an adult person leads to a tendency of fat mass increase and a relative decrease in muscle mass and, in many instances, decreased energy and quality of life [4]. The brain can't "tell your body to shrink", but the lack of "communication" between the brain and organs leads to less to absolutely no use of that organ, thus inducing atrophy. The lack of both external and internal stimuli leads to atrophy (in general) [5].

References:

Gupta N, White KT, Sandford PR. Body mass index in spinal cord injury -- a retrospective study. Spinal Cord. 2006 Feb;44(2):92-4. doi: 10.1038/sj.sc.3101790. PubMed PMID: 16030513.
Ji L, Dang XQ, Lan BS, Wang KZ, Huang YJ, Wen B, Duan HH, Ren F. Study on the safe range of shortening of the spinal cord in canine models. Spinal Cord. 2013 Feb;51(2):134-8. doi: 10.1038/sc.2012.99. PubMed PMID: 22945745.
Wikipedia contributors, "Growth hormone," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Growth_hormone&oldid=616959802 (accessed July 21, 2014).
Molitch ME, Clemmons DR, Malozowski S, Merriam GR, Shalet SM, Vance ML, Stephens PA. Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society Clinical Practice Guideline. J. Clin. Endocrinol. Metab. 2006 May;91(5):1621-34. doi: 10.1210/jc.2005-2227. PubMed PMID: 16636129.
Wikipedia contributors, "Atrophy," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Atrophy&oldid=611770442 (accessed July 21, 2014).

As they say in Texas don't slump or your get your grandmother's hump.

This answer is just wow!!


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How do liver and lung metastases cause death?
Metastasis to the liver and lungs are the main causes of death in colorectal cancer.(1)
I understand that colorectal cancer may have metastases. But how do these metastases cause death?
Reference
(1) A. Bolocan, D. Ion, D.N. Ciocan, D.N Paduraru. Chirurgia (2012) 107:555-563. Introduction.

As I understand metastasis doesn't cause death.. it just spreads the cancer to new sites and the body is parallely invaded at several areas.. worse than a single locus.. moreover it would be difficult to surgically remove the cancer in such conditions.

Metastasis is the spreading of cancerous cells to a new site within the body where they form a secondary tumour.  There is nothing special about how these metastases cause death, they do so in the same ways as the primary cancer eventually might:

Replacing functional cells with non-functional cancerous cells
Eroding into other tissues and disrupting normal body architecture
Causing haemorrhage
Putting pressure onto other structures

If we apply those principles to lung and liver secondary tumours, it is easy to see why they are likely to contribute significantly to mortality.
Cancerous masses in the lungs reduce the surface area available for gas exchange, reducing oxygen saturation of the patient.  The tumour may also erode into a primary bronchus, which if obstructed would cause lung collapse, or into the mediastinum.  If the mediastinum is involved then the great vessels or heart may be invaded into with significant consequences.
Liver metastases are more likely to cause problems due to the reduction of liver function as the cancer grows. This causes a plethora of problems as the liver is involved in so many pathways within the body.  Examples of serious effects would include the patient becoming coagulopathic due to a reduction in production of clotting factors, making bleeding much more severe.  The liver can begin to fail to clear toxins from the blood, leading to the risk of acidosis or hepatic encephalopathy (leading to coma and eventual death).  If the tumour were to invade the portal vein, this can cause portal hypertension, which in turn shunts pressure into the systemic venous system.  This can cause oesophageal varices which are prone to spontaneous and catastrophic bleeding. Similarly a tumour invading the common bile duct (or other part of the biliary tree) can cause obstructive jaundice and associated problems.
The reason your quote suggests that most deaths are from metastases than the primary tumour is probably because tumours in these locations have greater negative effects at a smaller size because they are in crucial tissues.
There may be another contributing factor in the form of data interpretation, however.  Tumours are often 'staged' via the TNM staging system, the last component of which is the presence of metastases.  The presence of distal metastases automatically makes colorectal cancer Stage 4.  This is often considered not to be curable, meaning a move to more palliative treatment options.  This may affect the survival curves for those with distal metastases and those without.

Fabulous explanation, thank you! Yes, the same paper states that these metastases occur in up to 25% of patients at presentation.


text:
What does "tumour budding" mean?
tumour budding, lymphocytic infiltration and resection margins are established factors that influence the outcome of colorectal cancer (1)
In this context what does "tumour budding" mean?
Reference
(1) A. Bolocan, D. Ion, D.N. Ciocan, D.N Paduraru. Chirurgia (2012) 107:555-563. Introduction/0

Tumor ‘budding’ is loosely defined as the presence of individual cells and small clusters of tumor cells at the invasive front of carcinomas. A study of the measure of budding can give an insight into how fast the disease might propogate.
Reference


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Are there any examples where 'magic bullet' drugs have worked in cancer treatment?
Magic bullets are drugs that can be administered on a micro local scale. In this context administration/binding would occur in or near the tumour by exploiting the different surface antigens that cancers expose. Basic lectures teach that a "magic bullt" drug could attach via an mAb (attached to the pro-drug) and then a conjugated enzyme cleaves or converts the pro drug to a drug. This would eliminate a lot of side effects from chemotherapy.
Use in clinical trials. Some mAbs have started to be used in clinical trials, almost 40 years after they were first proposed. My question is simply; have there been any cases of mAbs being used as a successful treatment for any disease? If not, what makes the R&D of this drug type so difficult?

Do you understand magic bullets only in the way of directly attaching to surface antigens or do you also see special made drugs for certain cancers under it?

I'm not necessarily interested in other “magic bullet” concepts. Paul Ehrlich’s magic bullet idea was first discussed in the early 1900's so I'm sure there are enough ideas out there to fill many textbooks by now! Hopefully my edit cleared it up - I only care about this mAb proto drug idea.

There are, indeed, several such mAb based treatments. From the Mayo Clinic:

The monoclonal antibody drug rituximab (Rituxan) attaches to a specific protein (CD20) found only on B cells, one type of white blood cell. Certain types of lymphomas arise from these same B cells. When rituximab attaches to this protein on the B cells, it makes the cells more visible to the immune system, which can then attack.

(...)

Cetuximab (Erbitux), a monoclonal antibody approved to treat colon cancer and head and neck cancers, attaches to receptors on cancer cells that accept a certain growth signal (epidermal growth factor). Blocking this signal from reaching its target on the cancer cells may slow or stop the cancer from growing.

(...)

The monoclonal antibody bevacizumab (Avastin) targets a growth signal called vascular endothelial growth factor (VEGF) that cancer cells send out to attract new blood vessels. Bevacizumab intercepts a tumor's VEGF signals and stops them from connecting with their targets.

(...)

Ibritumomab (Zevalin), approved for non-Hodgkin's lymphoma, combines a monoclonal antibody with radioactive particles. The ibritumomab monoclonal antibody attaches to receptors on cancerous blood cells and delivers the radiation.

(...)

Ado-trastuzumab emtansine (Kadcyla) is one such drug approved to treat HER2-positive breast cancer. Ado-trastuzumab emtansine contains an antibody that attaches to the HER2 receptors on the breast cancer cells. The cancer cells then ingest the antibody, which releases a few molecules of chemotherapy.

It does eliminate side effects, although the treatment is not side effect-free.
Personally, my suspicion with this approach is this: At its heart, cancer is a problem of uncontrolled cell division. Most cells in the body do not divide rapidly, and this slowing down of proliferation is integrated into differentiation into whatever tissue the cells are in. The most obvious cells that divide rapidly are stem cells (themselves carcinogenic!). Furthermore, it seems to be a common theme in cancer that the less differentiated (or more de-differentiated) you are, the more easily you divide, and hence the nastier the cancer you generate.
As such, the worst cancers out there are going to be very undifferentiated, and express few eligible surface markers. What's more, tumors evolve. If you start selecting against cells which express your marker, you will encourage the tumor to simply evolve and stop expressing that marker. Back to the benchside to look for a new marker - meanwhile your patient gets worse and worse.
This is why generalized chemotherapies (or radiotherapy) are so attractive. They attack the rapid division of cancer cells, and the cancer cells cannot evolve to lose this property, because if they did, they would not be cancer cells.


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What are the characteristics of a promising drug?
The drug development industry is a multi-billion dollar economy powered by a multitude of research bodies from industry and academia. A big risk is that drug development costs are in the tens of millions of dollars when looking at the most successful drugs
Generally speaking, what makes a good drug for research for those researchers working on these projects? Why are some potential drug pursued and others not? What traits, according to the experts, justifies such a vast investment?

Just a note, not all drugs are proteins.  Some are biologicals, others are small molecules, some are even mixtures of compounds.  This can make a difference, as I've heard it said that biologicals are sometimes expected to work better but are more likely to be toxic or have off-target effects.

Sadly no.  That advice was mostly word-of-mouth and from my notes.  Here's a link that somewhat implies support for that theory but it's not specific: http://www.bio.org/articles/how-do-drugs-and-biologics-differ

The specific characteristics sought after will vary widely, but that being said, there are a few key features many groups look for.  I've talked to and heard a number of individuals at a number of different companies, and there are a lot of different techniques and pathways looked for.  In general, however, the single, most important factor is value.  If the drug won't make money, it's almost never considered "promising."  Maybe that's a sad fact of the way the world works, but it's a fact.  The average drug costs around $1 billion (USD) to bring to market so the successful ones damn well better recoup that (Orphan drugs and companies actively pursuing them often have an easier time of this, as the FDA is understandably less restrictive and fast-tracks their progress).
That's not actually so simple.  It's a large, crowded market out there, and there is a lot of intellectual property floating around.  A wise businesswoman told me that her company focuses on the middle-ground.  A target that is too promising is probably already owned by Genentech, so they aim for the ones that are below the attention of the giants but still quite profitable.
After that, it's mainly what you might expect.  High avidity, long half-life coupled with low toxicity (more on this later), small size (if possible), and a realistic time frame.  A month can mean millions of dollars, so working for a decade is not necessarily a possibility.  Often, companies will use high-throughput screens of thousands, even millions of small molecules to look for an effect.  The screening process is usually extremely rigorous, and many potential candidates are eliminated as not good enough.  Sometimes they do some fancy stuff such as 3D modeling but it is definitely a field where brute force can still be successful.
Often those screens are used against primary cells to test for toxicity.  In fact, throughout the entire process, toxicity is a huge factor.  A full 20%-40% of drug attrition is due to safety and liability issues.  It's a constant balance: nothing can risk the health of healthy, control volunteers, but sometimes more risk is acceptable.  The first HIV/AIDS drugs were incredibly toxic, but that was okay because it was still better than the alternative.  These days, the toxicity requirements for HIV/AIDS treatments such as HAART are stricter.  Short-term antibiotics are allowed more risk since you only take them for five/seven days, whereas long-term medication for chronic illnesses are held to much higher standards.
Basically, loss of eyesight might be preferable to death, but it's unacceptable if treating the flu.  The mantra I've been told is three things:

Don’t treat one thing but cause another
Don't cause cancer
Don’t cause birth defects or alter the ability to have children

Toxicologists are conservative, willing to throw the baby out with the bathwater.  In short, Fail Early.


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What happens to an ant colony when the queen dies?
Does the colony collapse? Do workers keep following the last orders? Or can future queens replace the dead one? I'm guessing this might also depend on each specific sub-species.

Not ants unfortunately, but with bees if the queen dies the workers start rearing some larvae under queen-developing conditions. They're not normally as effective as 'proper' queens and you might end up with several at once, but you get something. Leaving this here in case someone feels like looking up whether similar processes occur in ants (although if I get time to I will try to do it myself at some point).

http://www.antweb.org/antblog/2010/12/can-ant-colonies-reproduce-and-sustain-with-no-queen-angela.html has an interesting answer (basically, they struggle but should survive by turning workers into temporary queens). That said, I'd like to have community experts confirm this, or detail whether it's species dependant before making it an official answer.
@arboviral: looks like it works just like bees if this is true.

Does your second question assume ant workers follow orders given by a qeen? I am not an ant specialist but how would that happen physically?

@BagiM: not sure if I've imagined this or read it somewhere, but I thought pheromones were used to spread general orders, influencing behavior throughout the colony.

Not really my field, but I can point to this review which discusses a couple of different ways in which ants organize their communities:
Heinze. 2008. The demise of the standard ant (Hymenoptera: Formicidae)
I know that in some species there can be several queens per colony (so more robust to queen deaths). In many species, workers can start laying eggs if the queen dies, but these will develop as males (since they are unfertilized). However, in some species (e.g. Platythyrea punctata) the workers can reproduce by parthenogenesis which can stabilize the colony to some extent after the queen dies.


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To what extent is immature eggs in insects (beetles) a good approximation for maximum fecundity?
To what extent is the number of immature eggs from dissected, newly emerged individuals a reasonable approximation for maximum/potential fecundity in insects (more specifically beetles)? I know that many species must feed for the eggs to become mature and viable. However, can a comparison between species on immature eggs still be used to capture the range of maximum fecundity between species or to accurately rank species from low---high fecundity?

There are a number of things to clarify here; Fecundity is the number of offspring that is produced by an individual, and this can be separated into potential fecundity (maximum reproductive capacity) and realized fecundity (number of offspring actually produced). Realized fecundity is very similar to fertility, which is defined as the number of viable offspring that are produced.
Potential fecundity can sometimes be a good proxy for future fertility, and this is especially true for species where all eggs are present after metamorphosis of the adult insect (Awmack & Leather, 2002). However, in some species the formation of eggs is a continuous process in adult individuals, and this is relatively common in beetles. Therefore, the number of immature eggs might be a poor proxy of both potential and realized fecundity in these species (Awmack & Leather, 2002), and this is more likely in relatively long-lived species that feed extensively as adults. In beetle species that do not feed as adults (often lacking functional mouthparts), immature eggs is probably a better approximation of potential fecundity.
It should also be mentioned that the quality of host plants will often affect the maturation of eggs (Sterns & Smith, 1960; Hopkins & Ekbom, 1999), and will therefore also determine to what extent the number of immature eggs is a good indication of potential fecundity. When feeding on poor quality hosts eggs may e.g. be reabsorbed by females to use for other purposes (see references in Awmack & Leather, 2002 & Hopkins & Ekbom, 1999 for further information).
The review paper by Awmack & Leather, 2002 is very comprehensive, and contains a wealth of useful references on this topic.


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Why do conker flowers grow upwards?
Most trees I know that have their flowers in groups hang these groups down. I noticed, however, that conker flowers grow upwards!
I guess that growing against gravity requires special effort, so conker may benefit somehow from growing the flowers upwards. Is this true? What's the benefit?

The main and maybe the only reason for me looks to be phototropism. Also read heliotropism though I can't guess if this is a factor with regard to the conker tree.

I would think that this is a inherited morphological trait within the subfamily. And I doubt it requires additional effort.


text:
What kind of mushroom(?) is this?
I found groups of these growing in the Lassen National Forest (Susanville, CA, USA). It looks like some sort of mushroom. I have Googled extensively, but can't seem to find a match.

Found it. It's a Sarcodes or snow plant:
http://en.wikipedia.org/wiki/Sarcodes

not a mushroom after all! How did you find it?

Wow this is allied to Monotropa. Thanks for link to wiki page


text:
Skeletal muscles in clam
Although skeletal muscle fatigues fairly rapidly, clams have a protein called paramyosin that allows them to sustain contractions for up to a month. What might be the role of paramyosin at the molecular or cellular level, which results in this peculiarity?

This appears to be a homework question, which is often frowned-upon without prior research. Where have you looked so far?

Without proper background knowledge I'd say that that's for keeping the shell closed.

actually this is an 'Scientific Enquiry'- type question in "Biology By Campbell & Reece"...

Older papers initially presumed that it was part of a mechanism called "catch" in invertebrates like molluscs which is a "sustained contraction."  However, paramyosin was also found in insects.  There is a very detailed review on invertebrate muscle from 2008 that you should read through (or, you know, search through) points out that recent evidence has shown that paramyosin is not involved in catch; that review also has this to say on the subject (emphasis added):

Furthermore, paramyosin’s presence in almost every invertebrate muscle (including those with relatively small thick filaments) suggests that paramyosin should not be considered a ‘special’ molecule whose presence needs explanation. Paramyosin is instead an everyday constituent of invertebrate muscles, similar, for instance, to the giant sarcomere associated proteins (see Hooper and Thuma, 2005). Indeed, a more salient question might be why vertebrates do not have paramyosin.

Following through; OP's questions seems poorly posed. Indeed, sustained contraction is nothing special. That's what muscle tone is.

From an anthropocentric position, though, it's a fair question, although as I point out the better question is why we can't contract consistently but many invertebrates can.

Yeah I'm confused by your point. Paramyosin is not involved in catch. Contracting consistently isn't difficult if you think about rigor tonus.


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Blood pressure during exercise
What happens to blood pressure when we exercise? Does it increase, decrease, or remain the same? If it does increase, why are patients with high blood pressure recommended to exercise?

As pointed out in the answers above, your blood pressure increases transiently as you exercise because more oxygen and nutrients are consumed by your muscles. However, regular exercise increases your "cardiovascular reserve"-this means your body will be able to function well at lower blood pressures. However, caution must be taken in hypertensive patients whose blood pressures are already up the roof. In these patients, gentle exercise and life style modifications (diet, stopping smoking, weight loss etc) may reduce their blood pressures over time. This will also reduce their risk of cardiovascular catastrophes in the future.
So whilst exercise will reduce blood pressure, it is not recommended as a first line of life style modification in hypertensive patients because exercise itself is stressful initially and stress is also bad for a hypertensive patient. Hence, exercise is good but gentle exercise is recommended for hypertensive patients. But again I doubt gentle exercise will do maximum good to your cardiovascular system because the type of exercise that helps lower your blood pressure is one that makes you sweat (e.g tread mill, etc). But once the blood pressure of a hypertensive patient is under control, then they can safely exercise and this should help lower their blood pressure long term. I hope this makes sense.

Blood pressure increases during exercise as shown in this paper, but the reason that experts recommend exercise for hypertensive patients is that increases in fitness decrease blood pressure (demonstrated nicely in this study of >2000 children, measuring fitness and blood pressure changes over 12 months).
In a way, the doctors aren't saying that exercise itself will decrease blood pressure, more: "increasing fitness will decrease blood pressure, fitness will increase with regular exercise, therefore you should exercise more."
Caution should be used though for taking up new exercise regimes and doctors should be consulted.
There are of course other well documented benefits to regular exercise and personally I find it is great stress relief which could indirectly aid lowering of blood pressure (stress increases blood pressure, mine is 80/50 - very low - and I would describe myself as quite easy going :D).

Increases during exercise, but as we get fitter it decreases. Vessels become more optimal, they grow to supply muscles better, the heart beats less as it becomes more efficient. However this goes beyond that, hypertensive patients are at risk of stroke and heart attacks. Exercise reduces many risk factors: stress, obesity and coronary artery disease and many others. Thus exercise is really helpful.


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What kind of tree could this be?
This may be a strange question, but does anyone know what kind of tree this could be?

I know, it's just a comic, but these trees, at “walking distance” within that comic are easily identifiable as Grandidier's Baobabs:

(That might indicate, of course, that the above tree also occurs on Madagascar, but it's a comic, so all bets are off.  And yes, we know, there are no squirrels on Madagascar.)

Is there any reason to believe that it is a real species at all?

@kmm it does look vaguely familiar, I'm pretty sure I've seen images of such trees.

I don't think this question can be answered, and it doesn't deal with real-world biology. The intent of the artist cannot be known and a silhouette can hardly be used for species determination.

I know, it's a cartoon tree, and might not be a real one, but the second one is clearly identifiable, which is why I believe the first one could be as well.

I noticed that in japanese animation, the fish are often identifiable, at least at the genus or family level. So the question makes sense to me.

Someone should just ask Randall Munroe, right?

I think these are two species.

Here's a link to the source: http://www.explainxkcd.com/wiki/index.php/1190:_Time/Pictures

It reminds me of the smooth-barked Australian gum trees / eucalyptus, like a salmon gum, ghost gum, etc.
Although there are no squirrels in Australia :)
This photo of a Salmon Gum is from http://www.fpc.wa.gov.au/content_migration/plantations/species/arid/salmon_gum.aspx

Of course, that's not a squirrel. It's clearly a brushtail possum. :)

As @fileunderwater suggested, this looks like an Acacia. Like many others with OSX, I have this incuded picture of an acacia as one of my screensaver rotations.
It looks very similar in bauplan to the illustration.

As Saxon Druce has pointed out it looks very much like a eucalypt. Specifically a desert or savanna species such as the ghost gum (Corymbia aparrerinja).

Other eucalypts (Eucalyptus and Corymbia spp.) have similar growth forms.

(source: masterfile.com)
The silhouette is obviously stylised and appears to have less foliage than a real eucalypt in order to make the profile neater. The branching pattern and the way the foliage is clustered in rounded clumps and textured in the image are representative of eucalypts. I would argue it is not an Acacia - they have very distinctive branching patterns and are more spreading with a flatter top than this.

It looks like a pine to me. Might be close to Pinus pinaster but take into account that
a) I'm not a botanist.
b) I'm only familiar with pines that grow in my area (Catalonia).

My guess (with an emphasis on guess) would rather be an Acacia species, since they are common on savanna/similar environments as Baobabs. They are fan/umbrella shaped (do a google image search). There are, however, more than 1300 species of Acacia worldwide.


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Inverse of dopamine reuptake inhibitor?
The wikipedia article on the dopamine transporter gives examples of some drugs whose effects are mediated by the inhibition of the dopamine transporter, such as cocaine and amphetamines.  Are there any drugs or substances whose mechanism of action involves increasing the activity of the dopamine transporter, i.e., a "DAT releaser?"

It's important to note the difference in mechanism between cocaine and meth. While cocaine blocks reuptake, meth makes VMAT - vesicular monoamine transport - leaky and actually reverses the transportation of dopamine, so that instead of transporting dopamine into the axon terminal, it actually transports dopamine out as it leaks from the vesicle that carry it. This is what is meant when referring to 'reverse transport' of dopamine through DAT. Feel free to read this abstract and the sources it cites (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2631950/).
Regarding the possibility of a DAT agonist of sorts, looks like current research has identified some potential targets. One of which seems to be luteolin and its derivatives (http://www.ncbi.nlm.nih.gov/pubmed/20971650). Current studies find new derivatives and test the EC50 to assess pharmacological efficacy.

Amphetamine isn't a DAT inhibitor. It actually causes exocytosis of dopamine vesicles. That is why cocaine is activity dependent as it's mechanism depends on presynaptic activity whereas amphetamine is activity independent.


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Meat and mushroom allergies, why are they so rare?
There are a lot of food allergies, but for some reason not to meat (mammalian meat or poultry) or mushrooms. I've googled a bit, and now I know that one can actually have a meat or mushroom allergy, although the odds of that are very-very small. Why is it so?
Is it because both meat and mushrooms are usually cooked and that kills potential allergens? What about undercooked or raw food like portobellos or carpaccio and steaks?
Or is it because animal tissues are so similar to ours and so are better digested? What about mushrooms then?
Is it something else?
Also, are there any data of what types of meat and mushrooms are most allergic?

Do you mean few mammal meat allergies? There are many fish and invertebrate (e.g., shellfish) allergies.

Yes, excluding seafood. I'll fix the wording.

I suspect that the reason mammalian meat allergies are so rare is that they cause extreme morbidity or mortality in kids. Essentially, most components of mammalian meat are going to be very similar or identical to self-antigens and therefore, your immune system will destroy your own body from the inside out.

Chinmay Kanchi, yes, that's plausible to me. But do you know anything to support this hypothesis?

What @ChinmayKanchi says makes sense, an allergic reaction is a response to unknown antigens, those antigens in meat are more likely to be our own - being allergic to these antigens would be like walking around with a giant self-destruct button on your forehead and hoping someone doesn't push it...

@ftt Nope. That's why it was a comment and not an answer ;)

Whilst it is true that animal cells are more like our own, I'm not sure that would be the reason for non-allergic responses. If we take xenografts (transplanting pig organs for example) we see a profound response.
The latter theory of it having a higher mortality is more closer to the truth. Typically we observe that things we are given from childhood causes induction of tolerance (T reg cells). However this occurs best at a young age and if given orally. Peanut allergies for example are incredibly infrequent in Japan for example. Meat is given typically from a young age.
However what about the vegetarian converts or exposure to new foods as you grow older. Well the theory suggested for this are some antigens act to signal the immune system. These proteins are similar to the cell signals our body uses to tell the body there's a fight on, we are being invaded by something dangerous. This causes an immune system reaction to build up, specfically IgE antibodies. Thus on subsequent exposure, the response is stronger due to a preformed response.
Although these are they hypotheses, they're being actively investigated because frankly they can't be that simple. And of course there is conflicting evidence.
Interestingly, I've met a person with mushroom allergy. It does occur. Maybe polymorphisms (slight genetic differences) means someone responds to antigens others don't?

I know two or three people with fungus allergies. In at least one of these people, mushrooms can trigger the allergic reaction.

@AndroidPenguin, you say these hypotheses are being investigated, can you point to any papers? Thank you!

See "the hygiene hypothesis"

Please add some references


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Ligase Chain Reaction: Determining the annealing temperature for gene synthesis
Using the tool Gene2Oligo I have a set of DNA oligonucleotides to synthesize a gene using ligase chain reaction (LCR).  The average melting temperature is 72 degrees Celsius.  I am going to use a the thermostable Taq ligase enzyme for the LCR reaction but I am unsure of the annealing temperature to use.  Should I use the standard recommendation as in PCR of 5 degrees less than the melting temperature or should I use another tool?  Taq ligase has a cutoff in activity at 65C so that is the highest I can use.


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What is the best way to clean plastic flasks that have been used for cell cultures - is virkon a good idea?
When you use cultures e.g. insect cells, which are infected with virus one way to clean the (plastics) shake flasks is with virkon. Which is the most effective way to clean your flasks in order to extinguish the virus?
Also, is it effective to use SDS in order to denatured the virus proteins?

I've always cultured either in disposable plastic vessels, or in glass flasks, so that they can be autoclaved and run through a depyrogenation oven. SDS will likely disrupt the virus particles, but it won't do anything about leftover DNA/RNA, which could still be infective/pathogenic.

I use a disinfectant solution of such as lizol (popular floor/toilet disinfectant).

Just to be clear, when you say clean, do you mean to disinfect to throw away, or do you plan on reusing them?  I would certainly not reuse.  Bleach is always a good idea, and when I did more serious BSL 3 work we had to use PAA.

I use virkon for cell cultures, but for viruses I tended to use standard bleach during the time I worked in a virology lab.


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Ammonia smell after physical exercise? What is the explanation?
After exercising vigorously one can sometimes smell ammonia and it feels like it's coming from within the nose actually. There is no indication that others can smell it when I do (i.e. seems to be internal rather than external). I know I'm not the only one experiencing this, but I was wondering what the physiological processes are that are responsible for that?
Also: is this merely a perceived smell or is there actually ammonia in/on my body after the exercise.

it might be the odour of the sweat. But I don't think that is the smell of ammonia.

Do you eat a lot of protein to promote muscle growth?

@NeoDevlin: well, I eat "a lot" of protein, yes, but not in particular for muscle growth. AFAIK the body cannot metabolize as much protein as for example body builders usually take in.

There are two explanations which come to mind answering your question:
I asked if you eat a lot of protein, because the amount of protein which some body builders consume leads to renal failure. And one sign of renal failure is the smell of ammonia. It's a quite common problem. But I don't think this applies to you. Your protein intake shouldn't exceed 2g per kg of body weight per day, some body builder eat up 4g per kg.
Ammonia is normally linked to your protein metabolism, which is higher during and after sport. The smell of Ammonia can occur when your carbohydrate reservoir is depleted and the body is mainly using protein as fuel. This effect also occurs when fasting or in patients with diabetes.
Try to keep your blood sugar level raised during exercise by eating something, like a banana, powerbars (also known as high energy bar) or directly dextrose. Or eat more long-chain carbohydrates. And this always depending the form of sport you are practicing. Just like the pasta party prior to marathons.

Wow, renal failure sounds severe. But I have this only after exhausting exercises, not every type of exercise either. Yeah, I think I don't get over the 2 g/kg limit, though. Will try the advice about carbs.


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Would my hands sweat this much if I wasn't wearing gloves?
I've wondered about this for a long time, and hopefully someone here has a reasonable answer. I'm a cell and molecular biologist, and much of my time at the bench is spent wearing (usually nitrile) gloves. I've noticed that if I wear them for longer than 10 or 15 minutes they start accumulating sweat. However, my hands aren't clammy or damp when I'm not wearing gloves, so my question is whether my hands are always sweating at approximately the same rate, and the impermeable barrier of the gloves just traps the moisture, or does the enclosed environment inside the gloves promote sweating? My hands don't seem particularly hot when I have the gloves on, and the gloves themselves are pretty thin, although they do have some insulating properties, as I can handle items taken from a -80°C more easily gloved than bare-handed. What causes this diaphoresis?

Skin produces a basal level of sweat all the time, so as far as makes sense to me, they simply prevent evaporation.

To the (potential) close-voters: This is not a medical question (I'm not asking for medical advice, I'm simply describing a phenotype). This isn't (or shouldn't be) primarily opinion-based, because I'm not asking for opinions, I'm asking if there is a clear, biological explanation for this. If you happen to disagree, please leave a comment and I'll try and clean up the wording.

Hand sweating has been fairly well-studied, both because sweating from the hands is one of the main mechanisms of heat dissipation at higher temperatures and because there is a significant effect on palmar sweating by the autonomic nervous system (the main cause of hyperhydrosis of the palms).
Disregarding autonomic effects (stress response), the single most important determinant of hand and foot blood flow is the thermal status of the body core. Heat dissipation is more marked in the hands than feet, and remains so as temperature increases.
Studies have been done of palmar sweating in extremes of temperatures, palmar sweating changes with aging (decreases), palmar sweating in disease, etc. But what has not been studied is the effect of localized heat on sweating of the palms, which would be of interest to you if sweating was a result of the insulating capacity of the gloves.
What is known about palmar sweating is that it is an ongoing and important process in both genders, at all temperatures, and at all ages. The most reasonable assumption then, given the limits of the literature, is that your hands sweat continuously and steadily at a given temperature, and it is highly likely that you are noticing it when wearing gloves only because the vapor barrier caused by the gloves prohibits evaporation.
The roles of hands and feet in temperature regulation in hot and cold environments
OBSERVATIONS ON THE ACTIVITY OF SWEAT GLANDS WITH SPECIAL REFERENCE TO THE INFLUENCE OF AGEING
Why do I get sweaty palms?

But then - If sweating reduces temperature, would the increased temperature not facilitate sweating? That was the reason for me not answering this, apparently, but actually not quite obvious question (+1 for the excellent answer btw :-)

@ChrisStronks - That's a real possibility! Palm sweating is a response to core temperature. Hand temperature isn't reflective of core temp (it varies much more), and there were no studies where the hands alone were warmed to measure it's impact on core temp or sweat production or evaporation was prevented. I have to guess, then. I think it's unlikely that the small heat gain from the hands would affect the core temperature, but I could be wrong. I wished I had found more on that (it was frustrating not to be able to say definitively). :-/

@ChrisStronks Sweating does reduce the temperature - you are right. But the glove prevents evaporation and thereby the cooling effect.

@Chris - yes! And therefore without the evap-cooling effect (I thought) the hands would start to sweat more because of the local temperature increase (sorry I wasn't clear). But as (@)anongoodnurse indicates: it's core temperature that drives sweating so my reasoning isn't valid I guess :) Interesting question after all :-)

Thanks for the answer, I had kind of forgotten about this question. It's too bad there hasn't been any work done on local temps, because I suspect that's why this happens - the gloves are somewhat insulating and there's no opportunity for evaporation, therefore raising the local temperature and causing a positive feedback loop. I guess I'll have to read up more on sweating disorders, as I tend to be rather... shall we say... damp frequently, but that's OT for here unless I anonymize it :)


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What is the difference between different brain regions
The brain is separated into different regions, and different regions perform different tasks. Well, what are the differences between these regions on the cellular/systemic level. The brain is made up of neurons and other cells, but how come one part is used to process sound and another is used to process, say, smell? Are they like different computer circuit boards - using the same components but are wired differently?
And anyways, why did evolution not come up with a brain that uses the entire brain to process something, would that not be more efficient?

The wiring is different as you mentioned. However, perhaps the most important is the brain knows where it's input is coming from. The brain knows where each fibre innervates and thus can compile and present this data to our conscious mind. We show if we stimulate the brain directly, than we feel a sensation in the part of the body that portion of the brain is responsible for. Plasticity means our brain can change what feeds into where, this is most commonly where we learn a motor skill. If we play the piano for example the part of the cortex feeding to this area increases.
Another way is the type of chemical transmitter and receptor. Dopamine is primarily used for things that cause us pleasure for example. However dopamine can affect our movement if it is secreted in from the substantia nigra, as this feeds into the motor cortex. Furthermore, neurotransmitters can be excitatory or inhibitory and this is an analogue rather than binary signal. All of these fine tune, and the position at which they inhibit and the location and the feedback from which they obtain their signal all indicates from where the brain is getting the information or to what it is responding to.
In summary it is wiring, signalling and location. However the components are incredibly similar but it isn't the small differences that have a profound effect.

OK, thanks for your answer, but WHY is this more efficient that if they are not separated? Why can't every part of the brain (at least the cortex) perform every function? Or can it? If a part of someone's brain is missing, would the other parts eventually be wired differently to 'replace' the missing part?

You have a machine that makes ice cream, a machine that makes bread and a machine that makes cookies. You lose the machine that makes cookies, would you use the ice cream maker or the bread maker? Would they be as good? That's how it works. Parts of our brain are specialised because they adapt as we use them. If we lose one part another part can take over that typically can mimic some of the function, but it isn't as great. If the part is unique then our brain has more difficulty. However it will unlikely be as efficient unless we train it to high degrees. That's a general theory.

If it wasn't clear why this means we have different regions catering for different things, then it is about efficiency. Using specialised well-adapted equipment is much better than using general stuff for everything.

It may be important to point out that different sensations (touch, smell, sight etc) are encoded by means of the same machinery (e.g. neurons, glia) using the same code (e.g. action potentials, calcium waves). If we stimulate a subject's visual cortex using an electrode he will experience visual sensations, although he would not be seeing real things.

The brain is separated into different regions, and different regions perform different tasks

Not really. This kind of claims stem from the early brain research, where every area was thought to specialize in one particular task. Sure, some categorization is possible (e.g. where the visual input is mostly processed). However, your question is basically an argument that is false.
Just look for example the temporal lobes and compare how the sulcal and gyral areas differ with respect to information processing.

We don't know yet in detail how different cortical areas are wired up, so it's difficult to say to what extent the wiring differs. But the overall structure of different cortical areas is remarkably similar, in terms of the layers of cortex and their cellular components.
Certainly the structure of the input is very different between cortical areas, and cortex seems to take great care during development how that input is structured.
We don't know why cortex is parcellated the way it is. But connections within cortical areas devoted to a single "function" are much more prevalent than connections between cortical areas. This suggests two things: many connections are required between neurons processing similar information, which implies that those neurons should be close together, because wire is expensive in the brain (i.e. requires resources and takes up a lot of space); alternatively, maybe the information is easier to process if it's kept physically separated.


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Can antibodies be formed against white blood cells after blood transfusion?
If antibodies are produced against other blood groups' red blood cells, why can't antibodies form against white blood cells, of any blood group? (even the same one, as MHC will be different in almost all individuals)

Antibodies and other immune responses do indeed occur against the donor's white blood cells. However, white blood cells are present in relatively tiny quantities (3-10 million WBCs per ml of blood vs 4-6 billion cells per ml).
Because the number of WBCs is so low, the immune reaction to them is also proportionally lower, with fever being a typical (and minor) complication of the reaction to WBCs. Some blood banks remove WBCs from blood to prevent these reactions.
For more information on the possible types of reactions to blood transfusions, see Wikipedia.
EDIT: Even in cases where the transfusion does not produce any symptoms, an immune reaction is most assuredly happening. In those cases, the immune system is simply killing off the foreign WBCs without any fuss.

Adding - very late to this - the most common symptom of a WBC incompatibility in a transfusion is a short-lived rash (looks like "heat rash") and low fever.
The HLA antigens are not very "antigenic" compared to the main blood group antigens, and the problem is mostly seen in people who have had multiple transfusions over a period of time.

Welcome and thanks for your answer. Could you add a reference to your answer?


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Do non-human animals suffer from insomnia?
And how do we know whether they do or not?
§
If sleep is a physiological need, it seems weird that we become unable to fulfill on demand even in the absence of any obvious physical issues. We would all probably would like to be able to fall asleep on demand on a long flight and we all know this can be hard even when we are tired.
Thus, my question is whether this is a mostly human dysfunction or a common animal property.

Cortisol is often used to measure stress levels in at least mammals and birds, and it is linked to insomnia in humans. I would therefore guess that stress-induced cortisol can cause insomnia in these groups of animals as well.

Commenting on the how, you can wire animals using EEG as you do with humans to see their brain activity. Provided you have a profile of the different patterns that correlates to different stages of sleep.

@Cornelius: You have almost the correct answer but why have you deleted it?

Insomnia most certainly occurs in other animals. One interesting example is the case of insomnia in Drosophila melanogaster. In this study 3 day old male and female flies that demonstrated reduced sleep time were crossed together over 60 generations to create flies insomnia-like (ins-l) that sleep less than 60 minutes a day compared to 800 min a day in their control flies, which are generation 0 (Fig 1B). These (ins-l) flies exhibited difficulty initiating sleep, maintaining sleep and showed cognitive impairment. They also had difficulty maintaining balance with elevated levels of triglycerides, cholesterol and fatty acids and although their core molecular clock remained intact, ins-l flies lost their ability to sleep in constant dark. Using whole-genome transcriptome profiling using Affymetrix high density nucleotide microarrays, these flies are compared against the control flies and many genes were over-represented (changed in expression compared to control flies) which are involved in metabolism, neuronal activity, behaviour and sensory perception with changes in lipid metabolism and synaptic transmission being consistent with increased adiposity and learning defects in flies. In addition, these ins-l flies were hyperactive and hyper responsive to environmental simulations and the over-representation of genes associated with sensory perception suggests that hyperarousal in insomnia may be attributed to increased activity in the sensory system and that these processes are under genetic control. Two genes in particular Filamin-A (Cheerio) and Malic enzyme (Men), which were found to be differentially regulated (changed in expression) in files are also modulated (changed) by sleep loss in humans, showing that the same processes are involved/get effected in humans and flies during insomnia.
The research above clearly demonstrated the genetic regulation and effects of insomnia in other animals and shows that its not just a human dysfunction.

Insomnia has also been observed in some fish: http://www.veterinarypracticenews.com/April-2009/Scientists-Say-Fish-Suffer-From-Insomnia/