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What is a sex-biased gene?
How do you define a male-biased gene and a female-biased gene as they are found in the abstract of this article.

perhaps by strong difference in expression between two sexes.

WYSIWYG yes, that's what I was thinking too. Let's wait and see if someone can make sure of this.

In the linked paper, the authors discuss this as sex-based gene expression that evolved by sex-specific selection. The expression is not limited to one sex (which are sex-limited genes). Sex-biased genes are expressed by both sexes, but differently between sexes.


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Distribution of fitness in wild populations
If I get out in the wild observe wild populations and measure the distribution of fitness $f(w)$ in a given population. What will I find out? Will I observe a Gaussian distribution, a Poisson distribution, an exponential distribution, ….?
It probably depends on the species under consideration, typically it may depend on whether there is an sexual selection in this species. I welcome any insights!

Long for a comment but consider this to be an extended comment and not an exact answer:
At least for Poisson I can say that the random variable should fit the three Poisson postulates. Poisson RV generally describe discrete events in continuous intervals. A fitness function doesn't seem to be such a type of RV; it is a property of a population rather than an event.
I would also not expect it to be exponentially distributed which would mean that probability is highest for the most fit (or most unfit) individual i.e the more fit are more frequent. I assume that it cannot be decided who is the most fit until selection happens. This may still be the case just after a selection event but not otherwise.
It seems that this function should be Gaussian: assuming that there is little variability between individuals and what exists is because of independent events of mutation, these should converge to Gaussian as per the central limit theorem.
But generally the term that best describes this RV is a performance function. Fitness would always be a conditional RV.
For e.g. I would very roughly define fitness like this:
$f(X) = P(m(X)\ |\ p(X),S)$
where $f(x)$ is the fitness of $X$, $m(X)$ is the survival probability of $X$, $p(X)$ is performance in different tasks and $S$ is selection event.

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What is the difference between these terms: clade, monophyletic group and taxon?
Wikipedia definitions for these terms are pretty similar:

http://en.wikipedia.org/wiki/Clade
http://en.wikipedia.org/wiki/Monophyletic_group
http://en.wikipedia.org/wiki/Taxon

They sound like the terms are synonyms. Why there are separate articles for them then?
Is it true that every person is a reptilomorph and an eupelycosaur just like he/she is a mammal?
Bonus question: what is the difference between a cladogram and a phylogenetic tree?
PS Please don't just give definitions and/or quote Wikipedia. Point out the differences, if any. Even better, provide examples that can be considered one but not the other.

A taxon (Plur. taxa) is any (monophyletic or not) group of species. For example the group of yellow flowers is a taxon. The group of primates is a taxon. The taxon of aquatic animals is a taxon.
A clade is a monophyletic taxon or monophyletic group if you prefer. A monophyletic taxon (or a clade) is defined as a taxon that contains only all descendants of a common ancestor and the common ancestor. On the following picture, only the Taxon 1 is a clade.

To cite few examples of clades: Primates, Eukaryotes, Rosacea, Reptilomorpha, Rodentia. (The links yield to tolweb.org. See below for more info about this site)
A cladogram is some kind of reduced evolutionary tree that only shows the branching pattern but the length of the branches does not carry any information. At the opposite on a evolutionary tree the lengths of branches usually indicate the inferred time from the divergence.
I think the best tree you can find online is tolweb.org. You can find here the clade of Reptilomorpha and here the clade of Eupelycosaur. As you can see from these links, the mammals form a clade within the Eupelycosaur which itself is a clade within the Reptilomorpha. So yes, every human being is a Reptiliomorpha/Eupelycosaur/Mammalia. You can have fun going through this evolutionary tree and see what are the common ancestors between human and other mammals, human and turtles, human and jellyfish, human and plants, etc… to cite just a few relationships you might be interested to look at.

+1 But I'd say, taxon is not any possible grouping, but a grouping proposed by someone. It's basically a formalized hypothesis about natural arrangement of  species. (This natural can be understood in multiple ways.) In this respect "yellow flowers" do not make a taxon.

A better example is that Reptilia is a taxon that has turned out not to be a clade because the descendants of the last common ancestor of modern reptiles also include birds.

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If the top epidermal layer is burned away, what is it replaced with?
If the squamous (top) layer of epidermis, or skin, is burned or damaged in another way, will it then be replaced by the next layer of below?
Also, from where does the basal membrane originate? Does it regenerate from a different layer of cells?

I edited your question so people might find it easier to answer.  hope that's okay - feel free to re-edit.

The epidermis is a four- or five-layered epithelium. The top layers are squamous whereas the bottom ones are more columnar (http://en.wikipedia.org/wiki/Epidermis_(skin)). The lowest layer is separated from the dermis by the basal membrane (a.k.a. basal lamina, basement membrane).
The process of wound healing in skin is extremely complex and obviously depends on the individual wound and how many layers are destroyed. There is a lot of detail on Wikipedia: http://en.wikipedia.org/wiki/Wound_healing.
If the basement membrane is not disrupted, there are two main components as a rule of thumb: 1) outwards-inwards migration, i.e. cells surrounding a wound will migrate into the wound. 2) bottom-upwards differentiation, i.e. the bottom-most layer contains replicating cells which will differentiate and squamify to regenerate upper layers.
Something like this (picture modified from Wikipedia):
If the wound is bleeding, this means the basement membrane is disrupted and the dermis underneath is also wounded (the epidermis itself contains no blood vessels). In this case, the dermis needs to regenerate first, in a process which is probably similar as described above. Simultaneously, the bottom-most epidermal cell layer will proliferate to close the gap, and then deposit new basement membrane. Remember that the basement membrane is a mesh of proteins, not an actual cell layer.

It would first be good to look at the different layers within the skin  as you mentioned in your question.

The skin is made up of:

Epidermis: the outermost layer of skin, provides a waterproof barrier and creates our skin tone
Dermis: beneath the epidermis, contains tough connective tissue, hair follicles, and sweat glands
Hypodermis: deeper subcutaneous tissue is made of fat and connective tissue

Different kinds of damage can occur to the skin, including burns, which have different degrees based on what layer of skin is damaged and how far down the burn goes.  Therefore, it is not as simple as the epidermis itself getting burned, it could also be much worse and the healing process may be hindered if too much damage occurs.

Burns can happen when the skin is exposed to heat (from fire or hot liquids), electricity, corrosive chemicals, or radiation (UV rays from the sun or tanning beds, or radiation treatments).
Burns are classified as follows, according to the severity of tissue damage:

First degree burns: affect only the outer layer of the skin (epidermis), causing pain and redness. The prototype is mild sunburn
Second degree burns: extend to the second layer of the skin (the dermis), causing pain, redness, and blisters that may ooze; deep second degree burns may progress to third degree burns over the course of several days
Third degree burns: involve both layers of the skin and may also damage the underlying bones, muscles, and tendons; the burn site appears pale, charred, or leathery; there is generally no pain in the area because the nerve endings are destroyed.
Fourth degree burns: extend through the skin and subcutaneous fat into the underlying muscle and bone; are stiff and charred

Depending on the type of burn, different skin generation occurs.  If it is a really terrible burn, then a skin graft from another area of the body may be needed, as it cannot regenerate the epidermis layer due to the excessive damage.

First degree burns are the easiest from which to recover [...] the dermis remains intact and can support the regeneration of the epidermis.  It may happen that the skin will get inflamed (due to responses in the underlying dermis) during this time; the inflammation is to encourage clean-up cells (macrophages) and nutrients to reach the damaged area.

It appears as though the dermis itself will help with the regeneration of the epidermal cells.

In a second degree burn, the dermis is also affected, at least partially.   But, with a second-degree burn, most (or at least some) skin accessory organs typically remain in tact.  Remember, these accessory organs (like glands and hairs) are built from invaginations of the epidermis, creating the epithelium of the glands or hair follicles.  If these organs survive the burn, the epithelial cells that remain will begin to divide to regenerate a new epidermis.
Third-degree burns are the worst.  In these, even the accessory organs are destroyed.  How can we recover from this?  Skin grafts are about the best way, but they cannot really be done across one's entire body, so a very widespread third-degree burn is not usually something that a person can recover from.

AND although this is a separate question and topic, the basal membrane is thought to be of epithelial origin, but this is very complex and still not completely known.  There is more information about it in this article; Cellular origin of the dermal-epidermal basement membrane (Marinkovich et al. 1993).  It is a dated article but has some interesting information.


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What is the evolutionary reason behind human preference for salty foods?
It's been established that food palatability is related to it's caloric density. This hypothesis is used to explain why humans are partial to sugar and fat. But it is also said that humans are partial to salt.
Given that salt has no calories, are there evolutionary reasons that explain why humans have a preference for salty foods?

The body needs more than energy to survive.
Salt is vital to the body's function. Ions of sodium and calcium perform numerous vital functions, but are particularly related to the function of the nervous system and contraction of muscles. Accordingly, seeking out sources of salt makes sense in a natural environment in which salt is relatively unavailable.


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Restriction endonucleases are found in?
Quoting from : Scientific American July 1975 The Manipulation of genes by Stanley Cohen :

Restriction endonucleases (and modification methylases) are widespread
  in microorganisms; genes for making them were found on viral
  chromosomes and extrachromosomal plasmid DNA as well as on many
  bacterial chromosomes.

Why would the genes for making RE be found on viral chromosomes ? Also, could you give some examples where they are found on plasmids ?

There are many proposals for the ecological role of restriction-modification (RM) systems, and why they would exist on mobile genetic elements (e.g. plasmids and viruses). In this case, I am specifically talking about the viruses that infect bacteria (aka, bacteriophage).
1) RM systems may have an anti-viral function. Normally we would think of such systems as being part of the host chromosome, but as Alan Boyd suggested, once a temperate phage has integrated itself into the chromosome, its fitness is tied to its host. Therefore, a RM system found in a prophage could prevent infections by additional phage. See here for a discussion of this issue:
http://www.ncbi.nlm.nih.gov/pubmed/23471617
2) RM systems may have "addictive" properties by acting as toxin-antitoxin systems. Basically, this means that if the genes for the RM system are lost, the host cell dies. This can provide selection for the maintenance of plasmids and prophage inside of the host cell. See here for a discussion of this issue:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3874152/
3) Finally, viruses need to destroy the host genome -- both to suppress any anti-viral response and to release nutrients for viral replication. While this is typically achieved with nucleases other than restriction endonucleases, there is at least one situation where a RE seems to be involved. This is discussed in the first link above (see the section entitled "Role in Nutrition")

If you have a dsDNA genome and replicate it by rolling circle like most bacteriophages and many plasmids do, an endonuclease is pretty much a necessity.

Could you elaborate your answer and include some references ?

this is a nice question and post!  the RE nicks the phage genome so that it can be replicated by the polymerase.  Without it there would be no copying off of the chromosome.

But the nicking isn't carried out by a restriction endonuclease but by a specific protein which remains linked to the 5' end of the DNA. If this was accomplished by an R-M system on the phage the site would presumably be modified to protect it from double-stranded cutting.

I generally think of REs as producing double-stranded cuts. If I understand correctly, this answer only applies to those that create single-stranded cuts. Are they also called RE?

i just wonder which has an older origin- CRISPR-Cas or RE?

@WYSIWYG Interesting question. Nearly all bacteria have a restriction modification system yet only about half have CRISPR/Cas. In archaea, CRISPR/Cas is more ubiquitous. Ancient ancestry and horizontal gene transfer make it difficult to make strong conclusions on which came first. CRISPR/Cas is interesting in that it requires an RNA co-factor (crRNA/tracrRNA). There may have existed (or still exists) an ancient CRISPR system that functioned without Cas or other proteins (e.g. an endonucleolytic ribozyme with a targeting domain that existed before the evolution of protein synthesis).

The familiar restriction enzyme EcoRI is plasmid encoded.

Betlach et al. (1976) A restriction endonuclease analysis of the bacterial plasmid controlling the EcoRI restriction and modification of DNA. Fed. Proc. 35:2037 - 43.

For an example of a phage encoded system see:

Dempsey et al. (2005) Sau421, a BcgI-like restriction-modification system encoded by the Staphylococcus aureus quadruple-converting phage Phi42. Microbiology 151: 1301-1311

This second paper suggests an answer to why a phage would have such a system: lysogens of Phi42 are resistant to infection by all 23 members of a standard set of S. aureus phages. Once a phage has lysogenised it is in its interest to prevent lysis of its host.


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How was Restriction Site of EcoRI sequenced?
The sequence of restriction site of EcoRI - GAATTC was identified in the early 1970s, before Sanger Sequencing was invented.(1977)
How was the restriction site of EcoRI sequenced ?

The first determination of a recognition site for a restriction endonulease was reported in:

Kelly & Smith (1970) A restriction enzyme from Hemophilus influenzae II. Base sequence of the recognition site. J Mol. Biol. 51: 393-409

The enzyme was then called endonuclease R, but is now known as HindII (or HincII).
The method used was to cut DNA with the enzyme and then remove the exposed terminal phosphates with alkaline phosphatase. These ends could then be labelled with 32P using polynucleotide kinase and γ-labelled ATP.
The end-labelled DNA was then treated with nucleases in three different ways to release mononucleotides, dinucleotides, and a mixture enriched for trinucleotides. In each case the labelled products were identified by their behaviour in 2D thin-layer chromatography, and were  further characterised for their total base composition after digestion to mononucleotides where appropriate.
The deduced site was/is
5'----GTY RAC----3'
3'----CAR YTG----5'

Thus the labelled mononucleotides were found to be A and G (purine=R), the dinucleotides were found to be GA and AA and so on.
The EcoRI sequence was determined by essentially the same methodology and was reported by

Hedgpeth et al (1972) DNA nucleotide sequence restricted by the RI endonuclease. Proc. Natl. Acad. Sci USA 69:3448 - 3452

Addendum:
Although Sanger sequencing (the plus-minus method) may have been developed through the 1970s, it really didn't catch on until the early 80s. So for example the first complete plasmid sequence to be determined was pBR322 in 1979:

Sutcliffe (1979) Complete nucleotide sequence of the Escherichia coli plasmid pBR322. CSH Symp. Quant. Biol. 43: 77 - 90
"I have determined the 4362-nucleotide-pair sequence of the plasmid cloning vector pBR322 using the DNA-sequencing technique of Maxam and Gilbert (1977). The DNA structure has several interesting features that lead to testable predictions."

The standard sequencing method in use at that time was chemical sequencing using the Maxam-Gilbert methodology. When I started a postdoc in the USA in 1979 M-G sequencing was the standard method. Sanger sequencing really only took off following the development of the M13 mp vectors (and later the pUC plasmids) by J Messing in the early 80s. And what a relief it was: M-G sequencing was extremely laborious, as anyone who ever did it will testify.


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Help Needed Identifying Corvids
I'd appreciate some help identifying these three corvids I photographed in Austria during the Summer:

I know identifying corvids can be difficult and I'm not an ornithologist -- just an amateur bird watcher. After looking through many images of various crow species and their hybrids, I've tentatively identified these as:

Carrion crow (Corvus corone)
Carrion crow × Hooded crow (Corvus corone × Corvus cornix)
Carrion crow × Hooded crow (Corvus corone × Corvus cornix)
I initially believed this to be a Hooded crow (Corvus cornix), but the broken coloration on the wings made me think it might actually be a hybrid as well.

Can someone here either confirm my identification or provide a more informed identification?

Have you solved this yet?

1. Carrion crow (Corvus corone)

The plumage of carrion crow is black with a green or purple sheen, much greener than the gloss of the rook. The bill, legs and feet are also black. It can be distinguished from the common raven by its size (48–52 cm or 19 to 20 inches in length as compared to an average of 63 centimetres (25 inches) for ravens) and from the hooded crow by its black plumage

3. Hooded crow (Corvus cornix)

ashy grey bird with black head, throat, wings, tail, and thigh feathers, as well as a black bill, eyes, and feet.

2. This one is a bit more difficult, but I think it is also a hooded crow or possibly a hybrid  Carrion crow × Hooded crow (Corvus corone × Corvus cornix).

 Hybrid
At first glance, #2 looked somewhat like a Western jackdaw (Corvus monedula) because the grey feathers travel fairly high up on its neck and because the bird appears to be somewhat smaller.

Measuring 34–39 centimetres (13–15 in) in length, the western jackdaw is the second smallest member of the genus Corvus...The cheeks, nape and neck are light grey to greyish-silver, and the underparts are slate-grey. The legs are black, as is the short stout bill.

However, C. monedula has fairly conspicuous grey eyes and its feathers travel up the neck/head almost as far superiorly/anteriorly as the eyes. Neither appear to be the case in your specimen.

All three species are common in Europe.

The first 2 are correct.
The third one is actually a hooded crow. The different color of the wing depends on the generation of feathers. Feathers of different generations (changed during different time) are abraded (used) in a different way. The wing feathers of this guy are older than the rest.
Cheers and good luck birding :)

Thanks, can you show some images of hooded crows at different generations (or perhaps just their feathers) for comparison?

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Why do we suffer abdominal pain after we get very angry or stress?
You also realize probably, when we get so much anger or high levels of stress, after some point we have terrible stomach ache, like really heavy pain. Why is that? How stress or anger can effect our stomach? What is the mechanism?

Cortisol produced from the zona fasciculata of the adrenal cortex is directly caused by stress.
According to http://en.wikipedia.org/wiki/Cortisol

Cortisol stimulates gastric-acid secretion. Cortisol's only direct effect on the hydrogen ion excretion of the kidneys is to stimulate the excretion of ammonium ions by deactivating the renal glutaminase enzyme. Net chloride secretion in the intestines is inversely decreased by cortisol in vitro.

This increase in gastric-acid secretion can irritate the lining of the GI tract, especially if there are ulcers or inflammation, resulting in pain. In addition, the fight-or-flight response causes

inhibition of stomach and upper-intestinal action to the point where digestion slows down or stops.

(see http://en.wikipedia.org/wiki/Fight-or-flight_response)
Those things, paired with increased muscle tension and vasoconstriction cause pressure changes in the GI tract, which can cause pain.


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What is the best time to exercise
So, after starting to gain weight on sitting in front of my computer too long, I have decided to take the plunge and maybe stick to an exercise regimen. As has been reported by some studies, exercising in the morning can be more beneficial than doing so in the evening. Now, personally, waking up in the morning is a huge chore for me. Furthermore, I have people advising me to hit the loo (toilet) before exercising as it may not be good for my health and leads to waste accumulation in the body. Now, search as I may, I cant find any basis that supports this theory. I understand that hygiene might be a factor but does exercising in the morning before going to the loo have any effects on health in general? Thanks.

WHO's definition about Health

Health is a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity.

In other words, Good health means active life where you can express yourself freely, you can succeed and can make mistakes, can reach your goals, can understand your body and others, and can say no when you see your limit to yourself and others - and can set new targets to yourself, feel accepted in your society and accept yourself as you are.
Best time to Exercise for successful results in competitions - dependent on Age

Endurance atletes during ages 25-30 years in this answer about Why does max heart rate decrease with age?

Short-term and long-term effects of exercise on Vitality
There are many stages in your question in Physiology, Pathophysiology and Microbiology, for instance.
I can cover here only the surface:

very short effect of short exercise (20 min) on brain
long term effect of regular short exercise (20 min) on brain, hypothalamus and biologic clock - wakefulness (limbic system)
long-term effect of regular weekly exercise (3.5 h) on brain
long-term effect of regular weekly exercise (3.5 h) on body muscles
long-term effect of careful regular stretching and appropriate resting on congestion of body
long-term effect of regular weekly exercise (3.5 h) on metabolism
effect of regular exercise on circulation system (blood and lymph) - known to increase i.e. include temperature distribution and defence bodies distribution
short-term effect of short exercise on PTH secretion (calcium); autoregulation of renal blood flow with two major theories: myogenic mechanism and tubuloglomerular effect

where I only briefly cover one term in Pathology.
There are two unanswered questions about the renal function [Costanzo, 2013]

(1) What component of tubular fluid is sensed at the macula densa? The
  major candidates are luminal Na+ and Cl−. (2) What vasoactive
  substance is secreted by the juxtaglomerular apparatus to act locally
  on afferent arterioles? Here, the candidates are adenosine, ATP, and
  thromboxane.

so to understand the effect of short-term morning training on PTH secretion, we should understand the two questions first.
Evidences to some things

Short-term exercise can work sometimes as prophylactics for allergic symptoms.
I think the most important thing is the irritation of your skin which is the most important endocrine organ in our body.
Skin's temperature change secretes many hormones than help us to stand irritations from the environment.
What are the effects of short-term exercise in the morning depends on the patient at hand.
I cannot say much general.
For instance, if your heart is not strained; that it has too high T peak, too heavy exercise can cause you harm.
My personal experience

Short-term exercise suited to a person with no deficits in sleeping can help to alleviate symptoms of allergies and decrease stress in a normally physiological balances without viral infections,

but the real world is not that nice.
The problem comes if the patient has any disease that uses our immune system against us such as some viral infection.
The immune response is also the source of pathogenesis for many viral diseases.
Unlike for a bacterial infection, the ultimate goal of the immune response in a viral infection is to eliminate both the virus and the host cells harbouring or replicating the virus, [Murray, Medical Microbiology, 6th ed].
Actually, some drugs are immunosuppressant like cortisone, and some procedures like radiation therapy.
However, with some medication plans, you should avoid drugs, living styles and habits that immunosuppresses your body.
For instance, HIV patients with HAART medication plan (medication combination is antiretroviral but possible immunosuppressive pathways may exist in different conditions) that involves a strategy depending on the condition, since HAART medications are life-long and cannot be stop, so other conditions etc TBC must be treated first, to avoid too much burden on the body at the same time.
In a similar way, avoiding living style or habits that puts immunosystem down can help with HIV.
Doing sport when you have slept badly many days and feel exhausted, puts your body under immunosuppression.
So the state of the disease or your physical wellbeing determines when sport is useful and when not.
Other part of your question
To hit toiled before exercise is good because then

you decrease the risk of gastrointestinal bleeding and venous congestion.
effect of exercise on constipation is one topic here; depends on you, since there are many types

The more stuff you have in your colon and gastrointestinal system, the harder it is to use fully your muscles of your body.
Try pull-ups with more empty colon vs full one.
Pull-ups require many muscles from upper trunk and lower trunk.
You cannot use all your stomach muscles if something is blocking your middle body muscles.
Good Hygiene is the easiest way to decrease the risk of any infections caused by many factors.
I estimate that 2-5 % of people visiting public toilets wash hands correctly; one video here about how one should do it.
Many people leave their hands wet.
If you have infection in your body, you should not exercise because failure to resolve the infection may lead to persistent or chronic infection or death.
It takes much energy from our body to handle with infections.
To recover from training, it requires good balance of many factors.
Summary
The best time to do sport when you are healthy

you do not have any infections (viral particularly) because a failure to resolve the infection can lead to persistent or chronic infection or death
when you have prepared early enough for the exercise with enough sleep

where pathologies and/or teratologies are not limiting your process.
You compete only against yourself and then grow from that to see you how good person you are really.
The morning exercise in a body which has rested well before the exercise and prepared accordingly to the exercise can be useful because

short-term effects on the brain (process things during exercise) (See Figure 1)
possible short-term effects during day after the exercise

and if the exercise becomes a habit in a healthy person, then

long-term effects: increased metabolism and many other positive effects described above
and many other possible reasons from social to better self-esteem

when the the person listens to his body and stops when it hurts or something goes over; can rest accordingly.
Good motivation is useful in gaining good health.
Motivation is the strength and direction of the effort.
If you are interested in morning exercise, then you can set target and make a realistic plan.
Listen your own body and be able to refit your plan accordingly.
Actually, here is an important step that the consultation of many doctors can be useful; one doctor cannot always see the main problem for instance of prolonged and deepened allergic symptoms.
Consultation and discussions of other people can also be useful - like discussing where to help for this and this; who has enough capabilities to understand it.
The person cannot always know himself what is a main disease underneath.
Anything can come that postpone some training sessions.
Sources

Infectious disease courses 2015-2016
Gleeson. The effect on immunity of long-term intensive training in elite swimmers.
Anderson. Effects of Exercise and Physical Activity on Anxiety. 2013.
Laires. Exercise, magnesium and immune function.
Gunzer. Exercise-Induced Immunodepression in Endurance Athletes and Nutritional Intervention with Carbohydrate, Protein and Fat—What Is Possible, What Is Not?
HAART and HIV in DynaMed Plus. Visited 7.8.2016.
WHO. Health Education. Visited 7.8.2016.
...

Can you please add references to your answer? Especially the first part about exercising and and allegies needs this.

@Chris To investigate such a thing is very difficult in a general subject. I need more specific patient data to give references: sleeping rhythm, age, gender, training history, allergies, blood picture etc to give exact references. Otherwise, the scope of this answer cannot be reached in a lifetime. Please, say exactly to which statement you want a reference so it is easier for me to find it. There are very many sources which I have used in my text. Please, specify what is your exact interest here.

This is not hard - you claim that exercising improves the symptoms of allergies. To do so, there should be some studies proving it. If these do not exist, than you can simply not claim this. If this is your experience than this is anecdotal and also no proof.

Your post could still do with references for it's points, particularly: "Short-term exercise can work sometimes as prophylactics for allergic symptoms".  HIV treatment is also not by immunosuppresant drugs (this is what you are trying to avoid).  There has been some very limited research into trialling immune suppression but clinically it's treated with HAART - antivirals not immune suppressors.


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Are spiders part of the study of entomology?
The definition of entomology says it is the science of studying insects.
I know spiders are not insects but does entomology include studying spiders as well?
Otherwise is there any name to the science of studying spiders (class Arachnida)?

Spiders are part of a taxon called Arachnida. Arachnida also contain scorpions, Oppiliones, acari, … The science of arachnids is logically called Arachnology
However, (wikipedia):

Entomology (from Greek ἔντομος, entomos, "that which is cut in pieces or engraved/segmented", hence "insect"; and -λογία, -logia) is the scientific study of insects, a branch of arthropodology. In the past the term "insect" was more vague, and historically the definition of entomology included the study of terrestrial animals in other arthropod groups or other phyla, such as arachnids, myriapods, earthworms, land snails, and slugs. This wider meaning may still be encountered in informal use.

In other words, in the informal sense entomology include arachnology but the strict definition entomology does not encompass arachnology.
You will find here on tolweb.org more information about the systematics of Arthropoda

I understand this. But generally the term Arachnology seems not very used; even the wikipedia's article seems incomplete or needs more "inline citations". In the other side, it was looking entomology includes spiders and some other non-insect animals in the past but it is not clear if it is still accepted or if any other animals should go in thier specific terms.

@ruffp I am not sure I understand your comment.. You know, all this is just a matter of definitions. And the definition of entomology has not real importance to science, just like the definition of biology itself is not of real important to biologists. So, what has to be known is that some people use "entomology" this way and some people use "entomology" that way. And yes, of course this kind of definitions are changing over time. It is indeed likely that entomology has evolved to be used in a more and more restrictive way as everybody accepted that spiders are not insects for quite a while.

I had this question when I start to use this site to ask questions about spiders and I did not know if I can tag them with Entomology because there is no Arachnology tag. I did not know as well if this question can be in the meta site or here, but because I wanted a general answer not specifically related with tagging on this site, I post it here.

As a general rule no. Spiders and other arachnids generally tend to have their own field of study called arachnology.

The term entomology is derived from the Greek words Entomo ("Insect") and Logia(word) . Considering that Entomo generally refers to insect(s) the question is whether Arachnids could be considered entoma in Greek as there is no other used term that refers to arachnids.

Although this answer gets at the etymology of entomology, it doesn't quite consider the usage which seems to be more important here, and doesn't have any citation for that usage. There are lots of words for which the etymology is not particularly instructive for the usage since usages change.


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Can jellyfish swim backwards?
Jellyfish use jet propulsion to move forward, according to http://earthsky.org/earth/how-do-jellyfish-swim. Otherwise, they drift with the ocean currents.
Does this mean that, without the presence of water currents, jellyfish cannot swim backwards?
(This question was inspired by watching countless SpongeBob episodes and seeing the efficiency in which SB catches jellyfish).

I don't know what you mean by swim backward. technically for a jellyfish, I don't know how you can state which is the front and which is the back..

Jellyfish move by a form of jet propulsion and it moves in the direction that the head is facing. If it needs to change direction, it just needs to pivot and propel itself in the direction that it needs to move. Comb jellies (which are not really jellyfish) have cilia that beat continuously in the water for it to move forward. So water currents are not necessary. Here is an article with videos on how jellyfish move.

No.
They're locomotion only allows for forward/upward motion. That said, their buoyancy control does provide a measure of 'backward' or 'sinking' motion, but it's negligible.
But to convert this all into the simplest terms: Jellyfish uses a form of jet propulsion. Ever seen a jet go backwards? (The Harrier does not count.)


text:
What is inside IDL (intermediate density lipoproteïn)?
I am studying about the endogene lipidcycle in the human body and I know that VLDL (very low density lipoproteïn) is made in the liver and that it contains triglycerides and cholesterol from your food but also made in the body.
Next with that, I know that VLDL brings triglycerides to the adipose tissue (or fat tissue) and to the muscles with help of the LPL (lipoproteïnlipase) just as chylomicrons do.
Enclosed; VLDL will go over to IDL (intermediate density lipoproteïn).
But what is the definition then from IDL exactly?
Is IDL just a smaller lipoproteïn then VLDL and does it only contains a sort of 'leftover' of the triglycerides? Or does it also contains cholesterol?
And if VLDL brings the triglycerides to the muscles and fat tissue, does it only contains triglycerides then? Or does it also carry cholesterol with it? If yes, what happens with the cholesterol then?
Because my book is only telling me about the transport of triglycerides to the fat tissue and muscles, but in the beginning it also says that it carry's cholesterol, and a little further in my book it even tells it can also carry cholesterolesters from HDL...
It's getting confusing...
Hope somebody can tell me what is exactly in all the kinds of lipoproteïns, where the lipoproteïns are all made, and where the products they carry come from, and where they go to. Because my book is being very indistinct.

Which book did you  read...?

"Is IDL just a smaller lipoproteïn then VLDL and does it only contains a sort of 'leftover' of the triglycerides? Or does it also contains cholesterol?" Yes / yes  / yes.

"but in the beginning it also says that it carry's cholesterol, and a little further in my book it even tells it can also carry cholesterolesters from HDL... It's getting confusing..." - The latter emotion is "adequate". From memory I'd say:  IDL turns to LDL by shedding "even more" fatty acids (as it did when it still was VHDL (Berg/Stryer, Biochemistry), and it carries cholesterol, as it becomes LDL remnant, and as such is able to take over  chloesterolesters from HDL (the latter "confusing" in a stricter sense, I guess)

Taken from Fundamentals of Biochemistry (Voet et al. 2013). Note the differences in apolipoproteins between LDL and IDL, as well as the ratio triacylglycerol : cholesteryl esters between VLDL and IDL.

The question is not specific enough to elaborate? Does Voet et al. tell about different fate and function of cholesterol and triacylglyerol? What are the inferences that must be made from the numbers? I mean, any answer should not be restricted to referencing alone...sorry.


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Feedback affecting myocyte metabolism in humans
I understand that there are several reserves available to muscle that can be tapped for ATP, and that each reserve is being used to some degree at all times.
Are these reaction rates purely due to the presence of reactants which are products of myocyte activity?
Or are there other controlling reactants involved that determine the rate at which each reserve is consumed?

Well, ATP is replenished from three energy sources, namely:
1. phosphagen system (very fast, but quickly deprived)
2. glycolysis (fast, but slower deprived)
3. oxidative system (slow, 'impossible' to deprive)
When ATP is used, for example for muscle contraction, ADP is formed. The formed ADP can be rephosphorylated to ATP by the enzym creatine kinase, which also requires creatinephosphate (the phosphate attached to the creatine provides the phosphate group for ADP to form ATP). Additionally, ATP can be formed out of 2 ADP molecules by adenylate kinase. The phosphagen system is largely driven by the law of mass action, i.e. the direction of the enzymatic reaction is controlled by the concentration of the products and substrates. In other words; when ATP is low, and ADP is high, the generation of ATP is favored and vice versa. The energy from the phosphagen system is depleted rather quickly tho.
The second system, glycolysis, simply refers to the breakdown of carbohydrates (e.g. glucose) to resynthesize ATP from the energy stored in those carbohydrates. Your muscles contain a buffer of glycogen, approx. 300~ gr for the average Joe (give or take). The glycogen can be broken down to glucose-6-phosphate, which can then enter glycolysis. The glucose-6-phosphate is broken down to 2 pyruvate and yields 3 ATP netto (2 when derived from glucose, rather than glycogen, due to a first enzymatic step which requires 1 ATP). The enzymatic steps of glycolysis are controlled by ATP, AMP, ADP and other factors, factually integrating the energy status of the muscle (primarly through allosteric regulation of enzymes, especially phosphofructokinase).
The third system, the oxidative system, refers to the breakdown of carbohydrates and fatty acids, requiring oxygen to 'burn' them (citric acid cycle). The yield of this is much higher than for glycolysis, but the process is way slower.
In essence, all are regulated by the concentration of substrates and products, as well as through allosteric regulation (binding of a molecule at a different site, inhibiting or activating the enzyme, often by intermediates of the pathways themselves). Additionally, there is some long-term regulation through gene expression (e.g. up- or down-regulating expression of genes involved in these pathways), mostly by hormones.
Edit:
Well, I guess this is described in any basic biochemistry book (I'm very fund of the book 'Fundamentals of Biochemistry: Life at the Molecular Level'). If you want to see a description of these energy systems in a more exercise related context (since you were aiming at myocytes) I suggest reading Strength and Condition: Biological Principles and Practical Applications from Marco Cardinale et al., and the NSCA book Essentials of Strength and Conditioning.

It would be great if you could also provide some references as an edit to this response!

Added a couple.


text:
What the difference between an inverted and everted retina?
I'm looking specifically for examples and comparisons, because the definitions of inverted and everted are remarkably similar; e.g. from Dictionary.com/Reference.com:

everted
  verb (used with object)
  to turn outward or inside out.

http://dictionary.reference.com/browse/everted
vs. (esp. #5)

inverted
  verb (used with object)
  1. to turn upside down.
  2. to reverse in position, order, direction, or relationship.
  3. to turn or change to the opposite or contrary, as in nature, bearing, or effect: to invert a process.
  4. to turn inward or back upon itself.
  5. to turn inside out.

http://dictionary.reference.com/browse/inverted
I'm curious because of this:

Structurally, the cephalopod eye differs from the vertebrate eye.
  Cephalopods do not have a cornea, and the retina is everted so that
  the distal end of photoreceptive cells lies directly behind the lens
  and points toward incoming light. As a result, photoreceptor cells
  connect to the optic nerve behind the retina (Packard 1972).

From: Evolution: Education and Outreach
October 2008, Volume 1, Issue 4, pp 439-447
http://link.springer.com/article/10.1007%2Fs12052-008-0084-1
http://link.springer.com/article/10.1007%2Fs12052-008-0084-1/fulltext.html
via
https://en.wikipedia.org/wiki/Cephalopod#cite_note-Serb2008-12

If you have the rep please tag this with cephalopod; the tag doesn't exist and I don't have enough rep to create it. Thanks.

Based on your title and description, all that means is that in vertebrates the retina is inverted in a sense that light sensing cells sit at the back of the retina meaning light has to pass through layers of neurons and capillaries before reaching light sensing cells, whereas cephalopod has the photoreceptors at the front side of the retina, with processing neurons and capillaries behind them hence retina is everted i.e. inside out. See this page (http://en.wikipedia.org/wiki/Retina) under "In other animals" section.
Hope this helps!

Oh, of course.  After re-reading this, it's actually very clear.  Also very interesting in the diagram was concerning the optical cavity vs. the cornea & lens; really "opens" the possibilities for "getting something in your eye"!


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Cancer growth and cell division
I am confused about the prerequisites for cell division and cancer.
Which of the following is necessary for the cell cycle to progress?

Hormones
Growth factor
Cyclins
Cyclin dependent kinases

Which of the following is essential for cancer proliferation?

Growth factors
Signalling molecules
DNA replication
A control mechanism

How do the cell cycle and cancer relate to each other?

Hi!These are homework questions and you MUST show at least some effort to answer them and do tell us specifically where you are confused.

@biogirl I swear they are not homewark, these are questions I want to know the answers in order to know where is the confusing part , please help me

Biogirl I am waiting for you :(

Its okay. .they looked homework :) try Googling cdk and cell division. ..

Do you actually understand all the terms in the options ?

Maybe :/ . Ok I will try then correct my answer If I wrong , I think the cyclic is the answer for first Q

Cuz hormones are form of growth fectors , and cyclic is essential cuz it will activate CDK

Growth factor is the answer for second Q , cuz they will stimulate other cell to divide . .  Am I wrong ?

See my answer ask if you still do not understand any part.

Please do not post homework questions verbatim on this site. Asking for homework help is fine, but this isn't your free biology tutor - questions must be phrased so that they are interesting and useful to many future visitors. I will edit yours accordingly.

Cyclin dependent kinase is the answer for the first question. Cyclin concentration increases during m phase and falls in g1 s and g2 phase as it is degraded. Cdk is always present in the cell but gets activated during m phase, when cyclin is present. (cyclin dependent)
Cancer cells do not require growth factors to stimulate cell division. They have mutations which disrupts the normal cell cycle regulation. Now can you think what should be the answer ?

There is a wide continuum from "cancer" in the sense of uncontrolled cell division (this could include even things like 2-3 extra cells making an imperceptible, microscopic bulge in your colon) to cancer in the sense of huge lumps of meat growing on your body and killing you painfully within X months. For the latter kind, many "stages" of "evolution" must be completed by "the cancer" (forgive the excessive quotes, but the terminology is a bit nuanced here). For a better idea of the nature of cancer, you could start by reading The Hallmarks of Cancer (and reading about it).

Which of the following is always present in the cell cycle?

There are eukaryotic cells like yeast which can be cultured in a medium containing only nutrients. Because these are unicellular organisms, there's no reason to expect that they have any growth factors or hormones or extrinsic signal like that (there's a caveat that often even unicellular organism can signal each other, but I believe there are also many that don't). All eukaryotic cells that divide have a cell cycle, so these cells also have it.
Therefore, hormones and growth factors cannot be required for the cell cycle. Cyclins and Cdks are a fundamental part of virtually any cell cycle ever seen by science, so you could say they are necessary (though I think it is conceivable that an organism could exist which progresses its cell cycle using proteins completely divergent from known cyclins and Cdks, but then again).

Which of the following is essential in cancer growth and division?

Without DNA replication, you obviously cannot make more cells, so that is necessary.
There are cancer kinds which are dependent on growth factors (perhaps they make their own growth factor) but there are also cancer which simply jam the receptor active, so that they can grow even without the factor. This is discussed in The Hallmarks of Cancer.
Signalling molecules (assuming that extracellular signaling is meant, because if you start taking away signalling molecules inside the cell like IP3, obviously you can break the cell to the point it won't divide) is just a superset of growth factors; same arguments apply because growth factors are the most potent "signalling molecules".
Control mechanism is also "obviously unnecessary" and "obviously necessary". Cancer is uncontrolled division, so if there was control, the cancer wouldn't be there in the first place, duh. But obviously cancer cells also control their own division to some extent - they still have a coherent cell cycle and so on.

Ultimately, the key to understanding cancer is being cognizant of "perspectives".
"The body" (actually the wild-type genome) has a certain plan in mind for what each cell should do, and to that end, it has programmed the cells here to divide so many times in so and so fashion and the cells there to not divide unless this event happens and so forth. If those cells are mutated, and that programming is disrupted, they may divide in ways the body "does not want" (ie. they create tissue which has not been evolutionary selected for over previous generations), so from the body's point of view the cancer is indeed out of control.
On the other hand, the cancer is almost like its own separate organism - for one, it certainly has a different DNA than you, as it has mutated. It undergoes Darwinian evolution and becomes gradually more adept at surviving and spreading inside your body. So from the cancer's point of view, the cancer cells are indeed quite well-controlled, with the goal of that control being to divide as much as possible.


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How are Maggots Sterilized (Disinfected)?
For maggot therapy, how are maggots disinfected? I'd imagine there's a limited scope of measurements that can be taken to sterilize the maggots - i.e. we don't want to sterilize them and kill them too.

Speculation : Maybe they are grown in laboratory settings, preventing them from any microbe infection...Something like germ free mice.

Of course, but what about the first generation? They have to have come from the wild.

They are grown in the same way that "clean" mice that don't have any gut flora are grown - originally they came from the wild, were cleaned, then kept in specific conditions after that. The first couple generations may be iffy, but dirt isn't inheritable...

How is gut flora taken care of? I thought gut flora was necessary for digestion.

History
Ambroise Paré is credited with being the first to note his observations on Maggot Debridement Therapy (MDT) in the 1500 though it is a technology that has been used for centuries (reference). It wasn't until the 1920's that therapeutic experimentation with maggots was instigated by William Baer, a clinical professor in orthopaedic surgery at the Johns Hopkins University in Baltimore, Maryland, whose unorthodox methods were successful in the treatment of osteomyelitis and pyogenic wounds. He is also considered the father of modern MDT since he was the first to devise a way to sterilize maggots (reference).
Procedure
In addition to removing necrotic tissue from the wound (a procedure known as debridement) maggots have also been proven to disinfect wounds, promote healing, and inhibit a pesky substance known as biofilm from forming on the wound bed. Maggots are nature’s cleansers, showing up to remove dead tissue and promote healing (reference).
Currently Lucilia sericata, or the greenbottle blowfly larvae is preferred for MDT because

Firstly, larvae have been shown to debride wounds with extremely low
probability of myiasis upon clinical application. Larval secretions
have been shown to help in tissue regeneration. L. sericata have also
been shown to lower bacteremia levels in patients infected with MRSA (reference).

Sterilizing maggots
In early applications, sterilizing the larvae was a major problem. Doctors had to first bathe the eggs in bleach and then soak them in mercuric chloride or formaldehyde. The bandages, gaudy and cumbersome for the patients, were held in place with either surgical tape or Unna’s paste—made of zinc oxide, gelatin, glycerine, and water. Other problems that doctors faced included the maggots escaping during the application process and the leakage of toxic waste secreted by the maggots into the wound, which led to infections such as tetanus. Today, commercial and research laboratories produce sterile larvae. And instead of the bulky gauze bandage, a form-fitting cast with a nylon net to corral the larvae is placed over the wound. An absorbent pad put on top of the netting soaks up the larvae’s toxic waste products. The number of larvae used has also changed. Early prescriptions ranged from 5–6 maggots for a fingertip injury to 500–600 for a more serious wound. Today, the scientific standard of 10 larvae/cm2 is used (reference).
William Baer proposed a method to produce sterilized maggots and it is understood that sterilization has to start from the egg stage in itself (reference). The sterilization solution that he proposed was.

Stock Solution of bichloride of mercury, strength one in 1,000 parts.
Stock Solution of fifty per cent. ethyl alcohol. Take equal volume of
each Solution, mix, and add one-half of one per cent. chemically pure
hydrochloric acid. The final Solution will contain bichloride of
mercury, strength one in 2,000 parts, twenty-five per cent. alcohol,
and one-half of one per cent. hydrochloric acid.

He did not sterilize the maggots as such but took care to feed it sterile food. His work can be read here. Another solution used for sterilization was  5 per cent solution of formalin plus 1 per cent sodium hydroxide (reference).  Sterilization of maggot larvae in itself was found to be hard with some success being reported (reference). Current maggot sterilization techniques include.

UV Sterilization
Rapid washer sterilization
Egg to maggot sterilization (reference)

There is no first generation that has been detailed as such. Mostly sterilization starts from the egg stage. As far as bacteria in the gut is concerned, if sterilization is carried out well, it has been found that there is a significant decrease in any harmful bacteria present (reference). Most details of sterilizing maggot larvae is given in this paper. Consider reading this paper as well.

Medical maggots are FDA approved. Their use for wound debridement of bullet wounds was recommended in the US Army Special Forces Medic handbook back in the 80's. I assume it is still there.

How could sterilized maggots cause tetanus? Or was it case with un-sterilized maggots?

@abukaj That is in the case of un-sterilized maggots

There is an interesting and authoritative paper on rearing of larvae of blue bottle flies for debridement purposes, cited below.

Essentially the eggs are disinfected (rinsed) using .25 % chloramine solution (NH2Cl), then the larvae are hatched and reared in aseptic conditions and fed sterilized food. There are some additional controls after initial disinfection (eggs are placed in agar and the resulting growth is compared to non-disinfected eggs). The procedure is detailed on page 127-128.

Whether the eggs are perfectly germ-free may be somewhat moot. Historically this was done without disinfecting the eggs (or anything else). Secondary infections were probably not uncommon but the advantages of the technique far outweighed the disadvantages until the advent of antibiotics. Apparently these things are great at debridement of wounds (but shouldn't be used too close to organs or blood vessels).
See Wolff and Hansson, Rearing Larvae of Lucilia sericata for Chronic Ulcer Treatment--An Improved Method, Acta Derm. Venereol. (2005) 85: 126-131.


text:
Relation between respiration and concentration of citric acid

A and B are 2 reactions.
If there is an excess availability of citrate, then which of the above reactions will prevail?
I know that citric acid is formed when oxaloacetic acid reacts with acetyl coA. But how does concentration of citric acid influence the above reactions

This image is a bit misleading since both ways seem to be the reversion of each other, but in fact they are not (although the same metabolites are used).
Reaction A takes only place in gluconeogenesis which makes glucose from other metabolites (coming from the metabolism of fatty acids for example) and this pathway is only active when there is an abundance of energy present in the cell. Citrate activates the Fructose-1,6-bisphosphatase. The gluconeogenesis takes only place in liver and kidney.
Reaction B takes place in glycolysis and is the rate limiting for the whole pathway. It takes place when glucose is taken up and then used for the production of energy. The Phosphofructokinase (PFK) is inhibited by signals of excess energy as ATP (which is an allosteric inhibitor of PFK) as well as citrate and NADH/H+. While citrate is a weak allosteric inhibitor on its own, it acts as a strong inhibitor together with ATP. This makes sense since both molecules are indicators of free energy metabolites in the cell.
See these two publications for details:

"Allosteric regulatory properties of muscle phosphofructokinase."
Effect of citrate on the activities of 6-phosphofructokinase from
nervous and muscle tissues from different animals and its
relationships to the regulation of glycolysis.

If there is an excess of AMP/ADP then the enzyme is activated and phosphorylates Fructose-1-phosphate.

Although it is true that citrate can act as an inhibitor of PFK, I see to recall that the relevance of this in vivo is questionable. The key effect, not mentioned in the answer here, is that citrate is an activator of fructose 1,6 bisphosphatase, the enzyme for reaction A. Also worth mentioning that gluconeogenesis only takes place in liver and kidney.

@AlanBoyd It has both effects - and since they are adverse, this makes sense. PFK is activated by AMP/ADP which inhibits the Fructose-1,6-bisphosphatase. Thanks for mentioning.


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Why are flies not scared when landing on a monitor with changing graphics?
I have been wondering why would insects in general, not be scared when important changes happen on your monitor where they have landed...
If you move even just a finger, they are scared to death and fly away, but anything on my monitor and they remain completely placid.

Ha ha interesting question. Maybe 0.5 second of no change in graphics on your monitor is enough for a fly/mosquito/other to infer that the thing is not moving. And once they landed they may not see what under their feet and can't detect further movement. Or they might just understand that the thing they're walking on is not moving and therefore whatever they see, they grasp there is no danger. Also are you sure that the insects that land on your monitor are those that are really scared of movement such as mosquitoes for example.

Today it was a large fly. I've mainly got flies, but saw some other insects there too. Note that I, on purpose, would say... move a window under the insect and saw absolutely no reaction. So I can say that there was rather heavy movement.

Hypothesis: Flies can resolve each individual frame and recognize that the screen is just changing color/don't notice that some of the flashing is changing colors. Hypothesis 2: The fly isn't looking at your finger but feeling your finger move with pressure senses.

Hmmm... my finger is on the mouse, the fly is on the screen, so I'm not too sure about hypothesis 2...

My guess: A fly's eyes are probably half a centimeter away from the screen, which means that they see pretty much all of the screen from a 90 degree angle. Try looking at your screen in a 90 degree angle and you wont see any changes either.

Flies see motion. When the monitor screen changes, the visible spectrum of the pixel is changing and nothing is moving.

Flies have limited color vision. Each color has its own wave frequency, but flies have only two kinds of color receptor cells. This means they have trouble distinguishing between colors, for instance discerning between yellow and white. Insects cannot see the color red, which is the lowest color frequency humans can see. However, houseflies have the ability to see polarized light, but humans cannot differentiate between polarized and unpolarized light. Polarized light is light in which the waves travel only in one plane. [1]

Monitors have polarized film on them so you could test the color hypothesis by taking an old monitor you are willing to sacrifice and removing the polarized film. Then you could test if the flies jump when the screen changes. See here for removing the polarized film on the monitor, or if you have access, this article on A behavioural study of polarization vision in the fly, Musca domestica may hold the answer without needing to ruining a monitor.

I can't reconcile your answer with the well-studied optomotor response of fruit flies (e.g., http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846117/), where in flies are tethered in place and their visual field is changed via LED screens, simulating movement. Photo here: http://depts.washington.edu/flyarama/

@kmm here it discussed the flicker affect. That is, insects with compound eyes respond better to moving stimuli then stationary. I am about to eat a cupcake so I will read your link in a bit.

That's what I can't figure out. The OP describes things moving on the screen, which should activate the flicker effect.

@kmm movement on the screen isn't 3D movement since nothing actually moves. What is happening is the pixels are changing colors. Since flies cannot distinguish nearly as many colors, they won't perceive the change. However, if I wrapped my hand in red (which is hardest for them to see) and moved it towards them, the movement will be picked up since their is depth perception amongst other characteristics in play as well as background colors being removed from view by my movement.

@kmm did you read LED Arena and Visual Behavior Assay section at the end? They used UV, blue, and green light. Flies can see UV light. Your computer screen has polarizating film blocking UV. So the experiment seems to be geared to benefit the limited visual ability of the fly. Also, they were started by vibration before each experiment to heighten their visual senses.

As indicated by @kmm there is little reason to believe that a difference in polarization or color would cause a differential escape response. - Which also is not claimed by the paper cited in the answer. Flies do not like a darkening: http://link.springer.com/article/10.1007/BF00197657  ;  also note that flies have little reason to visually monitor the platform on which they stand (and that the movement of the pixels poses no danger to them) - whereas they sense dangers from above (such as a finger) - also you can still scare them to death by hitting your monitor and inducing vibrations

Flies monitor the space above them:
Flies have a very strong innervation of the back of the head, which contacts the surface ( http://flybase.org/reports/FBim0000875.html ). While working in a fly lab, which studied behavior, I was told that these nerves sense changes in the light intensity above a fly - and it is this "third eye", which usually triggers the escape response of flies.


text:
Regulation of Cra protein level in E coli
Catabolite Activator/Repressor, Cra protein (formerly known as Fructure Repressor FruR) plays a significant role in central carbon metabolism of E coli. Its activity is inhibited by fructose-1,6-bisphosphate (FBP); Cra up-regulate gluconeogeneis pathways and down-regulate glycolysis and carbon-uptake pathways. I found enough literature on how Cra plays a regulatory role in metabolism.
However, I am unable to find out explanation of one experimental observation: with increase in glucose uptake rate the transcript level of cra decreases. What is the mechanism for this. Further, are Cra proteins degraded as the glucose uptake rate increase, if so what is the regulatory mechanism?


text:
Breathing under water
Why can fish breathe under water but land mammals can't? How can fish extract oxygen straight from water but humans can't?

It's always helpful to other users if you show what you have found on the matter so far so that any input is a constructive one.

shortly speaking. Because they have gills! You may want to have a look to the wiki article for fish gills. You may also want to google "How do fish gills work?". I think you will easily find all the information by yourself. Note: You say that land mammals can't breath underwater. Neither do the aquatic mammals. All aquatic mammals have lung and therefore need to come back to the surface to breath.

I believe that terrestrial animals tend to consume far more oxygen as well, so that even if a land animal had lots of gills, it could still not survive underwater.

@Superbest - I would imagine that great white sharks consume a lot of oxygen when they're hunting, and last time I saw one it was just slightly larger than I am :)

isn't this just a matter of a small Google search..

I'm taking this question at face value. Yes, fish have gills, but we also have a respiratory surface in our lungs so why couldn't we 'breathe' water and extract the oxygen (since extraction is a simple matter of diffusion from the content of the lungs into the blood).
Apparently we use 550 L of pure O2 per day. This works out as approximately 400 g.
The solubility of O2 in fresh water is around 10 mg L-1. Assuming a hypothetical situation where we could breathe water and extract all of the O2 from each lungful this means that we would need to breathe 28 L of water per minute, compared to the 8 L of air that we breathe.
Now of course water has a much higher density than air so that a lot of energy would be expended in moving this much water in and out of the lungs (which in turn would require us to consume more oxygen). Couple this with the fact that realistically we would only be able to use a fraction of the O2 dissolved in each lungful and you can begin to see why this is a non-starter.
Gills allow this problem to be largely circumvented by having a one way flow of water over the respiratory surface, which in the case of fish is often achieved at least in part by moving through the water.

+1 good answer. Note also that because water is more viscous than air, fish can have thiner structures than terrestrial organisms allowing a greater surface exchange.


text:
How much mechanical stress can a skeletal muscle bear?
In the movie- Saw, for the last trap Bobby was told to insert metallic hooks into his pectoralis major muscle. In his fake story Bobby has raised himself successfully, but when he was "really" trapped, his muscles were broken under his own weight.
Is it true, that muscles can be broken so easy? When human is pulling up on the bar, aren't these muscles undergo much more tension, because of lever effect made by his arms?
Also, what if Bobby insert hooks under his ribs, would he die immediately due to pneumothorax?
The question is biological, no interest of how it was possible to overcome trap with mechanical means.

Can you edit this to make it more about biology and less about a fictional character in a movie? Are you interested in the tensile strength of vertebrate muscle?

I don't watch the SAW series. But with regard to muscle tear, it depends on a lot of factors like the weight applied (was this Bobby heavy or muscular) and whether he moved around a lot. You might have heard of crocodiles rolling around to tear off flesh of their prey. So if he was thin or was muscular and did not move around much, the muscle should be able to handle the weight.

worth noting SAW uses a lot of handwavium when it comes to biology, like there is no hacksaw no matter how dull that will cut through a leg faster than a link of chain. cutting through a human leg is tough.

The skeletal muscle is not isotropic and therefore the effect of stress would be different from different axes. The strength also depends on the density of fibers and the composition of tendons (aponeurosis) that connect the muscle tissues; these can change (positively) with long term exercise [ref].
In this article the authors show the effect of different mechanical stresses on the skeletal muscle tissue — digitorum longus, from rabbit hindlimbs.

Tests were performed on extensor digitorum longus (EDL) muscles,
  chosen for its regular cross-section and low pennation angle (Lieber
  and Blevins, 1989). To ensure that only muscle tissue was tested,
  aponeuroses were carefully dissected away

Figure from the same article by Morrow et al. (2010)
You can notice that the yielding point to longitudinal extension is somewhere near 180kPa. It can be assumed that a hook into the tissue on pulling would generate longitudinal extension stress (unless the hook pierces through the muscle tissue or has sharp edges that can rip the muscle transversely). The stress in the Bobby situation would be: $$\frac{\text{weight (mass)}\times \text{gravitational acceleration}\ (9.8\ ms^{-2})}{\text{area of the muscle covered by the hook} \times \text{number of hooks}}$$
This is the best I can answer your question based on data; this cannot be directly extrapolated to the Bobby situation because:

The muscle tissue is different
The strength of the tissue depends on how much has Bobby exercised his muscles.
There would be additional mechanical stresses in other directions because of his movement while being suspended from the hook.

Ribs are not very strong bones and attempt to hook something on it may cause punctured lungs, not pneumothorax. Death will depend on the severity of the wound.


text:
How does yeast dissolve in sugar?
There's this fascinating "kitchen experiment". Take a "brick" of baker's yeast (not dry yeast), and a couple teaspoons of sugar, put them together in a cup and stir together. There's no doubt both are solids: yeast is a firm block, you must use quite a bit of force initially to crush it and even then it should remain a rather thick paste. The sugar is crystals, nothing tricky about that. And then, within a minute or so of stirring, your cup contains only liquid - not entirely fluid like water, but not much thicker than cream. Solid+Solid -> Liquid.
What process leads to that? What happens with the baking yeast when it comes in contact with sugar, that it turns from solid to liquid, and releasing enough water to dissolve the sugar?

If if you find that impressive, try baking something that calls for a mashed banana. It's typically listed as a liquid ingredient for a reason.

There are a few solids that when mixed dissolve into a liquid. It's a pretty neat thing.

The whole process is called osmosis. In it there is the flow of liquid along a concentration gradient. Water then flows from the side which contains the low concentration of dissolved molecules (this can be salts or sugar for example) to the side with the higher concentration until it reached equilibrium. This principle is shown in the image below (all images from the Wikipeadia article on osmosis):

The blue dots are the dissolved material, the concentration is high on the right side and lower on the left. Through the dotted line in the middle (which is a semi-permeable membrane) only the solvent can pass to reach a concentration equilibrium. There is a pretty cool osmotic pressure simulator available on Molecular Logic which can also help understanding the principle.
And this is exactly what happens to the yeast cells. The sugar crystalls get dissolved (at least partly) by some of the humidity from the yeast block (this will not work with dried yeast) and form a highly concentrated sugar solution (also called hypertonic). The sugar concentration inside the cells is relatively low (called hypotonic). This leads to the effort to balance the concentration inside the cell and outside of it which then leads to a massive efflux of water from the cells. This goes so far, that the cell membranes break and the interior of the cells is released (nucleus, DNA, proteins and so on) and the sugar is completely dissolved in the released water. The reason why this mixture is so "gooey" afterwards is the DNA, which forms long, thick strains.

This method can be used in the lab to break up cells relatively gently without applying too much force.
When baking you should make sure, that your yeast is not coming directly into contact with undissolved sugar (or salt which works the same way), as this will kill a part of your yeast cells. However, for baking you usually dissolve the yeast in water or milk, so there is a huge excess of water which dissolves the sugar (or salt) and protects the cells. Addionally your yeast is much better distributed in the dough and gives better results.


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Genes, chromosomes, base pairs and the 23 pairs
OK so I'm a bit confused. Does a chromosome consist of genes and do genes consist of DNA? What about the 23 pairs in sexual reproduction? I can't remember what the pairs consist of

Please show what you have found on the subject matter so far so that any responses are constructive.

The Wikipedia articles for chromosomes, genes, and DNA contain all the information you need, and are literally the first links of the respective Google searches for those words.

@MattDMo This is perfectly right. But I tend to differ here: Wikipedia is nice but tends to explain things with a lot of words and sometimes in a complicated way which is hard to understand. So I think it is important to answer this kind of questions here as well, even if it is pretty basic.

Wikipedia's articles on things like DNA and Genes are far more friendly to the Layman if you switch to Simple English.  I've found that reading that first, then moving onto the English article is a good way to get a decent understanding.

I will start from the small and go to the big organisational unit:
All of this is constructed by DNA, the sequence of the four bases: adenosine, thymidine, cytidine and guanosine.  They are abbreviated G, A, T and C and are called the letters of DNA.
Genes are organisational units formed by a specific sequence of the four "letters". Genes encode for all the proteins (in fact this is a simple view, but should be enough for the moment) and are the way the information of how the protein sequence looks is conserved.
All DNA is organised in the form of a long string of bases, which would be very long in higher organisms. To come around this problem, the DNA is organised in chromosomes, in which the DNA is wound around special proteins (the histones) and further wound up to get a compact form.  The image below (from here) shows the relationship:

The 23 chromosome pairs are the 23 organisational units in humans, in which our genetic information is stored and organised.  A picture of them looks like this (image from the same website as above):

Please note that the chromosomes are not X-shaped, although they might look like on the image. They are pairs of long DNA molecules, which are not connected.

Pet peeve of mine - chromosomes are not X-shaped! They only look like that at one particular point in mitosis, and not even at the point where they make karyotypes. Sorry, nothing wrong with your answer, I just had to vent :)

They are not, you are absolutely right.

+1 good effort. It is not the first time this kind of basic question raises and it often get closed and we can't find them to point it out to newcomers. It is good if we can keep this post I think.


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Why do some fruits have their seeds disintegrated
Sometimes I'd come across a Lychee or a Naseberry whose seeds are kinda disintegrated.. in a thick powdered form, either completely or partially. What could cause such a thing? And is the fruit with such seed harmful?
I wish I had pics to show but it happens rarely.
Here's a normal Lychee with normal seed:

And what I sometimes find in place of the solid black seed is something that has the texture like this wet dirt:

but obviously more like the seed itself that has disintegrated into a thick wet powder.

Just a guess, but I would say that the process of the seed growing into a plant started. The fruit will still be eatable in most cases. We have a similar phenomenon with peaches where the inside of the hard core changes.


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Meaning of "auto" in trans autophosphorylation?
Why this process called "auto"?
Is it because each tyrosine kinase receptor subunit of the RTK dimer has the ability to phosphorylate tyrosine or other amino acid residue present in other subunit of the RTK dimer's cytoplasmic tail? Is it because no new set of kinase enzyme is needed to phosphorylate them?

Receptor tyrosine kinases are proteins which float around in the cellular membrane. Upon binding of their ligand, the dimerize (two units form a dimer). This releases the kinase domains and the proteins start phosphorylating themselves over cross (meaning part a phosphylates part b and vice versa). This looks like in this figure below (from here, it is an interesting article):

Besides ATP this process needs no further co-factors so the "auto" refers to the ability of the RTK to phosphorylate itself upon activation. See more about autophosphorylation here.

OP may not see your comment if you don't @mention him... :/

@N00B Instead of thanking me here in a comment you could upvote answers to your questions and accept to show it answers your question. This is a nice gesture towards the people who answer questions (also probably in older questions).

@Chris I did that already


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What is "bacto" peptone?
Standard recipes for yeast medium often include "bacto-peptone". Is this the same as bacteriological peptone? Is there an authoritative source that spells it out?

See here. Bacto is a brand which used to be marketed by Difco. It is a casein (milk protein) hydrolysate.

@leonardo that's a pity since it included a lot of useful information.


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Blood groups - why is O the universal donor and AB the universal recipient?
I do not understand why individuals with type O- blood are often called universal donors and those with type AB+ blood are called universal recipients.
My thoughts on this are:

It should be that because O+ blood has all antibodies but no antigens that all other blood types including O- would be incompatible making O not a universal donor - so why is O the universal donor?
Also if O is the universal donor, it should be O+ that is the universal donor and O- that isn't because Rh+ is compatible with Rh+ and Rh-, not just Rh+ or Rh-.
It should also be that because AB- has all antigens and no antibodies that AB is not the universal recipient - so why is AB the universal recipient?
Here is what I would expect from blood group mixtures:
O-A: A clumping in O
O-B: B clumping in O
O-AB: AB clumping in O
and that being true for the reverse order as well
AB-A: AB clumping in A
AB-B: AB clumping in B
as well as the one that everybody knows which is A-B: A clumping in B and B clumping in A
I would also expect for Rh compatibility:
Rh- with Rh+: Rh- clumping in Rh+

@Arsak Nominating for re-opening does not happen automatically. This needs to be done by you and decided by the community.

@Chris Thank you for the feedback! I've found that the reputation threshold for close and reopen votes is at 3000, so I'll leave it's up to the higher-rep user to decide.

In blood groups you always need to consider two things: The antigens present on red blood cells (RBC) and the antibodies present in plasma, which lead to clumping of RBCs if they match. Don't mix up the words antigen and antibody! A healthy individual will never have antibodies against the antigens on their own RBCs, but they will have antibodies against antigens which are not present on their own RBCs. (*)
Also always remember that blood transfusions consist only of RBCs! The plasma and antibodies are removed. If you mix blood of two people directly, all combinations will coagulate unless the blood types are identical. Thus, when thinking about donor and acceptor match, you have to consider the acceptor's antibodies and the donor's antigens - nothing else.
Finally, Rh+ means RBCs have the Rh antigen, Rh- means they don't.
A universal acceptor will thus be someone who has no antibodies at all (because their antigens don't matter - they receive no antibodies from the donor). This is the case if the RBCs have all antigens: AB+
A universal donor will be someone whose RBCs have no antigens at all (because their antibodies don't matter, they get removed before transfusion): O-
As a side note: The ABO system and Rh are only the two most dangerous blood groups when they are mismatched. There are many more RBC antigen types (around 35) and in fact hospitals will consider several of these when matching donors and acceptors.
(*) We don't completely know why we make antibodies against antigens not present on RBCs yet. One hypothesis is that the bacteria in the intestines produce antigens which 'look' similar to our blood antigens. Also, this only applies to the A/B/O antigen. All other antigens work like normal antigens such as bacterial ones - after your immune system has seen them the once, you have antibodies against them.

O- should be the universal donor not O+because when rh- blood is given to rh+ person ,the rh+ person can not make antibodies against rh- blood because there are no rh antigens in the rh- blood.(So what will rh antibodies be made against ?)
Now I think u can figure out about why AB+ is the universal recipient !

this I think is why it should be O+ that is the universal donor. You see O- is only compatible with O-, B-, A-, and AB- from the Rh compatibility and ABO compatibility combined whereas O+ is compatible with O+, B+, A+, AB+, O-, B-, A-, and AB- as far as donating and as far as recieving these are the compatibilities.                                             O+: O-, O+ and O-: O-  so already O+ is compatible with more blood types than O- is on both the donor side and the receiving side.

No..if you give O+ blood to a person with -ve blood group, that person will make antibodies against the rh antigens on O+ RBC. But if you give O- blood to any blood group they can not make antibodies (reason explained above. ) so your notion that O- is compatible only with negative blood groups is wrong.  Receiving and donating compabilities for a blood group are different. You can NOT say that if O+ can receive blood from O-, it can donate blood to O-..

ah but negative blood types have antibodies against Rh antigens in positive blood already there so that means less making of antibodies. Plus when you have a blood transfusion you get an RBC transfusion and a plasma transfusion so there comes the problem of antibodies in plasma. You might also get a WBC transfusion or a platelet transfusion.

Various  factor are considered before blood transfusion. Not only abo and rh+  and -  blood group... I am unable to understand what you are asking in the first statemen of the above comment.

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


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Is the human body composition real?
In Fullmetal Alchemist when Ed goes to disprove to Rose the Sun God's "miracle" to bring humans back to life by proving that science (in the form of Alchemy) can create people by saying

Water (35 L), Carbon (20 kg), Ammonia (4 L), Lime (1.5 kg), Phosphorous (800 g), Salt (250 g), Saltpeter (100 g), Sulfur (80 g), Fluorine (7.5 g), Iron (5 g), Silicon (3 g) and trace amounts fifteen other elements.

I am wondering, is this composition true in real life? if so what are fifteen trace elements?

You'd probably get better answers at [biology.SE]. See also Composition of the human body - there's more than 15 trace elements thought to play a significant role in human physiology.

The composition of the human body has already been linked in the comments above. It takes a bit more than to mix a few buckets of elements together to get a human.

@Chris - That's actually one of the major plot points of this particular anime.  Just because they can describe the body in terms of ingredients doesn't mean they can transmute those ingredients into a human.  Bad Stuff happens when they try.

@Bobson Ah, ok. I was not aware of that :-)

@Chris - I figured, given the question got migrated out of its original context. It's a good anime, if you're into such things.

@Bobson I will have a look at it some time in the summer. Its always interesting to see new things.

No, it's only a very rough approximation.
I actually made a spreadsheet to figure this out.

The rows represent the composition as described by the quote.  I translated each into its appropriate chemical formula and converted all measurements to grams.  Then I found the atomic weight of each.  The gray area represents the grams of each element made up from that particular description, which are summed up in the first summary line.  The second summary line are the values as specified in The Last Word's link, which are based on a 70 kg (154 lb) person.
You can see that while some of the numbers are in the right ballpark, most are still off by significant amounts (the bottom row is percentage error - negative means the anime was too low, positive that it was too high).

It's been a long time since my high school chemistry.  Please let me know if I made any glaring errors in the process.

Really this is just a comment towards Bobson. The only things that I notice is that you have saltpeter as NaNO3, sodium nitrate, but that's Soda Niter. Wouldn't Saltpeter be KNO3, potassium nitrate. Also, you have no column for potassium which is said to make up .35% of the human body. Hope you see this because I'm not a high enough reputation to actually comment...

@user8184 - Nice catch.  I've updated the chart to properly use K.  Thanks!

@Bobson. Good job +1. You could improve the presentation of the table though. We can barely read the numbers for the moment.

@Remi.b - I don't think I have that spreadsheet anymore, but if you click the image, you'll get the full-sized version.

Indeed "right-click > open in a new tab" is the solution then :) Thanks

Alright, so this answer is partially based off the ideas presented by Bobson above. What i did was take his Excel spreadsheet idea and put that into the upper section. Then, I used the amounts used on the website he linked to check the proper amounts needed in the body. I then used those numbers to reverse engineer how much of each compound would be needed for the measurements to be correct.  Some of the measurements added up while others didn't. The red and blue text are the measurements used for sodium and chlorine, respectively, because they worked against each other. Also, the oxygen and hydrogen didn't add up exactly with the water so that's what the green and yellow text is. From this we see that most of the measurements are off by substantial amounts. This also shows that certain elements exist beyond the compounds stated in the show throughout the body. So although the show is simpler and fun to quote, it's not scientifically correct.

(Full size image)
If you notice anything that stands out or that I missed, feel free to leave a comment and I'll try to correct myself or see your perspective. And sorry the Excel sheet may seem a bit sloppy, I tried to work quickly late at night.

Is it possible to put a link for the spreadsheet and upload it somewhere so that we could get an enlarged version of it. Currently as it is, it is hardly visible.

You can open the image in a separate tab by right clicking and selecting "Open image in new tab". You can magnify that image easier. I don't really know how to link the spreadsheet but hopefully that works.

yes it does.. that bit skipped my mind.. thx

No problem. I realized that the other day when I was trying to view Bobson's spreadsheet

I edited in a link directly to the image, so you can just click it for the full size version.

The Internet can be such a beautiful place sometimes :P

Water can be essentially split into hydrogen and oxygen. Also the amount of salt content can be split into calculating the composition of both sodium and chlorine. Almost 99% of the mass of the human body is made up of six elements: oxygen, carbon, hydrogen, nitrogen, calcium, and phosphorus. Only about 0.85% is composed of another five elements: potassium, sulfur, sodium, chlorine, and magnesium. The remaining elements are trace elements, of which more than a dozen are thought to be necessary for life, or play a role in good health (e.g., fluorine, which hardens dental enamel). A straightforward elemental composition of the human body with the elements given by weight can be found here. I would also suggest going through the wikipedia article linked in the comment section.

funny that down-voters have nothing really to say about what is wrong with the answer. :)

I think it might be the tone of your answer.  Interpreting the anime's proportions also results in 99% of the body made up of oxygen, carbon, hydrogen, nitrogen, calcium, and phosphorus, and ~0.62% other stuff.  The content of the answer is good, but downplaying the source isn't useful.

@Bobson probably what it is. Will edit it


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mFOLD prediction result interpretation
I am trying to predict the secondary structure of certain predicted pre-miRNAs through mFOLD which is the generally accepted technique for structure prediction in most studies. I am finding it hard to interpret the result and accept if the pre-miRNA which I have picked and the miRNA I have can be accepted and included in my result.
This is one predicted pre-miRNA structure with the predicted miRNA position shown in green.

Is this a good/bad structure and if so, can anyone give me a reason why. Thank you.
edit: I understand that energy levels are also something that is looked for in the prediction. In this particular figure, ΔG = -75.00 kcal/mol which I think is fine.
Sequence used for folding is
AAAAATAAAAAACAGAACCATGAGGCAGCGCACCAAGAGCGTCGTGAACGTCCGCGAATA CTTCCGCATGGACGGCAGTGGCGCCCCCGAGCAGGAGGACGACGATGACAACGATGACTG GATGGCCATCGCCATGCAGGGCGCACCGCGTAAGGTCAGCGTGGAAGTCGTTAAGCCTGG CAAGAAGGCACGCGCTCGTACGTCGACGTGTGACTCAC

and the highlighted match area is
ACGATGACAACGATGAC

So this structure should be fine because the sequence lies along a stem-loop structure.

I am worried about that bulge on the left top corner though. That doesn't affect the predictability of this structure does it?

As a non-specialist reader, I wonder when you say mMFOLD is a "technique" if you mean it's software?

@daniel yup software

Can I know more about the settings of this prediction? Temperature, ionic strenght, molarity etc? You could post the link to the job results on the mfold server so I can better evaluate the likelihood of this structure.

@alec_djinn I have moved past this project but I generally stick to default parameters for prediction. The paper titled "Bioinformatic discovery of microRNA precursors from human ESTs and introns" gave me a guideline for identifying a viable precursor which I follow currently. But it would of course be helpful to know how the prediction is done. I will make sure to contact you the next time I do a precursor prediction and give you a link. Thank you.

The green region will definitely not make an miRNA: It is not a part of a stem loop. See typical miRNA structures from miRbase.
EDIT
Bulges can sometimes determine which strand is chosen as mature miRNA. However, this green region is also is unlikely to form miRNA because the stem is just 15bp.

Please look at the edit of the question.

I didn't know if I should ask this as a separate question so, I am posting it as a comment. In one paper (http://bioinformatics.oxfordjournals.org/content/21/18/3610.abstract, I found that ~70 nt of the matched flanking area was taken as pre-miRNA while in this paper (http://www.hindawi.com/journals/ijg/2012/957607/) ~100 flanking nt of the match area was taken for pre-miRNA structure prediction. Any idea why so?

no idea.. it is best to take 60-70 nt from either side (because you don't yet know that your read is -3p or -5p). I suggest that you use a machine learning algorithm to predict the right miRNA structure. Co-incidentally a friend of mine was working on similar problem and was talking to me about it (for a moment I thought you and her are same people :P ). I'll let you know if we make some progress.

I'll post it as a question then to see if anybody else could get some light on the issue..


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Steps to confirm if predicted miRNA is good or bad
I aligned all miRNAs available to the supercontigs of a particular genome with certain parameters (e value of 0.01 and a word match of atleast 7 as suggested in this paper). I have also isolated the pre-miRNAs (+100 nucleotides from either end of the match area). What would you suggest as ideal ab-initio methods to confirm that these miRNAs do exist in that particular genome? Some papers I found use mFOLD like this.
What would you suggest as best steps to confirm if a predicted miRNA/pre-miRNA is really present in the genome.

you can look at my answer in your previous post.. BTW, How did you obtain the miRNA sequences?

@WYSIWYG I downloaded all the available mature sequences in miRBase. Removing duplicates is an issue. What would you suggest is a good tool to remove duplicate miRNAs among 30,000 sequences.

There won't be any duplicates in miRBase (for a given organism). Choose the taxon nearest to your organism if you are doing homology based discovery. If you want to take all/many organisms then you can use fastx_collapser to collapse redundant sequences. However you will lose the name of the miRNA. You can use awk also for this and it will keep the sequence header from the first organism in the list.
awk '/>/{$0=h} !(/>/){if($0 in a){next} else{a[$0];print h"\n"$0}}' organism1.fa organism2.fa ... organismN.fa

Make sure that there are no extra newlines, otherwise you might need a small modification
To know if something is an expressed miRNA you would need to do a small RNA sequencing. There are some tools like mirdeep and mirSVR which you can use to discover miRNA sequences.

Do I really need to use mirDeep now that I am trying to match the already existing list of all available miRNA to the genome rather than find new novel sequences. I thought that was what miRdeep was for.

It does not just find novel miRNAs but it also checks for the features such as hairpin formation and assigns scores. mirSVR uses a machine learning algorithm to find miRNAs (I have never used it though)


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Biological advantage of electric synapses
Electric synapses are synapses that do not process information but simply foward one action potential from one neuron to the next. There are no neurotransmitters, no inhibitory and exitatory postsynaptic potentials that would cause different responses in the post-synapse.
So, I'm wondering: What are the biological advantages over just one long axon? My research has only told me the advantages over "normal" synapses (speed), but I couldn't find any advantage over just using one longer neuron which, I suppose, would be even faster.

I can't answer this but just to consider: firstly, this may be a way to overcome the limit of length of an individual cell before intracellular transport of proteins and organelles becomes impracticable. Aside from this, the difference between one long neuron and two connected ones is that they are separated by a membrane and can have different interiors. This means different internal cell states e.g. signalling molecules, ion concentrations,...

Having just read this article (http://www.ncbi.nlm.nih.gov/books/NBK11164/) there are several advantages/functional reasons that seem apparent and important in having electrical synapses with gap junctions compared to just a very long neuron.
a) signals in electrical synapse can be bidirectional.
b) electrical synapse synchronize electrical activity among populations of neurons.
c) The large pores in gap junctions allows passage of ATP and other important intracellular metabolites, such as second messengers between neurons.
I'm sure there are plenty of other reasons but these should provide a better picture in terms of the functional significance of having electric synapses.
Hope this helps!

Also. If there is one long neuron then the nucleus will have difficulty coping up with the maintenance of the cell

The advantage I have heard of is synchronization, as can be found in the Wikipedia article on electrical synapses:

The relative speed of electrical synapses also allows for many neurons
  to fire synchronously.

Synchronization in turn has many advantages and is supposed to play roles in different contexts, e.g. in binding.

Synchronisation through electrical synapses, which is covered by the previous answer, is much faster and stereotyped compared to gamma synchronization hypothesized to underlie feature binding.

Ah, I did oversee b). Should I delete my answer or just the hint on binding?

@vkehayas: You mean the maximal firing rate of neurons (1000Hz) compared to the 40Hz of gamma oscillations?

Correct. That said, gap junctions may not be responsible for the characteristic frequency of the oscillation, but they could increase the level of synchrony in the population (https://ac.els-cdn.com/S0896627304000431/1-s2.0-S0896627304000431-main.pdf?_tid=de9b03ec-af4d-11e7-add4-00000aab0f6c&acdnat=1507813644_721ef4edc7c1752e1634aa21b6f2eaa2), so there is a point to be made there.

This reassures me, i.e. I am not on a totally misleading track. (General increasing the general level of synchrony is something.) This is what I found today: Neuronal synchrony measures (http://www.scholarpedia.org/article/Neuronal_synchrony_measures)