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Biological origin of shuddering during sleep
What is the biological origin of the following behavior:
Sometimes, during the early, formative phase of sleep (when you have a gradually dimming consciousness of what all is happening around), you feel some kind of a tremor of sorts - a feeling as if you are about to fall off. The body responds by twitching the limbs, so as to "balance", and you end up waking up for a second or two, where you realize that you aren't about to fall and all is fine.
Since Cerebellum is involved with maintaining equilibrium and balance, I have the intuition that this is related to some transient behavior where the Cerebellum is dimming down. When you are in deep sleep, you do not have a sense of balance, so I guess Cerebellum does dim down the sense of equilibrium.
But the apparent flaw in my reasoning is - if this was indeed the origin, one would have experienced these tremors every time one slept. That doesn't happen, it is only occasional (AFAIK).
So, biologically, what is the true origin of this behavior?

FWIW, I am aware of the fact that answers on SE are well-intended to have a broad scope, but still, I feel necessary to point out my familiarity with Biology is quite basic and limited to as much as is taught in a typical high-school (to people who take up Biology as a chosen stream). Hence, I'll request the answerer the please point me towards some introductory literature, in case using more advanced terms is unavoidable. Thanks :)

These are called hypnic jerks, also known as hypnagogic jerks or sleep starts. They are normal part of the wake-to-sleep transition. Hypic jerks consist of non-periodic myoclonic movements, generally involving an isolated limb.
The exact physiologic origin of hypic jerks is unknown. We can say that they correlate with a particular waveform on the EEG known as a K-complex:

Picture from http://en.wikipedia.org/wiki/K-complex
K-complexes are a normal part of Stage II sleep and can evoked using auditory stimuli, even if sleep is not interrupted. In the case of hypnic jerks, the K-complex is usually followed by alpha (wake) activity. To my knowledge, there is no evidence that hypnic jerks originate in or are routed through the cerebellum. K-complexes themselves are related to cross-talk between the cortex and the thalamus, a circuit that doesn’t involve the cerebellum.
In addition to the EEG findings, it has also been shown that the jerks are accompanied by autonomic activation — transiently increased heart rate and respiratory rate. There is also an (unexplained) subjective aspect. You described it as feeling "as if you are about to fall off,” which seems to be consistent with the published literature on this. As mentioned in the review cited below, some people report a sensation of "falling into the void.”1
The clinical implications, in case you were wondering, are summarized well by Vertugno et al.:

Sleep starts are common physiological phenomenon affecting up to 70% of the adult population and their course is benign, resolving without any neurological sequel. Therefore, reassurance and counselling are all that is needed to treat the patient. Though an adequate explanation and reassurance may be sufficient, some patients may require a small dose of clonazepam (0.5–1 mg at bedtime) to ameliorate the symptoms on a short-term basis.

1. Vetrugno R, Montagna P. Sleep-to-wake transition movement disorders. Sleep Med. 2011 Dec;12 Suppl 2:S11-6.

You requested in a comment a reference to introductory material on the topic. What we know about the neuro-physiology of sleep is mostly based on the analysis of EEG (brain-wave) tracings. I therefore refer you to this introduction to sleep polysomnography if you would like to get a better handle on how scientists think about sleep.

Thanks for your response. I have +1'd it and will go through the linked articles a bit later (a bit short on time right now), and get back to you if I need any help in understanding them. I'm deferring the accept for until then, but I'm sure this is only temporary. Thanks again :)

@TheDarkSide Unfortunately, the Vetrugno paper requires access through a library (or paywall) for viewing the full text. It was the only review I found that includes significant discussion of the topic in a relatively recent issue of a top-tier sleep journal. If you're not able to access it, let me know and I can see about finding something else. The PDF of the polysomnography chapter should be viewable in full, though.

I do not think sleep starts are associated with sleep starts. K-complexes are a characteristic of sleep (Stage 2), although they can be seen is deeper stage 3 and 4 sleep as well. Sleep starts tend to occur during the wake-sleep transition. Sleep starts can also be "Hypnagogic hallucinations" which can vary to sensations of falling (common) to loud noises leading to the infamous "exploding head syndrome". Sound is not the defining characteristic of Hypnagogic hallucinations.  ;)  See https://www.sleepassociation.org/patients-general-public/exploding-head-syndrome/

Sleep starts can be exacerbated by caffeine and "stress" . See also - http://www.sleepeducation.com/news/2013/08/22/sleep-starts

@bodhi.zazen Re. your first comment - you’re confusing a lot of things here. 1) Yes, K-complexes are a defining characteristic of Stage 2 sleep, but they are also frequently associated with brief arousals (alpha frequency), i.e. sleep-wake transitions. 2) The literature about auditory-evoked K-complexes within sleep is extensive. 3) Hypnagogic hallucinations are REM-sleep phenomena, most often seen in narcolepsy, sometimes in sleep deprived young healthy people. Totally different deal. 4) Exploding head is different still, a type of HH but likely different mechanism.

@bodhi.zazen Re your second comment - agreed. The review cited above mentioned triggers: fatigue, stress, sleep deprivation, vigorous exercise, and stimulants like caffeine and nicotine.

Most K-complexs are not associated with arousals and not all alpha activity is awake. An awake rhythm is low amplitude mixed frequencies and the "alpha rhythm" is a relaxed rhythm with eyes closed. The alpha frequency seen with K-complexes has a completely different distribution as K complexes are over the central head regions and thus completely different from the posterior dominant alpha rhythm.

K-complexes can be evoked, but they are not a defining characteristic of sleep starts and it is not clear if the K-complex is the cause or the result of the sleep start, ie, just as they can be evoked by auditory stimuli, they can also be evoked by internal stimuli or the arousal of sleep starts.

Hypnagogic hallucinations are not always associated with Narcolepsy and the hypnagogic hallucinations seen in Narcolepsy are not really Hypnagogic hallucinations, they are REM sleep intrusions into either wake or light sleep and are detailed visual "dream" imagery. See http://www.sleepeducation.com/sleep-disorders-by-category/parasomnias/sleep-hallucinations/overview-facts . The main difference with Narcolepsy, other the the type of hallucination, is that the HH occur when Narcoleptic patients are AWAKE where in "normal" people they occur when transitioning into sleep.

Hypnagogic hallucinations is thus a non-specific term. In Narcoleptic patients they are intrusions of REM sleep physiology into wake or light sleep . In "normal people" they occur in light sleep, during the transition to sleep, and not associated with REM sleep or REM sleep physiology at all. There no evidence to support or refute that exploding head syndrome is or is not different from sleep starts. And I am not confused, I happen to know quite a bit about sleep ;)

Thanks very much for these inputs. I am accepting your answer since you pointed out a nice 'correlation'. However, I feel that the graph is not representing a correlation, but rather a direct response to the (unknown) source. That kick in the graph is the EEG equivalent of the kick we feel physically (rather an EEG representation of the same). That sentence "The exact physiologic origin of hypic jerks is unknown" seems overwhelming, but if that correctly represents the current understanding, there isn't any more I can expect from the answer. Many thanks again :)


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What is genodiversity good for?
I saw some documents which were trying to say that they can prove via sweat smell selected by women that humans are developed to find a partner with similar genes. At the first glance, I refused it as absurd for many examples of organisms behaving in reverse but then I realized that I don't know any satisfying evolutionary explanation for this (and more: I could even explain the contrary: If less developed and more developed human had a baby, the better genes could be maybe annulled by the worse genes, on the contrary two very developed partners would have not only a lot of descendants, but their descendants would have also lot of descendants and so on.)
And more thing: if genetic diversity is truly evolutionary practical, could for example even people with genetically transmitted disease help our gene pool?
Thanks a lot.

You should add a link to that document.

@WYSIWYG Sorry, I've seen it in TV and I can't find it anymore (apart from   the fact that the document was in czech :-)

Identification of potential partners by body odors is actually selecting for different genes, not similar ones - see this article on "genetic matchmaking" for some additional details.

@MattDMo Yeah, that's what I though, in that document was definitely the contrary.

Genetic diversity is indeed very important for many reasons, most notably resistance to diseases.
The Gros Michel banana used to be the most cultivated banana, until it was almost completely wiped out by a fungal disease due to lack of resistance in the genetically homogenous cultivars grown in plantations. As a result, it had to be replaced by the Cavendish banana across most of its former range by banana growers.
Furthermore, the answer is a definite "yes" to people with genetically transmitted diseases helping the gene pool.
For example, the case of sickle cell anemia clearly shows why even people with genetic diseases can help the gene pool by providing useful alleles. Heterozygotes for the sickle cell allele are resistant to malaria. This has led to the allele having a high propensity in subsaharan Africa, where malaria is endemic.

The first example of genetically controlled innate resistance to human malaria was the demonstration in 1954 that sickle-cell heterozygotes have less severe Plasmodium falciparum infections than do children with normal adult hemoglobin. This observation has been repeatedly confirmed, most recently by independent studies of genome-wide associations in severe falciparum malaria, which have identified the HBB locus as the major signal of association.

Additional examples are the cystic fibrosis gene, which confers resistance to cholera, and thalassemia, which confers resistance to heart attacks.

source: Stack Exchange

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

sort: votes


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How accurate does the alignment of molecules in DNA have to be?
We have learned that the same information is saved in the DNA in the same place. So when DNA splits and then connects again (during reproduction); how does it maintain the integrity of the information? In other words, do they split and come back like a zipper, or does something else happen?

It is not clear what you want to ask

I think he's asking if whether the DNA post-division needs to be the the exact same spacial configuration as in the mother cell.

DNA and nucleotides don't separate and come and go on their own. Spefific enzymes mediate these processes. So it's not like the two strands of DNA suddenly separate and nucleotides wandering around just come and hybdridize. I suggest you to do some research on DNA replication. If you're interested in that, please edit your question, and we'll be happy to answer.

I still don't understand this question and am unsure why it was reopened. It's not even clear if the edits reflect the original intent. This doesn't seem answerable unless the OP clarifies what they are asking.

In the case of replication the parent strands do not pair up back into the original helix. Instead, as your picture and the one below show, the complementary bases are paired up on one of the parent strands, resulting in two copies, each with one parent strand and one new one.

Source: Kathy's webpage on DNA

When I was reading the question, I had a flash of insight into what I presume the question the OP is asking: how do we maintain "integrity" of DNA when we get a set of DNA from mother, and the other set from father (ignoring mitochondrial DNA and other neat things). I would assume this is the question due to the key word reproduction, but anyway,I am here to provide an answer.
As an answer:
I believe the OP has a misconception. DNA of the parents do not pair up in the progeny. Rather, we have 23 pairs of chromosomes, or 46 total chromosomes. What does this mean? The set from the mother and the father do not come together, like a zipper, and have certain bases that just happen to be different (due to single nucleotide polymorphisms and whatnot). Instead, there are two sets of DNA, each with a double helix.
I think this may be what AliceD is also conveying, but I wished to add some more points such as bringing to numbers to help clarify. If I misunderstood, please clarify!

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


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What is a new biotechnology issue?
I'm looking for any new biotechnology issue related to Biochemistry, Metabolic processes, molecular Genetics, or other relevant fields. If anyone knows of an issue that has solid resources around I'd love to hear all about it.

You use the term 'biotechnology' in a wrong way. It is a field of science and is somewhat mixture of what you've listed. I don't know what you're looking for, so could you pleas clarify what you mean by biotechnology? I'm voting for close this question as 'unclear what you're asking', that I'm willing to retract.

Edited, hope it makes more sense now.

It makes more sense, yet it is till unclear and / or too broad. There are tons of biotechnology papers, journals, full of research. Interesting to who? For eg. plant biotech. is could be interesting to someone (for eg. you), but I'm totally uninterested in it right now. Interesting at what level? For an average person beer and champagne production can be interesting ( it is a sort of biotechnology)....

Biotechnology is a gigantic field. You should have a look at the wikipedia entry for biotechnology.
Because of the size of the field "biotechnology", because the word biotechnology accept different definitions and because the word interesting is extremely arbitrary it is pretty much impossible to give a good answer to this question.
I am using below wikipedia's definiton of biotechnology that encompass...pretty much everything! The wiki definition include fields such as:

chemical and bioprocess engineering
bioinformatics and biostatistics
biorobotics

From @poka.nando's comment, the UN definition is
Hoping it will help you, below are few random examples of research in biotechnology: "Biotechnology is the use of living systems and organisms to develop or make products, or "any technological application that uses biological systems, living organisms or derivatives thereof, to make or modify products or processes for specific use" (UN Convention on Biological Diversity, Art. 2)" Under this definition fields such as bioinformatics would probably not really fit within the field of biotechnology.
Using wiki's definition of biotechnology below are few examples of s^hitngs you might be looking for.

Improve the statistical tools to detect differential selection pressure in a phylogeny (methods such as PAML)
Improving fungiculture by improving our understanding of the mushroom life cycle variation in response to temperature.
Track down genes of resistance to drought in tomato (GWAS)
Design better artificial hearts or get a better understanding of cell differentiation in order to be able to rebuild lost tissues or even organs (see regenerative medicine).
Improve understanding of the transmission of the African swine fever in order to improve its use as a biological warfare.

I think we have different understanding of biotechnology : "Biotechnology is the use of living systems and organisms to develop or make products, or "any technological application that uses biological systems, living organisms or derivatives thereof, to make or modify products or processes for specific use" (UN Convention on Biological Diversity, Art. 2)" taken from wikipedia, an basically this is what I was taught under biotech.

I am using wikipedia's definition which also include bioinformatics and this kind of tools. Let me update my answer with your comment in mind.

The very page you link list quite different fields and to make it clear:
"In many instances, it is also dependent on knowledge and methods from outside the sphere of biology including:
bioinformatics, a new brand of computer science
bioprocess engineering
biorobotics
chemical engineering

" I think you copied the wrong part...

Oops you're right.... ok. I got lazy to work for a poorly defined question. I vote for closing! Hum... I can't delete my answer as it has been accepted now!


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Does suffocation pain involve nociceptors?
I never suffocated myself so not entirely sure, but when you suffocate, it's painful, right? But of course different kind of pain than being injured or sick. What I'm wondering is, if the "painful" (or suffering) experience of suffocation involves the standard pain pathway mediated by nociceptors? Or is it some other kind of pain pathway due to a lack of oxygen? I don't mean psychological pain.

I've heard it more commonly described as a sensation of panic rather than of pain, resulting from a rising [CO2] as detected by carotid chemoreceptors

It looks like this question is based on an unfounded assumption that asphyxia should be painful. Hold your breath for as long as you can. Does it hurt?...  I vote to close this question as opinion based as it is likely to generate wild guesses for answers as to whether nociception is involved yes or no. Quite frankly it is impossible to investigate this issue thoroughly due to experimental and ethical difficulties :)

@RoryM and probably also J receptors in the lung itself.

This is more of a hypothesis

I am not sure if suffocation per se would cause pain. Asphyxia, as RoryM indicated in their comments, can lead to anxiety and panic but not really pain. However, forceful breathing may lead to muscular fatigue which may result in pain. Pain induced by muscle fatigue is called myalgia. Myalgia is possibly triggered by low pH generated by lactic acid, via ASIC3 (Acid Sensing Ion Channel) receptor. Carbon dioxide has no role in this process either directly or as a synergist.

Reference:
Alan R. Light, Charles J. Vierck, and Kathleen C. Light. (2010) Translation from Mouse Sensory Neurons to Fibromyalgia and Chronic Fatigue Syndromes. Boca Raton, FL: CRC Press; Chapter 11 (Myalgia and Fatigue)

I think connecting myalgia and asphyxia is kind of far-reached. https://en.wikipedia.org/wiki/Myalgia

@AliceD this is farthest I can go :) I'll add a disclaimer

With a disclaimer you have my vote :) And a tiny edit ;) +1

Being no expert on pain, I will share some thoughts on the issue.
According to the following site(http://www.helpforpain.com/arch2000dec.htm), there are two types of pain: nociceptive and neuropathic pain. Neuropathic pain involves the central and peripheral nervous system, a possibility I would discount due to no apparent link to suffocation.
Thus, it is likely that, if "traditional pain" is felt, nociceptors are involved. A possible pathway is the decrease in oxygen, possibly detected by certain nociceptors which respond to lead to pain. However, I have not suffocated either, not met anyone suffocating so this is only a possibility.

Kudos for the attempt to answer this difficult question. However, it seems to be a wild guess and a reference is really needed here.

Good point. the problem is that I could not find any :(. If anything, I just wanted to add some food for thought; I'll keep looking though!

Yes, thank you :) Does anyone know how I can get more answers? Can I ask this question as another new question?

This is a reasonable stab at things, but has a number of inaccuracies (as does the website linked as a reference). I wouldn't call the pain of suffocation "traditional pain", as it is not usually described in such a way, but one thing that is correct here is the likely receptor is a particular type of nociceptor -- the "J-receptor".


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Which protein complex is composed of the greatest number of different kinds of proteins, and how many types are involved?
Why are some protein complexes composed of many different types of proteins? How many different types are they composed of? In particular, which protein complex has the greater number of different types of proteins in it?
For example, I've read that the ribosome consists of 70-80 different types of proteins.
How many different types of proteins are in the spliceosome for example?
I'm using the phrasing "types of proteins" to distinguish aggregates/complexes composed of many different copies of the same protein (i.e. some viral capsids) from those composed of many different kinds (i.e. ribosome, exosome complex, spliceosome).

it is better to say "70-80 different proteins". Saying types impose that there is a classification. They are just different proteins aka polypeptides

I've edited your question to include suggestion by @aandreev. Please feel free to revert at any time.

thanks for the criticism @aandreev. I edited the question to try to clarify why I used "types." Is there a more appropriate terminology to use?

In this paper detailed analysis has been made on spliceosome (U2-type) composition. It should be noted that this complex has dynamic composition. In the paper authors state that up to 170 proteins may associate to a metozoan spliceosome during its course of action. Individual assemblies contain approx 110 proteins (human). Similar complex of the yeast contains approx 60 proteins (precatalytic B complex), while C complexes have 50 proteins, altogether 90 different were identified in yeast. See the linked paper for details.


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Is it in principle possible to revive an extinct species having no living relatives?
Is it, in principle, possible to revive an extinct species having no living close relatives but whose DNA and other tissues have been preserved?
What about the case where there are no living individuals of a species but there are some living somatic cells?
What about the case where only individuals of only one sex are alive?

This may absolutely be possible. Check this for some info. But really it appears that using somatic nuclear transfer, using the same principle used to generate Dolly, we may be able to recreate an extinct species by swapping in the genetic material into a new cell. One current problem that we face with this is that while the genetics should be fine in nuclear transfer, controlling proper epigenetic programming is difficult.

How would one go about raising the zygote if this processed occurred? With no living relatives, what would you use as a surrogate mother?

It depends, if there are close enough relatives its possible that the zygote could then be implanted in them. For instance it may be possible to regrow a woolly mammoth using an elephant mother to carrier the embryo. But this has not been done, this is now getting in to current leading edge science.

I only ask because the question specifically references "having no living relatives"

yeah that is true. honestly in that case who knows, I'm sure somebody at some point will be able to figure out how to grow an organism entirely in-vitro.

@TheNightman http://www.huffingtonpost.com/2015/04/27/woolly-mammoth-genome-video_n_7137764.html?ncid=fcbklnkushpmg00000010 we will see soon :D

"...controlling proper epigenetic programming is difficult" might be an understatement...


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How did the introduction of artificial light changed the life cycle of a plant?
Plants in urbanized areas are constantly exposed to artificial light after sunset. In their natural habitat there is a more distinct day and night cycle.
Since light is an important factor in a plant life cycle, I wonder if the introduction of the artificial light forces any changes in the life cycle of plants in urbanized areas?

According to this study, artificial lighting similar to that provided by streetlights in the UK can reduce flowering in at least one plant, which also affects the aphids that feed on it.
This article discusses it in more general terms - night lighting doesn't affect photosynthesis, but can affect the length of day/night perceived by plants and alter growth accordingly. There are two examples given of how it is harmful:

Young trees grow longer and don't enter dormancy, making them increasingly susceptible to cold temperatures.
The stomatal pores of leaves remain open longer, making some trees more susceptible to pollution and water stress.


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What is this insect? Found in Peru
I took the pictures today in Cusco Peru. It is the third insect of its class in a month. I never see it before. I thought that it is a wasp, but I think it's really thin to be a wasp. It's about 4 or 5cm.
I want to know what kind of insect is and if it's dangerous. Thanks!

Very good picture for identification, even I am not the one who can answer here.

Yeap! Very good quality of photos.

http://www.nhm.ac.uk/resources-rx/files/keys-for-nocturnal-workshop-reduced-109651.pdf

So that looks to me like the Ophioninae family of wasps, genus Ophion. I'll query the list of known species to try to find a more direct match.

Some evidence exists which notes Ophion may sting when threatened, but at the same time (and I don't have the reference ready) it's believed that the sting contains no toxin.
As for a positive identification, it's difficult without examining the the features of the wasp extremely close up. Identification keys exist here.

It seems, that I haven't found more direct match, as you promised in your answer. Nor, you haven't answered OP, whether it can be dangerous. An edit would be nice, to clear these things (i.e. remove promise for searching for more details). Thanks!


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Neuroscience of mathematicians
I've tried to google this but everything that comes up are things like "mathematical neuroscience" rather than the other way around.
Specifically, I'm interested in the workings of a mathematician's brain that sets her apart from others. For example, is there evidence to be found in MRI scans or EEG recordings of mathematicians as to why they excel in math?

i think you are looking in wrong direction. Mathematicians are same species as other folks, so look for information on how brain processes mathematics, don't bother with occupation. This article might be of interest: http://phys.org/news11473.html It is not who does math, but rather what brain s doing. Or are you interested in how brains of accomplished mathematicians differ from that of artists?

Thanks for the pointer! That is perhaps more of what I'm looking for. Though I'm much more interested in what happens when mathematicians research more abstract stuff than just numbers, like topological or algebraic reasoning. Do you know any research on those things?

numbers seems pretty abstract to me. Maybe this paper will shed some more light: http://journal.frontiersin.org/article/10.3389/fnhum.2014.00068/abstract

I'm voting to close this question as off-topic because it is a cognitive science question http://cogsci.stackexchange.com/

Most people choose a particular subject not just because of an inherent predilection. You should perhaps study the mathematical savants.

Since when is neurobiology off topic?

Taking the comments into account I have edited the question to give it more focus. Comparing math versus other disciplines cannot be done at the imaging and electrophysiological level as one needs a control group. Both the math group and control group need to be doing the same task. Comparing a musician playing an instrument versus a mathematician solving a complex mathematical problem is comparing apples and oranges.

It's not completely off-topic, but the cogsci SE is a better fit and the question should logically be there to a) ensure it gets the best possible answers and b) gets the right traffic.

@GriffinEvo - Neurobiology questions and their overlap with Biology are hotly debated at CogSci. It is definitely on-topic there, but not because it is a better fit there. This question has a strong neuro-anatomy and neurobiology component and it is a borderline-case. Possibly the neurobiology debate needs to be addressed here at Bio as well. Anyway, I edited the question to make it more scientifically sound.

@AliceD I think it would be a very good discussion for meta - its a part of the SE model to not post the same Q on multiple sites, while both the question, and the site it is on, benefit most by being on the most appropriate site. Personally I'm not sure that it the best way, questions such as this (and many other cogsci type Q's) are suitable for both. I've only raised the close vote because that is how SE is supposed to work, not because I feel the question is massively off topic, just more on topic somewhere else :)

Short answer
People competent in mathematics have been shown to have higher activation of the left angular gyrus according to fMRI. EEG recordings have shown larger activity in the posterior parietal cortex.
Background
I think you are interested in what makes a good mathematician. A brain imaging study by Grabner et al. (2011). showed that the left anterior gyrus was more activated in individuals more competent in math. Specifically, the authors argue that the stronger left AG activity in the more competent subjects reflects a higher proficiency in processing mathematical symbols. The anterior gyrus is involved in mathematical symbol processing.

Left angular gyrus, lateral view. Source: Kenhub Neuroanatomy Atlas
ERP studies (event-related potentials deduced from the EEG) have shown higher activity in posterior parietal cortex in subjects excelling in math (Waisman et al., 2014). This region is associated with algebra and handling mathematical functions.

Posterior parietal cortex among other regions not relevant to the question answer. Source: Live Science
References
Grabner et al. Front Hum Neurosci 2011; 5: 130
Waisman et al., Int J Sci Math Edu 2014; 12(3): 669-96

What type of Algebra? Algebra that everyone learns is a low form of mathematics. Being able to process Algebra doesn't necessary equate to a high competence in math. However, if by Algebra, you mean Abstract Algebra, Algebraic Geometry, Lie Algebras, Sigma Algebras, etc. this would be a different story. So what is meant by Algebra since I would be skeptical to someone simply good in Algebra $x+3 =5$ equates to math greatness.

Quoting from the study: "A computerized test that required of the participants a translation between symbolic and graphical representations of function was designed with 60 tasks (trials) using E-Prime software. [...] The tasks we used in our study are basic items for the Israeli curriculum and were learned by all study participants in a similar way."

I actually think that this is a fairly good compromise. If we delve too deep into higher mathematics the available pool of subjects diminishes rapidly; on the other hand function manipulation is much closer to actual mathematical research than the plain numericity studies that @aandreev has been pointing out in his comments.

@dustin - I tried to keep the answer short and sweet without too much detail on methods. But I am happy to edit.I

@SorcererofDM Israeli curriculum at what level? Even if it is just college math for non math majors, I don't think that reflects a mathematicians brain. If it is high school, that is substantial worse. All subjects should be MS, PhDs, Post Docs, and Professors (hence PhD). Anyone else else shouldn't be referred to as a Mathematician and mathematicians will say MS holders aren't mathematicians either but including wouldn't be wrong.

In the US, the Bureau of Labor Statistics says a Mathematician typically needs a Masters Degree.

@AliceD, it is great, that you use Kenhubs image. But please also use the correct link for source: https://www.kenhub.com/en/atlas/gyrus-angularis

@dustin - the problem, as AliceD mentioned, is that we can't test, say a categorical theorist and a musician, on proving the Yoneda lemma. So we need a task that should use similar faculties in all people, regardless of what occupation they have. Perhaps questions from math competitions would be more appropriate than from the standard curriculum, but olympiad problems are quite different from problems arising from mathematical research.

@SorcererofDM we can't call something neuroscience of mathematicians if the subjects are layman. Would you say neuroscience of doctors (MDs) if we based it on the educational level of anatomy 1?

@dustin - I think we are parsing "neuroscience of mathematicians" differently. You want to find out the difference between fields medalists and the "regular Joe" mathematicians. I'd be interested in this question too, though I can't see an easy way to randomize this, or even how to test this. After all, fields medalists are known for building grand and important theories, not for solving problems in one sitting.

@SorcererofDM I am not talking about field medalists. I am talking about mathematicians. People who simply take a math course are not mathematicians.

@dustin - so now I'm confused. What is the question you are trying to answer? What is the quality about mathematicians you want to extract? Do you want to separate the good mathematicians from the average mathematicians, or to separate mathematicians from nonmathematicians?

Perhaps I was misleading in my previous reply. By fields medalists I simply mean much better mathematicians than the average. I probably should have added "for example" in there.

@SorcererofDM I am not asking any questions. Your title doesn't jive with what you want as an answer. The word mathematician means mathematicians not people who take math courses. They are totally different.

Let us continue this discussion in chat.


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Stop codons and exons?
If we had a hypotheical gene called gene exampleGene and this gene had 5 exons, labeled A, B, C, D, and E in that order on the chromosome, could it be the case that the stop codon for this gene be on exon D and the exon E still being a exon that would be transcribed in? I can not see this to be true, since If I  remember correctly, transcription stops BEFORE the stop codon, and when stopped, the pre-mRNA is then further processed, but everything after that stop would not be a part of the exampleGene ?
My lazy diagram of how I think of the supposed exampleGene to be:
---A-----B---C---------D(stop codon)-------E---
After transcription via RNA polymerase:
A-----B---C---------D

Take a look at this schematic of a mature mRNA.

[source]
The coding region (ie the part that is translated) is between the start and stop codons, but the 5' and 3' untranslated regions (UTRs) are also transcribed by RNA polymerase; these are part of the first and last exons, respectively. The transcription start site is labelled right in front of the 5' UTR. For the purpose of this answer, transcription termination can be said to occur at the poly(A) signal (the poly(A) tail is added post-transcriptionally, as is the 5' cap).
To be clear, the point I'm hopefully making is that transcription does not involve codons. RNA polymerase does not stop at the stop codon nor does it start at the start codon. In fact, it doesn't even "know" what codons are.

Thank you, this makes alot more sense now, but when you say RNA polymerase does not "stop at the stop codon" , could you detail that more?  What I do not get is how RNA polymerase is initiated then. From what i remember various protein complexes initiate it, and then I assume various protein complexes end it.

@RoSiv In eukaryotes, the mechanism behind transcription termination is somewhat unclear. After the poly(A) sequence (AAUAAA) is transcribed, proteins recognize it and cleave the mRNA, after which it is polyadenylated. However, RNA polymerase continues to transcribe past the signal sequence. It is thought that, after cleavage,  either RNAP is modified to become less processive and eventually falls off or an exonuclease begins degrading the second RNA until it catches up to RNAP and pulls the transcript out.

You mix up translation and transcription. Transcription creates mRNA from DNA template. Transcription also includes splicing, that is excision of introns so that mature mRNA contains only exons. In your example it goes like that:
DNA (chromosome): ---A----B--...--Dstop---E---
premature mRNA: A----B---...---Dstop--E---polyA
mature mRNA: AB..DstopE-polyA
Translation is the creation of polypeptide from template mature mRNA.
If codons in exon A correspond to polypeptide sequence a and so on for other exons, your polypeptide translated from mature mRNA will look something like that:
$NH_2$-ab..d-$COOH$
Stop codon stops translation. mRNA might still contain a lot of information after the stop codon, for example, for targeting mRNA to compartment of the cell (e.g. presynaptic site).

@anndreev       Yea i made a typo but will leave it in so your post is in context, thank you. But What I dont understand is for the E exon, how is that transcribed? Is that not the role of RNA polyemerase, to transcribe until it hits the point before a stop codon? How then, would that E be included into the premature mRNA, when it would be past the stop codon? And also, my chemistry is poor, but the NH2 would be the amino group, and the COOH  the carboxyl  group, which generlizes the form of a long polypeptide chain right?

proteins are produces by ribosome from N to C end (yes, one is amino-, other is carboxyl-terminus); 2) RNA polymerase stops at the terminator sequence, it has nothing to do with codons, some RNAs are not even coding a protein! 3) Since exon E is before terminator, it will be processed via RNA polymerase. As I said, RNA after stop codon might be very useful for e.g. localization


text:
Reliability of Sanger sequencing
Hailed as the "gold standard" of sequencing, I was wondering to what Sanger sequencing owes its incredible accuracy to. If possible, I would like a quantification of the accuracy (because I doubt it is 100%, though possibly very close).
I understand ddNTP chain termination and the strategies involved in Sanger sequencing but I lack the connection to accuracy.
Thanks!

In searching, I have located something known as "phred programs" which had provided early confidence levels for Sanger sequencing. I do not directly see the correlation though to modern Sanger sequencing

I don't think it's referred to as the gold standard solely because of its accuracy but rather because it was virtually the only method used for some 20 odd years before second generation techniques were even talked about. Chain termination sequencing is accurate though and is theoretically only limited by the error rate of the polymerase. That said, next gen techniques are also accurate.

Here's some accuracy comparisons: http://www.hindawi.com/journals/bmri/2012/251364/tab1/

Thanks for the comparisons! Personally, I have heard that Sanger sequencing is sometimes even used to confirm next gen tests, and its 99.999% accuracy is as expected. But I do agree that next gen is improving, in both accuracy and convenience

Reliability comes from the fact that in Sanger sequencing (AFAIK) the synthesis of the new strand to the template and the actual reading of the sequence is separated. As you may know Sanger seq uses capillary gel elfo. thus separating the newly produced DNA fragments on a single nucleotide difference, and the reading is done by fluorescence detectors (then base calling etc.) Now compared to this the other sequencing methods like Illumina and 454 detect each nucleotide incorporation that may produce less reliable signals. For eg. in Illumina colonies may overlap on the plate, or in 454 incorporation of multiple nucleotides at homopolymer regions cause a hard time deciding how many nucleotides have actually incorporated. Also it must be noted that quality of the singals / reads is not constant through out Sanger sequencing. The beginning and the end of the reads tend to have noisy and low quality signals, thus actually only the 100-500(-600)bp segment of the whole fragment can be read reliably. Also ABI's SOLID uses a 2 color color-space and each base is read twice and is extremely reliable (99.96% is said by the inventors). Also clever base calling and error correction algorithms may improve accuracy.
It is noteworthy to say that next gen sequencers also achieve high accuracy by taking advantage of their immerse throughput / output - due to clonal amplification of template sequences each original fragment is sequenced multiple times and errors in a single read can be corrected by the use of others.


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Has a new functional structure ever been observed arising spontaneously?
Have we ever observed a new functional biological structure arising spontaneously such as a new functional organ (sensory or otherwise. such as tracing some creature in the past few hundred years which had no electroreception organ and now has evolved this organ)
Or has what we observed been limited to changes in existing structures.
(Lenski's E. coli bacteria is not what i am looking for since it is a change in an existing metabolic system (not a new functional structure) and furthermore e-coli already had some ability to use citrate as an energy source )
Looking for a completely new functional organ (such as a new sensory organ) that we have actually observed - not deduced from fossil record.
Also not looking for something trivial such as a new/modified enzyme or protein molecule but rather a new organ in a species at least the size of an insect.

Can you define "functional biological structure"? As it is now, this is a good question which is not very clearly defined. For example, would a single new enzyme count as a "new function"?

@MarchHo looking for a new organ, such as an electroreception probe or a poison gland with delivery system. i.e. a new working functional system of non trivial complexity

@MarchHo new enzyme is not a sensor or organ. looking for a new functional system like a new organ or a new sense. I updated the question to reflect your point. thanks

how about story of epigenetic inheritance of fear? http://www.nature.com/news/fearful-memories-haunt-mouse-descendants-1.14272 Although it wasn't spontaneous

@aandreev what new organ arose there? thnx

organ in form of memory about never-encountered before adorant.

@aandreev new memory is not a new organ. memory infrastructure is already there. that's obviously not the question here. interesting article on epigenetics though. it seems that our understanding of DNA could change dramatically

What do you mean with "spontaneously" (without human influence? in a short period of time/instantaneously?)? The reason why I'm asking is that creationists often formulate questions in a similar way, from the perspective of doubting evolution as a whole (we haven't "seen" this/that happen), misunderstanding the evolutionary process (e.g. mutation -> new function) and their artifical boundary between macro and microevolution. I'm not saying that you believe in this, and I'm just asking for clarifications, since the current framing of your question might lead to misunderstandings.

correct. spontaneously means without human influence. time means since human recorded history.

Would an organelle do?

@WYSIWYG need a limb or organ in something the size of an insect or bigger. dont want to waste this question on trivial complexity arguments. could be a new functional limb or antenna or eye. something non trivial complexity. thnx

could even be a duplicated eye or antenna and this was advantageous and spread into the population. i.e. some species which had 2 eyes and now has 3

@r2d2 And what do you exactly mean by "trivial complexity arguments"?

@WYSIWYG exactly what it says. not some trivial change or strucutre. this is why i asked for new limb or organ, etc. in size of insect or bigger. or even a duplicated antena, etc.if you dont have. thnx

@r2d2 and you think changes that do not lead to a new limb formation are trivial? Please get the concepts right.

no. but at least those that lead to a new limb,etc in an insect, are usually not trivial. have to set some kind of bar. otherwise, will get some trivial organelles or enzyme molecule and the question is wasted

It is hard to know what examples would be satisfying to you. How about the classical case of human lactose digestion (see this answer)?

It seems like you are attempting to frame this as a question about current evolutionary theory. However, current evolutionary theory doesn't expect anything as complex as an organ to arise spontaneously without any precursors. You suggest a new claw in an insect would be something "spontaneous" enough for you. This again shows that your question and the answer you are looking for are not related to evolutionary theory. The insect organs you are talking about are all modified appendages. This includes claws, mandibles, antennae, legs, fangs. These appendages all share a common genetic and developmental framework that has been slightly modified over long periods of time to give raise to the variety of insect appendages that we see today.
The idea that evolutionary theory supports the spontaneous creation of organs is a willful ignorance of evolutionary theory. The molecular mechanisms that generate novelty (e.g. genome duplication, gene duplication, de novo genes, mutation, gene regulation) for natural selection to work on are relatively well understood. Since we have an understanding of how novelty is created it is known that spontaneous organ generation has never happened or is expected to happen under evolutionary theory.
Here is link to the University of California, Berkeley's webpage designed to teach the public about evolution.

Welcome to Biology. Great answer to a controversial question. +1. If you could add a reference to the evolutionary theory to allow people to read about it more that would really help.

nice dodge. of course it is not expected to happen because then random evolution would need to be observable and that would be the end of theory. and we cant allow that to happen, right

@r2d2 You may continue your efforts to associate these false hypotheses with Evolutionary Theory. However, I believe your time will be better spent reading and understanding Evolutionary Theory than parroting old and disproved creationist miseducation literature. At the very least, a better understanding of evolution will allow you to form coherent arguments against it.

this "answer" should be changed to a comment. show me please some real empirical evidence or admit that none exists. i dont want to waste this question on pitiful dodges whose stregnth of argument is only that the creationist alternative cannot be true

can even be duplicated structure such as some insect species which had 2 eyes and now has 3. or 2 antenna and now has 3 and this was advantageous and spread into the population. please, i'm begging you show me at least this

@r2d2 You should check your condescending attitude. "i dont want to waste this question": really!!? Stop behaving as if you are some kind of supreme being. Provide details in your question if you expect an answer with "empirical evidence".

How about the Italian wall lizards that evolved new muscles around their intestines after being introduced to an island? (other article, actual paper). The paper reports that these cecal valves are "a structure previously unreported for this species and rare in this family and scleroglossan lizards in general"; indeed, "The fact that <1% of all currently known species of squamates have cecal valves ... illustrates the unusual nature of these structures in this population.".
It is possible that these values are an ancestral structure that was reactivated by natural selection; however, we know that natural selection can act very quickly to change the size of morphological structures, so it's also possible that existing muscles quickly changed size in response to selective pressure. Figuring out the developmental mechanism of cecal valves would sort that out.

comment there: "I’m assuming this is a predominance of one possible phenotype, not a change in the genetic structure of the lizards, and that the genes for this phenotype were already present in these lizards..." answered there: "it’s still just the phenotypic expression of a bunch of stupid base pairs... There are other herbivorous lizards with cecal valves" makes sense given that took only 30 generations. i.e. sounds like this was already built into the lizards and was waiting to come out when needed

Do you have EVIDENCE that it was "built into the lizards"?  Or did you just make that up so you can deny that the example you asked for was given to you?  Why ask the question if you are prepared to say that EVERY possible answer "was always built in" with no evidence to support your claim?

@r2d2 I've updated my answer to reflect your point. Don't forget that for most (all?) animals, every individual starts as a single cell, so everything is "just the phenotypic expression of a bunch of stupid base pairs", plus whatever else was contained in that cell.

morphological changes not what i am asking. the "new valve" they found between the small and large intestine is simply an enlargement of muscles already present in the gut wall at this juncture. looking for completely new functional structure. like a new primitive claw in insects or new antenna. also, just curious how do you know the changes were from random mutations/NS? given that 30 generations is nothing for genetic algorithms (have worked with some) it seems far more likely those changes were built in responses/activations of existing DNA - not new genetic info from random mutations

@swbarnes2 a simple test. If we compare the full genome of the lizards on the original island to those on the new island, the genomes should be essentially the same. However, if the cecal valves are the result of new genes (or significantly modified old genes) that were produced by mutation and natural selection, the genomes should be noticeably different. No one has done this comparison, however, as it is not easy. They did do the easy comparison, looking at mitochondrial DNA in each population of lizard. They found the two populations indistinguishable. from http://blog.drwile.com/?p=7699

Again, do you HAVE the results of that test, or are you just jumping from "the evidence could theoretically show this" to "I conclude that this is what is happening" without having the evidence in hand?

@swbarnes2 you are the one jumping to conclusions here without evidence. arent you a scientist? given that it was <30 generations. it was either a very lucky dice roll or pre-existing phenotype expression. let's wait and see. secondly, it was not a new organ or limb as that link explains

What is your point in asking this?  If you are so sure that novel 'organs' can't evolve in a century, when evidence did you expect people to come up with?  Surely you are aware the the genetic evidence we can see TODAY shows the homology between flagella and type III secretory systems, why isn't THAT good enough evidence of the evolution of a novel structure?

To be sure a new trait actually evolved before our very eyes and wasn't simply mistaken for a wild trait we never noticed, you probably want to look at domestic animals. We have directly observed, through animal husbandry, the evolution of new fingers in cats, new ribs in pigs (wild pigs have 14, some breeds now have 17), new fins in fish (here I'm talking about the double tail mutation in golfish).
These new structures act, for the most part, like the old ones. I assume because of this you might be interested too, in the observed evolution of completely new functions from old parts:
The Norwegian Lundehund (dog breed) has evolved the ability to seal its ears shut with muscles that other dogs/wolves use to simply move their ears.
As someone else mentioned,  In an island population of Podarcis sicula (lizard species), muscles in the digestive tract which normally function to squeeze food through the intestines, have bunched up to form a new valve, thus creating a fermentation chamber.
Off the top of my head, I can't think of other directly observed changes in function but there are MANY super solid inferred changes in function:
Bee stingers are modified ovipositors (egg-laying organ). We know this because they are nearly identical to the ovipositors of other insects, and because the queen uses hers as a stinger and as an ovipostor.
Snake venom is modified saliva and snake fangs are simply a merger of tooth and saliva duct.
Bird wings are modified arms with 3 fingered claws. I could go on but I'll call that good.

just curious is there any evidence that these changes occurred by random mutations? i could think of other possibilities such as inherent mechanism within the organism which changes itself. after all, we are far from fully understanding even the most simple bacteria

There are two main issues in your question that make it hard or fundamentally impossible to answer. The two issues are

What you would accept being an 'observation'
What you would accept being significant enough to be an example of interest.

A big issue in your question is based upon what you call an observation!
When you say

observed - not deduced

, you highlight the whole issue of what you would consider being an observation.
In science, observations often take complex form. It is not only direct visual observation recorded on a standard camera. It is like asking for, recorded-on-camera evidence that quartz exist. Such evidence don't exist (and cannot exist), yet we know of their existence through other means of observation. It would make no sense for someone to only consider camera recording as valid mean of observation.
Of course, We have never recorded on a camera the evolution of an entire new organ because it takes a lot of time. Yet, evidences are numerous.
This technic of limiting arbitrarily the field of methods that one accepts to recognize as bringing evidence and call "observation" is a common technic from science denier (e.g. flat earth society, creationist). I made a similar point as the one I made here on this post if you want.
How to solve this "What is an observation" problem?
There is only one way to go. It will be for you to be able to understand the forms that observation can take. For this, you will have to learn a little bit about evolutionary biology and evolutionary genetics. For a very short introduction to evolutionary biology, you can have a look at Evo101 by UC Berkeley.
You may have hoped for someone to give an entire course on evolutionary biology to fill up this gap of knowledge of yours but I am afraid it would be way too much work for a single post. If this was your position, then it would be like refusing to accept that earth is a sphere without having yourself explain how GPS data work. We just can't give you an entire course here.
So you have two solutions; rely on authority or understand by yourself. If you rely on authority you have two main options; Rely on those that rely on evidence (science) or those that don't rely on evidence and either rely on other forms of justification (justification theory;such as a religious book for example). (either those that work through observations, scientists). You second solution is to understand the field by yourself and therefore start studying for it.
A second issue is that it is unclear to know what you would accept being "not trivial"
When you say

Also not looking for something trivial such as a new/modified enzyme or protein molecule but rather a new organ in a species at least the size of an insect

It is hard to know what you would call a significant enough evolutionary event to be accepted. The risk is that you may define it large enough so that it fundamentally cannot be observed by a mean that you would accept.
For your curiosity, this post talks about evolution of lactose digestion in humans and this post about the evolution of cardio-vascular system.
Somewhat related post
You might want to have a look at post Is evolution a fact? and the link posts in the top voted answer.
Just another comment

random evolution

In the scientific literature, "evolution" is never said to be "random". The fact that you're using this expression shows what kind of literature you are used to.
For all reasons explained above, the question cannot be answered, not by lack of evidence, but because the question is unclear. I am therefore voting to close as unclear. Good luck in your investigation of the question.

listen to your words. then it sounds like the whole area is not at all scientific. yet it is taught as science

My answer is more of an explanation for the philosophical difficulties behind the question. My answer is more of a long comment to explain why I think the question is unclear and deserves to be closed as such.

its not my question thats unclear. its the whole theory of random evolution thats unclear

@r2d2 I am quite convince there is no way to change your mind, so I won't try too hard. If you wanted to learn something you would have by the time (and would have stopped to stop to call this field of knowledge the "theory of random evolution" as creationist do; nobody call it that way in science). I am a researcher in the field of evolutionary biology and I know a thing or two about this theory and it is always a bit funny to face someone who knows nothing about it but thinks he knows best.

that was not me. it was a random computer glitch. i;ve studied the theory extensively. but it boils down to taking seriously something which is foolish and stupid. the scientists cannot reject it though, because it's the only explanation that "fits" the way they view the world

i've studied the theory extensively Really? Let's make a test. Here are a number of questions that one could find in an exam to a course of evolutionary biology. 1) In a population of constant size $N$, what is the expected coalescent time? 2) Why does the average $F_{ST}$ decreases with the effective population size? 3) Is the change in allele frequency at a bi-allelic locus faster when the deleterious allele that is a low frequency is dominant and recessive? 4) Is there a positive or negative correlation between recombination rate and heterozygosity in the D. melanogaster genome and why?

How can you estimate recombination rate from linkage disequilibrium and genetic diveristy patterns? 6) What is the shifting balance theory? 7) How does the methods of contrasts is helpful in comparative genomics? 8) What is a monophyletic group? 9) What is the concept of antagonist pleiotropy and how does it help us understand the evolution of ageing? 10) What is incomplete lineage sorting?

all your building of foolishness collapses once you realize random processes only result in nonsense. but that will never happen. i know

@r2d2 Anyway. I shall not feed the troll more than that. I hope your inability to answer or even understand these small questions will allow you to realize that you don't know much about evolution. Cheers!


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Why Doesn’t Hypercalcemia Cause Muscle Spasms?
If you have more calcium in the cell, wouldn’t more attach to troponin and initiate muscle contraction? Why does hypercalcemia cause muscle weakness instead of spasms?

Muscle weakness caused by hypercalcemia might come from a decrease in excitability (so that less contractions are initiated) rather than from the contraction mechanism itself.

Hypercalcemia does indeed cause muscle spasm, but as someone else wrote, hypercalcemia indicates the calcium levels in blood and not in the sarcoplasmic reticuli.
One example where you can observe that increased calcium leads to increased contraction is when you take the cardiac glycoside, digoxin. Digoxin inhibits the Na+/K+ ATPase causing an increased concentration of intracellular sodium ions. Indirectly, the increased levels of sodium will disturb the sodium gradient (because of the accumulation of sodium ions inside the cell) and stop the Na+/Ca2+ exchanger. The consequence of the disturbance of the sodium/calcium exchanger will lead to the increased levels of calcium and the increased storage of calcium in the sarcoplasmic reticulum and thus cause positive inotropy of the myocytes.
You can read more about it here:
Gheorghiade, Mihai, Kirkwood F. Adams, and Wilson S. Colucci. "Digoxin in the management of cardiovascular disorders." Circulation 109.24 (2004): 2959-2964.

Can you please provide a textbook/paper reference for your statements?

Look under "Mechanism of Action" here : http://circ.ahajournals.org/content/109/24/2959.full

Lets think about sodium channels for a moment. Empirical studies show that calcium has the ability to transiently block sodium channels (1). So if you have a high amount of calcium floating around, what you're doing is blocking the flux of sodium through the neural membranes. Neurons aren't going to fire if there's little or no flux through these sodium ion channels, so if the neurons decrease in their firing rate, yo end up with muscle weakness.


text:
Can scientists name themselves in the scientific name when they discover a new taxon?
There are sometimes people names in taxonomy, like Myotis keenii was names after Mr. Keen who contributed to discover the species. So, if you discover a species and someone else is constructing the scientific name and names you, it's clear. But when you discover a species and you publish it in a paper, can you propose a scientific name that contains your name? Has it ever happened, or is it considered an unhealthy practice?

The answer is that in general, self-naming is severely frowned upon in the scientific community, but the act itself is not disallowed.
There have been at least two instances of self-naming recorded in literature, as stated in John Wright's book The Naming of the Shrew, page 34, where Jules Bourguignat named a species of snail after himself as Ferussacia bourguignatiana. The naming was apparently very poorly received (being referred to as taxonomic onanism), although I was unable to confirm this by locating the original citation.
Another example was given in the book on Sigismund Hochenwarth who named a species of moth (now Syngrapha hochenwarthi) after himself (original citation here).

So, effectively, no?

@SiyuanRen Pretty much, you can if you want, but it will lead to you being ridiculed by the community.

@Tomas Isn't this answer enough for you, please mark it as accepted.

"Taxonomic onanism" is a great term.

As this example shows, it's not terribly uncommon to name a species after a family member. Linnaeus, for example, named the plant genus Linnaea after his wife.


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How can we differentiate between respiration and breathing?
I am a student of 10th grade, and I eagerly want to learn biology. What is the difference between respiration and breathing?

Think of respiration as ‘cellular respiration,’ which is the process by which the body extracts energy from glucose molecules. Breathing is the mechanism of the lungs that brings oxygen into the body and expels carbon dioxide.

It is good that you are eager but you should make an attempt to look for an answer before asking here. I did not vote to close this question because I know that there are certain misconceptions related to some subtle aspects of this topic, even amongst researchers. However you should at least do a google search and ask a specific question. Also, making a habit of putting in your maximum effort before asking for help would be good for you in the long run.

@WYSIWYG i appreciate your suggestions and in future i will try to follow your suggested way.

There are two uses of the term respiration: physiological respiration and cellular respiration
Physiological respiration involves the intake of outside oxygen and its distribution to the tissues of the body. Breathing is a part of physiological respiration and functions to bring oxygen into the lungs and expel carbon dioxide.
Cellular respiration is a chemical process by which energy is obtained within individual cells from biomolecules like glucose. In aerobic respiration, oxygen is used. Cells can also use fermentation and, for some, anaerobic respiration to obtain energy.

I think this is the most interesting example of anaerob respiration: http://www.nature.com/nature/journal/v467/n7314/abs/nature09415.html

@inf3rno Just skimmed the abstract; it is amazing.

I found the full text with google: http://rothlab.ucdavis.edu/publications/huseby_2010.pdf . Btw. this is not a unique ability, B. anthracis (anthrax) uses the same method: http://www.sciencedirect.com/science/article/pii/S1089860314000561 gasotransmitters like H2S, NO, CO promote inflammation in a large quantity.

Breathing is a part of respiration but respiration is not a part of breathing.
Breathing is a process through which oxygen is taken into the body for use in respiration. This involves physical movement to take oxygen (into the lungs) and also chemical action (haemoglobin-carries oxygen from lungs to blood and carbon dioxide from blood to lungs).
But respiration is a chemical process that involves the break down of the glucose that was formed during digestion to form energy (chemically, energy is Adenosine Triphosphate) for our everyday or metabolic processes.

thank you for your response . Your answer helped me a lot.

Your points and claims seems fine, but you can enrich your answer by adding references to it.

Cellular respiration does not actually include breakdown of glucose

@WYSIWYG  You write "Cellular respiration does not actually include breakdown of glucose –" <-- How can you say that , please give a source, particularly when  Googling cellular respiration glucose, and tons of links come up saying it is involved. Google says straight away "Cellular respiration is the enzymatic breakdown of glucose"

@anuragak breathing is not necessarily a part of respiration, as some respiration doesn't require oxygen.. but besides.. who is to say that getting the oxygen that aerobic respiration requires,  needs to be considered part of the definition of respiration? i.e. aerobic respiration could just be the chemical reaction that happens after the oxygen is in.

An addition to previous answers plus some clarification
The term respiration originally meant breathing i.e inhaling and exhaling (See here). It was believed that it is the oxygen and in turn the act of breathing is what lets an organism survive.
After substantial research it had been found that, in individual cells it is the ATP production by mitochondria that requires oxygen (as a terminal electron acceptor) and therefore for a cell, respiration is basically the electron transport chain (ETC).
Note that glucose or any other food molecule or its breakdown has got nothing to do with respiration. The process of glucose breakdown i.e glycolysis is not a part of respiration. TCA cycle is however considered a part of respiration because it is coupled with the ETC.
Later it had been found out that molecules/ions other than oxygen such as Fe3+, Fumarate etc, can also serve as the terminal electron acceptor. So cellular respiration expanded to include these cases as well;  these fall in the subcategory of anaerobic respiration.
Note that fermentation also is a pathway that generates energy in the absence of oxygen but it is not considered respiration. It was previously classified as anaerobic respiration (if I am not wrong) but not any more.
So you can see that respiration which was originally synonymous with breathing now denotes a very specialized process. However, respiration is still used to mean breathing and distribution of oxygen in the body when cellular physiology is not in discussion.

who is to say whether glykosis is considered to be part of respiration or not?  many links describe it to be the first step of respiration e.g.  http://www.rsc.org/Education/Teachers/Resources/cfb/respiration.htm

can you define respiration?  of course, breathing is not synonymous with respiration, as anaerobic respiration (what i've read fermentation to be!), doesn't require oxygen so doesn't require breathing.

furthermore, this article http://study.com/academy/lesson/anaerobic-respiration-lactic-acid-alcoholic-fermentation.html   is an article that carefully describes aerobic respiration, and anaerobic respiration, and the place of fermentation..

@barlop  re my second comment asking difference between fermentation and anaerobic respiration..  I've found the answer.. it's the same difference as between fermentation and any cellular respiration. Cellular respiration (aerobic or anaerobic), involves the ETC, which are a bunch of things in the inner membrane of mitochondria and are involved in a stage of respiration..

To my limited knowledge, I believe respiration is the chemical process of the body converting glucose and oxygen into energy, whereas breathing is the physical process of inhaling oxygen and exhaling carbon dioxide. Breathing is somewhat like an "external" respiration.

Thanks for your quick response. Is there any other difference?

@NigHterz  I guess this answerer has just defined each, and the definitions are different, and that's all the difference there can be.


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Is it possible to express the cistrons from a polycistronic insertion fragment in a single plasmid?
I have a insertion fragment that I wish to express from pUC19 in Escherichia coli. The insertion fragment is a sub-section from a larger operon sequence and contains just the last two cistrons from this operon.
I plan to insert this fragment into pUC19 under the control of its single lac promoter. Therefore, there will be two cistrons under the control of a single promoter (which is of course, very similar to how it would be expressed in the WT operon).
In my mind, expressing both the cistrons under the control of the single pUC19 lac promoter should allow both genes to be translated; once the mRNA is transcribed, both cistrons have their respective Ribosome Binding Sites upstream of their ORFs, and should be translated.
My question is, has anyone ever had experience expressing poly-cistronic fragments from plasmids using just a single promoter for the entire fragment? I cannot see any glaring issues with this in theory, but I thought i'd ask before I went ahead. Ultimately, I'd rather express both cistrons from a single plasmid, rather than express each cistron on a separate plasmid.
Cheers!
Izaak

If I understand correctly, you are seeking option for polycistronic expression. Have you considered using T2A or P2A sequences? These come from virus and essentially break polypeptide into two parts, so-called self-cleaving peptide T2A. Real mechanism of its work is that ribosome stalls on the sequence and unable to create peptide bond, effectively re-starting translation with next after T2A amino acid.
Of course, you lose independent control over expression, both products will be expressed at same level (but degradation might be different).
So, you should consider creating construct that looks something like that:
lac:gene1-T2A-gene2-stop
Thing is that a) it might not work in E.coli and b) it might not be necessary, because primary purpose of T2A is equal expression level of two polypeptides. And, if your 2 genes are big, for bacteria it is easier to handle two separate plasmids, rather than one but much larger.

Ahh, intresting! I don't T2A is necessary though; the genes themselves have their natural transcription termination sequences, so the ribosome should be able to 'parse' the ending of each ORF separating the products. The genes are prokaryotic, so I think the natal RBS's of the operons should work. I just wanted to check it over on here to see if there is any big no no's.

The genes form a hetrodimer together so equal expression is what I'm after  ;) cheers for the help. I didn't know about T2A, but its a useful one to know!

your guess seems correct. I never bothered with several-genes expression, so idk. however, since there is a plasmid for what you describe, it should work: https://www.snapgene.com/resources/plasmid_files/pet_and_duet_vectors_%28novagen%29/pETDuet-1/

never bothered with expression several genes in bacteria

pETDuet is close, but its not exactly what I want to do. pETDuet requires me to split the PCR fragment (containing both genes) so each of the two genes will be expressed under one of the two promoters on the pETDuet plasmid. There are two promoters and two separate MCS in this plasmid. I want expression under just one promoter.

However, I think I may order pETDuet just in case single promoter expression from pUC19 expression doesn't work ;) Cheers for the help man!


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Energy transformations in chemiosmosis and ATP synthase
In terms of energy, how does chemiosmosis drive ATP synthase? How does electrical energy turn into mechanical energy and then into chemical energy? Would the movement of $H^+$ be considered passive diffusion or secondary active transport?

Why close this question? It is a complex topic and the question is clearly formulated. Vote for leave open here.

@AliceD because it is a problem statement question, aka, here is problem community do my work to produce answer.

Do you want to know the exact mechanism of the binding change mechanism, i.e. which subparts of the synthase are altered and how their binding with other units ultimately bring about ATP synthesis, or just how, intuitively speaking, would a concentration gradient drive something apparently unrelated, ATP synthesis?

ATP synthase is basically a pump operating in reverse: while transporters such as the Na/K ATPase uses ATP to push ions against a chemical gradient (resulting in potential energy), ATP synthase uses the H+ gradient across the mitochondrial membrane to make new ATP.
A pump uses ATP (chemical energy) to achieve one-way transport by inducing conformation changes in the protein (mechanical energy), which either opens the channel only when ions come in contact with the low-concentration side, or closes the channel when ions come in contact with the high-concentraton side. In either case, the result is that ions can pass only in one direction, and a concentration gradient will build up (potenial energy).
In the case of ATP synthase, the process is simply reversed: an H+ ion entering the channel from the high-concentration side (the intermembrane space) causes a conformation change that opens the channel, and is coupled to the synthesis of ATP. Precisely how the ATP synthase accomplishes this on the molecular level is a complicated topic, and still an active area of research. See this article for an overview.
Note that ATP synthase is clearly reversible: if the mitochondrial H+ gradient collapses, for example if respiration is blocked, then ATP synthase can run in reverse, consuming ATP to pump H+ out of the matrix. There is even an ATPase inhibiting protein dedicated to blocking the ATP synthase in this situation, to prevent the depletion of ATP. Also, the lysosomal ATPase is structurally similar, but operates in the reverse direction to create low pH in lysosomes.

ATP synthase is a wonderful protein. I'll try to answer to your question without going into too much detail.
The protein complexes of the respiratory chain actively pump H+ to form a proton gradient between the two side of the membrane. ATP synthase uses the movement of the protons down their electrochemical gradient to synthesizes ATP molecules.
The transmembrane domain of the ATP synthase (FO) is a passive proton channel. Flow of protons causes the rotation of FO. Rotation of FO causes the rotation of the gamma subunit that connects FO with the catalytic domain of the ATP synthase (F1). Rotation of the gamma subunit causes the rotation of F1 that causes the synthesize of ATP. So the mechanical energy is transferred from FO to F1 via the gamma subunit. In F1 the mechanical energy is transformed into chemical energy via the synthesize of ATP.


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Resources of all known biochemical pathways?
I am looking for a encyclopedia or biochemical pathway atlas of all known or reported pathways. I am very much interested in network and systems biology. Also the references can be open databases, books or whatever. I came to know about a site called wikipathways , but it is not opening for me.

You can find biochemical pathways on KEGG pathway for example.

KEGG PATHWAY is a collection of manually drawn pathway maps representing our knowledge on the molecular interaction and reaction networks for:
  1. Metabolism
      Global/overview   Carbohydrate   Energy   Lipid   Nucleotide   Amino acid   Other amino   Glycan
      Cofactor/vitamin   Terpenoid/PK   Other secondary metabolite   Xenobiotics   Chemical structure
  2. Genetic Information Processing
  3. Environmental Information Processing
  4. Cellular Processes
  5. Organismal Systems
  6. Human Diseases
  and also on the structure relationships (KEGG drug structure maps) in:
  7. Drug Development

To illustrate the information you can find there, here is a screenshot:
If you click on kegg atlas, you get an atlas with all metabolic pathways. You can zoom in to great detail en click for further links.

If you click on glycolysis or oxidative phosphorylation for example, you will get linked to the following page (see picture). In these detailed schemes of the metabolic pathway, each intermediate can be clicked on, leading to a more detailed page.

Nice answer, but I am waiting for some more responses before accepting this.

I don't know if you will get any more :P


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What does it mean: carrying the stably integrated gene
Reading this study
http://www.nature.com/cr/journal/v23/n10/full/cr2013122a.html
They writing

Multiple exogenous and endogenous genes can be simultaneously activated
  by CRISPR-on
We tested single, double and triple activation of a TetO::tdTomato
  transgene and the endogenous SOX2 and IL1RN genes (Figure 3A) in
  HEK293T cells carrying the stably integrated TetO::tdTomato transgene

Could you please help me to understand: They talking about exogenous gene. But saying "carrying the stably integrated". Does that mean that this gene (TetO::tdTomato) is in the cell genome (integrated to genome)? If so, what is the meaning of exogenous here?
Thank you!

According to Merriam Webster, an exogeneous gene is defined as " introduced from or produced outside the organism or system; specifically :  not synthesized within the organism or system—compare endogenous".
I believe they refer to the tetO::tdTomato transgene as an exogeneous, or not originating from the species of study

Yes thats what I am understanding from this too. Thank you.

@Barbos if this answered your question, please consider accepting it by clicking on the check mark to turn it green.


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Evolutionary distance between Canidae, Felidae, and Rodentia
Comparing the families Canidae and Felidae, which have the shorter evolutionary distance to the order Rodentia? Less sophisticatedly put, are cats or dogs more related to rodents?

I just wanted to reiterate what Remi.b said that neither cats nor dogs are more closely related to rodents: they are exactly the same phylogenetic distance apart

I guess this might depend on the definition of "evolutionary distance". If you count something like "number of generations since nearest common anchestor", I guess the family with longer (average) generation length would win.

Online Ressources
Here is exactly the kind of question where tolweb.org is your best friend. tolweb.org is one of the most updated phylogenetic tree online. It also contains tons of reference, very useful to understand controversy over some nodes. onezoom.org is another online source that offer you to seek through the tree of life. Also, onezoom shows only the tetrapods (incl. mammals, birds, amphibians, lizards, snakes, turtles). However, onezoom has an awesome display and is a great tool for displaying diversity (they use the total length (in years) of all branches within a clade) within a clade and the threaten index (IUCN (red list) categories).
Dogs, Cats and Rodents
You will find the placental mammals here (tolweb). As you can see, the cats and dogs are both carnivora, while a rodent is a Rodentia (as you said). This means that cats and dogs have a more recent common ancestor than does either the cat or the dog with any rodent. Stated differently again, cats are not closer or further to rodents than dogs are. There is exactly the same distance between cats and rodents than between dogs and rodents.
One onezoom, the carnivorans is presented as a sister group to the ungulates. I have no idea what representation is the most correct but in any case, cats and dogs are carnivorans and share a common ancestor that is more recent than the common ancestor shared by carnivorans and rodents. So again, there is exactly the same distance between cats and rodents than between dogs and rodents.

»Please note that this tree has not been updated since 1995« ... is this really the most updated one?

The tree of the main branches of the placental mammals hasn't been updated since 1995. Seems pretty old indeed. In general, tolweb is a often updated, great source of information on phylogenetic relationship. If you seek for more updated and more accurate representation I think there is no better option than seeking directly through the literature.

Another very good source of knowledge on the subject is onezoom.org (I edited my answer to add oneZoom) but I can't tell if onezoom is more updated. Also, onezoom cannot support polytomy and will therefore not represent doubts. If I am not mistaken onezoom also don't offer list of references. However, onezoom has an awesome display!

Wrong.. You can actually have polytomies in onezoom. Actually looking a bit more at onezoom, I realize that it actually really is a very cool tool. It also offers great visualization of threaten statues!


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Problem involving selfing (inbreeding it with itself) a plant to generate purebred lines
I am working on a past exam problem where the first bit is as follows

A plant is repeatably selfed to generate inbred lines. Let $\mathbb{P}(He|He)$ denote the probability that a heterozygous parent gives rise to a heterozygous offspring, and let $\mathbb{P}(Ho|He)$ denote the probability that a heterozygous parent gives rise to homozygous offspring.

I am asked to work out the two probabilities as well as an interpretation and state the value of $\mathbb{P}(Ho|Ho)$. The interpretation is obvious and I calculate the conditional probabilities to be
$$\mathbb{P}(He|He)=\frac12, \quad \mathbb{P}(Ho|He)=\frac12, \quad \mathbb{P}(Ho|Ho)=1$$
Next I am given the following

The inbreeding protocol is carried out $i$ times in an effort to obtain representatives of all alleles that can occur at a locus of interest. Suppose that there are 3 alleles, equally prevalent in the population at large and not under selective pressure during the inbreeding experiment. Let $p_j(i)$ denote the probability that, after $i$ repetitions the lines share $j$ distinct alleles between them. Let $p(i) \in [0,1]^3$ be a vector whose $j$th element is $p_j(i)$. Consider the following equation: $$p(i+1) = M p(i)$$

I would like to calculate the transition matrix $M$ and explain the boundary condition $p(1) = [ 1, 0 ,0 ]^T$.
I am lost on how to do this, I'm given the answer for $M$ to be $$\begin{pmatrix} \frac13 & 0 & 0 \\ \frac23 & \frac23 & 0 \\ 0 & \frac13 & 1  \end{pmatrix}$$
But for example looking along the first line I would interpret this as $$\mathbb{P}(\text{There is 1 distinct allele between all lines at time t}) = \frac{1}{3} \mathbb{P}(\text{There is 1 distinct allele between all lines at time t-1})$$
However if there is a single allele between the lines at time $t-1$ then this means every line is homozygous for a single allele so why would that change at the next time step?!
As for the boundary condition, I would of thought it would be $[0, 0, 1]^T$ since is the alleles occur with equal chance and you select a large enough number of lines, you should find all $3$ alleles between them. I was thinking perhaps there is a mistake in the question/solution and the vectors are defined the wrong way round, but even then I would be confused. Surely the number of lines we have makes a large difference, if every line is of genotype $\alpha_1 \alpha_2$ and we would like the probability that there is a single allele between lines at the next selfing step, then every single line would need to become homozygous for the same allele, which seems unlikely if we have a massive number of lines.
Can someone help me work out what is going on here?


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Human bone density and Brown Bear bone density?
It is stated on this website that the density of a Grizzly bear bone is ten times our own. And since I am not into biology at all, I am confused as I don't understand the meaning of bone density here.
I know what the "bone mineral density" term means, and I know it is measured in $g/cm^2$, but there is also the "physical" density term which is the mass by volume and it's measured in $g/cm^3$.
Now, what does it mean when we say that an animal has a bone that is 10 times more dense than ours ? Does it mean that the bone weighs 10 times more for the same size (or volume) ? Or does it mean that it has 10 times the amount of minerals and so it is somehow stronger ?

The word density in the medical term bone density is used to quantify only the mineral content of the bone (bone mineral). It's not intended to describe the total mass density of the bone like we are used to from physics.
This is all on wikipedia: http://en.wikipedia.org/wiki/Bone_density
Thus, when one say that a Grizzly bear have 10 times the bone density, it implies that its bones have 10 times the mineral content compared to humans, and this is indeed seen as a proxy indicator for bone strength. However, this claim does seem unsupported and unrealistic as kmm points out.

I have to think they are using density incorrectly, and since they provide no reference, we really can't check. There is no way that bone density, in the scientific sense, can be 10 times higher in bears. It says "for a given size," which indicates to me that it must mean some kind of skeleton as percentage of body mass. Or it's just made up, with no basis in observation.

@kmm I found some data on the bears here: http://www.asbweb.org/conferences/2006/pdfs/20.pdf, now we just need the same numbers for humans to compare.

And I found a story about a man with a LRP5 mutation that is said to have had eight times the normal bone density, haven't been able to verify though.

The "ash fraction" value is the key here. Bear bone is 66% mineral. Typical human cortical bone is 65-70% mineral. So, no, bears don't have denser bones than humans.

@kmm, may I ask where you got these numbers ?
Also, do different spices have similar "physical" bone densities ? That is, in terms of mass over volume, can an animal have bones that are double or triple the density of ours ?


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Can intron become exon in alternative splicing?
From this image
We can see several exons that are actually introns in other genes. It's not a really a different gene, it's an alternative splicing of a gene. My background is not biology so is it possible for alternative splicing to behave like this? I only know that alternative splicing is just exon skipping and introns will just stay introns and not become exons. Can someone explain this to me and give any suggestions on which part of biology (or genetics) I need to learn. Thank you.

I'm not sure what you're asking. If a portion of sequence ends up in the mature RNA, it is by definition not an intron.

Hmm, you are right. So, do you think from that picture, it's just exon skipping? What does that kind of gene called? Is it still called isoform? I have a hard time to do RNA-seq analysis for this gene because of overlap position near the end can be mapped to 9 gene.

Just did some brief reading. It seems each form is under the control of its own promoter. This means that A8 will have to splice out the first exons of all other forms (this would be exon skipping). On the other hand, the A1 pre-mRNA doesn't contain any other first exons to begin with. These would be classified as gene isoforms.

Thank you. Can you suggest where you read those explanation? My knowledge in biology is really limited so I need to read many material to improve my knowledge.

http://www.ncbi.nlm.nih.gov/gene?Db=gene&Cmd=ShowDetailView&TermToSearch=54658

http://www.ncbi.nlm.nih.gov/m/pubmed/16399340/

Thank you so much. So, all of those gene will share 4 exon and just different in the first exon right? Does it mean, if I can count the reads of the first exon, I can estimate to total count of the gene (for example UGT1A1). Because the problem is the result for the last 4 exon is ambigous.

I don't know a lot about the analysis of RNA-seq data, but that sounds plausible to me.

Most of the transcripts you show have different transcription start sites. In other words, this happens because of alternative transcription start sites. So this is not typical alternative slicing. Some genes have different transcriptional start sites, but the case you show has exceptionally many start sites.

If a portion of sequence ends up in the mature RNA, it is by definition not an intron (save for abnormal splicing events and rare intron retention).
Specific to your question, it seems each form is under the control of its own promoter. This means that A8 will have to splice out the first exons of all other forms (this would be exon skipping). On the other hand, the A1 pre-mRNA doesn't contain any other first exons to begin with. These would be classified as gene isoforms

References:
Owens IS, Basu NK, Banerjee R. 2005. UDP-glucuronosyltransferases: gene structures of UGT1 and UGT2 families. Methods Enzymol 400:1-22.
NCBI Gene: UGT1


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How is the "fine mapping of pelvic regulatory region" done in this paper?
Could anyone please explain to be in very basic terms how Fig 2, and the associated text(located above the figure) is done? The jargon is too much for me to understand and I really need a simplified, step by step, version of the process to aid my understanding.
Here is a copy and paste of the text, the figure, and the figure description in that order from the paper:
"Fine mapping of pelvic regulatory region. To further localize the position of the cis-acting changes, we looked for the smallest chromosome region co-segregating with bilateral absence of pelvic structures in a cross between pelvic-complete [Japanese marine (JAMA) and pelvic-reduced (PAXB) fish (13)]. High-resolution mapping identified a 124-kb minimal interval, containing only the Pitx1 and Histone 2A (H2AFY) genes, which showed perfect concordance between PAXB alleles and absence of the pelvis (fig. S1A).
Recombination in natural populations can also be used to narrow the size of regions controlling polymorphic traits in sticklebacks (18). We therefore tested whether markers in the Pitx1 region were associated with the presence or absence of pelvic structures in lakes with dimorphic stickleback forms: benthic and limnetic sticklebacks from Paxton Lake, British Columbia (PAXB/PAXL), and pelvic-complete and pelvic-reduced sticklebacks from Wallace Lake, Alaska (WALR/WALC) (fig. S2) (13, 14). Microsatellite markers located in an intergenic region approximately 30 kb upstream of Pitx1 showed highly significant allele frequency differences in fish with contrasting pelvic phenoytpes (P < 10−35) (Fig. S1B and table S2). In contrast, markers around thePitx1 and H2AFY coding regions showed little or no differentiation above background levels. These results suggest that an approximately 23-kb intergenic region upstream of Pitx1 controls pelvic development. This region is conserved among zebrafish and other teleosts (Fig. 2A), suggesting that it may contain ancestrally conserved regulatory enhancers."
http://scienceintheclassroom.org/sites/default/files/stickleback_2.jpg

"Fig. 2.  (A) VISTA/mLAGAN (http://genome.lbl.gov/vista/) alignment ofPitx1 candidate region from pelvic-complete stickleback (SALR), medaka, and zebrafish. Red peaks indicate >40% sequence identity in 20-bp sliding windows; grey bars at topindicate repetitive sequences; and circles indicate microsatellite markers used in association mapping in fig. S1. (B) Reporter gene expression in transgenic animals. (C) Pel-2.5-kbSALR from a marine population drives tissue-specific EGFP (green) expression in the developing pelvic bud ofSwarup stage-32 larvae (36). (F) Detail of (C). (D and G)Altered Pel-Δ2.5-kbPAXB sequence from pelvic-reduced PAXB stickleback fails to drive pelvic EGFP expression. (E and H) A smaller fragment from marine fish, Pel-501-bpSALR, also drives EGFP expression in the developing pelvic bud of multiple stage-30 larvae. This region is completely missing in PAXB."
Source :http://scienceintheclassroom.org/research-papers/what-pelvis-can-teach-us-about-evolution/university
Paper:Adaptive Evolution of Pelvic Reduction in Sticklebacks by Recurrent Deletion of a Pitx1 Enhancer.  Chan et al.

This is conceptually similar to our discussion about QTLs, except that I believe that in this example the authors had already narrowed down (which means crudely mapped, as opposed to finely mapped) the actual genetic region by some previous experiments.
Based on that prior work they may have already deduced that they were seeking a single gene (or a Mendelian factor). Note that this is different than a QTL. QTLs are used when the phenotype of interest is polygenic, and cannot be mapped to just one single Mendelian locus.
The other important thing to realize is that the genetic map (derived from meiotic recombination between genetic markers), is an abstract concept, and on its own cannot be aligned to the physical map. The physical map is built by either creating a DNA library and making a restriction map of the clones to form contigs, or more likely by sequencing all of the clones in a library--or just using an NGS shotgun approach.
It is the RFLPs (the small DNA sequences that can be used as genetic markers)  that tie, or pin, or link the physical map of DNA to the genetic map. Once this alignment has been achieved in the region of interest you just need to establish the left and right boundaries of your region of interest. That should yield one, or more, candidate genes. Rough mapping, or gross mapping, might narrow the genetic interval to a segment containing dozens, or scores of genes, while fine-mapping lets you zoom in to perhaps just a handful of genes.
So the authors do a cross between a wild-type and a mutant, and then figure out some way to homozygose the recombinant chromosomes (I am assuming that the phenotype is recessive). Then they do two things. For each recombinant chromosome the score the phenotype (in this case that involves an anatomical structure for the pelvis). Then they also isolate genomic DNA from those scored animals and use their RFLPs to establish the molecular markers that map genetically the closest to the segregating phenotype.
With both a genetic and a physical map in hand they can establish the left and right boundaries.

That helps a bit, but I guess I am still confused on how QTL's come into play in this experiment. I guess I do not have a concrete idea about what exactly a QTL  is. I wish there was simple picture summary for the concept. Thank you though.

I'll try to help clarify the picture, but given that I have not read the paper, I am not too clear on the context.
A. IT compares the DNA of the stickleback (the SALR), medaka, and zebrafish. If there is a red peak, there is relatively high sequence identity (or similarity), indicating similarity (in evolutionary ancestry in this context?). Gray is repeating sequence, perhaps due to duplication or some kind of evolutionary history. For microsatellite markers, I believe that the paper is referring to the use of microsatellites (small tandem nucleotide repeats) as markers to compare the three.
B. Reporter genes are expressed and help the researcher identify something (by giving information, such as fluorescence etc.) (eGFP indicates green fluorescent protein e= enhanced)
C-H. These are just pictures of the fishes. Note the fluorescence (green). It indicates some expression (of the gene of interest). The absence or presence of the fluorescence indicates something, based on what the eGFP was attached to.
Hope this helped! But you need to do the analysis yourself, or at least I can't :P