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The evolution of poor eyesight: is there weaker selection in modern humans?
Short question:
Poor eyesight might have been a major impediment to survival and reproduction in early man (say, 100,000 years ago), but, with the advent of agriculture, major cultural changes, and modern medicine, one might imagine that genes for poor eyesight would persist more easily.
Is that true? Has selection on eyesight been relaxed, or changed significantly, in modern humans? If so, when? Do we know what might explain relaxed selection? If there are any genes associated with, for example, myopia, has their population frequency increased through human history, or has it remained constant?
This New York Times article discusses genetic changes 8 to 4 thousand years ago related to skin color, amino acid absorption, and eventually milk digestion, but it does not mention eyesight.
Background on why I find the question interesting:
A friend of mine speculated that human eyesight is worse today than it was only a few centuries ago, due to the invention and widespread adoption of glasses: a person with poor eyesight genes will now survive and have children, whereas in 1600 they might have died without reproducing.
I'm skeptical: first, glasses became widespread only a few generations ago; second, blurry vision plausibly has little effect on evolutionary fitness. I see no reason why someone with slight myopia would on average have significantly fewer offspring than someone with 20/20 vision, even in a tribe of hunter-gatherers. A short-sighted person could specialize in making hand-axes, for example, and trade them for food -- so I find it plausible that eyesight-related allele frequencies have not changed much over time.
However, I recently heard someone on the radio speculate that eyesight might have worsened significantly a few thousand years ago with the invention of agriculture; the story is that above-average eyesight is a major fitness advantage for a hunter, but not for a farmer.  What does the evidence say?
Side note: I realize that eyesight is affected by more than just genes -- for example, age as well as time spent reading books probably both affect eyesight. That's not what this question is about -- I'm interested in genetic selection.
Edit:  this question is indeed similar to Bad Eyesight and Evolution, but it isn't identical.  That question asks why poor eyesight can persist at all, while mine asks whether evolutionary pressures have changed over time.  In particular, do we know of any genes associated with, say, myopia?  Do we know whether their allele frequencies have changed over human history?

Hi Adrian, I've substantially edited your question to make it more concise, normally that leads to better answers. Let me know if I've changed it too much for you.

@rg255 Hmm, that's a big edit -- I'll try and come up with something intermediate.

I like the edit better. Note that the question is still relatively long.

I think the use of the phrase "poor eyesight" is a little problematic because we don't have a solid reference point. In reference to "perfect" eyesight (how to define that, there are always costs and benefits)? In reference to historic humans (probably largely speculative without definitive evidence)? In reference to other primates or mammals?

@Remi.b I'm asking a different question.  That questions asks "Shouldn't there be evolutionary pressure towards better eyesight?"  Mine is "has eyesight-related evolutionary pressure changed through time?"

@HarryVervet maybe it would help to think about specific genes.  For example, is there any known eyesight-related gene with a "bad" allele associated with higher rates of myopia?  If so, do we know anything about how allele frequencies in 2016 have changed relative to, say, 10,000 years ago?

@rg255 thank you for your edit, I agree that it was an improvement

There is no evolution towards bad eyesight. Generally, myopic patients are not hereditary, but are prone to it because of modern lifestyle.


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What's the mechanism or structure responsible for new species genetic code generation?
I always had this question in mind. I think, If humans find answer to it then we can trigger the next evolution of human specie.
What is the mechanism or structure responsible for evolution ? I don't mean the nucleus and the genetic code. because it's the consequence (the result) of evolution.
I mean all that I found right now as studies materials, treat only the consequences of the evolution, similarities between ancestors and descendants..etc
But what process triggers this evolution ?
For example, the birds ancestor (which couldn't fly ), how did his cells generate genetic code to build new proteins needed to build new protein structures and organs and also to keep this evolution's result for next generations ?
Is there any current research on this matter ?

Thank you All for your explanation, but they treat only the case when there is only a certain length ADN chain and this chain will change in time to produce let's say "more effective population ".
but if we say that all the species came from one cell. than this cell had necessarily less ADN then we have now (for ex: it doesn't have yet ADN to code for hemoglobin and other complex proteins)
So my question was Where did the new ADN came From ?
This question came to me, when we were studying bacteriology and one bacteria had all my attention, it's the staphylococcus, they produce a coagulase that trigger the coagulation process to stop the blood stream so the phagocytes and immune cells can't reach there position.
Random mutations ? well random process can have some result in variation and deletion of existing species, but not in building new ADN chains.
don't tell me that the staphylococcus acquired the ability to produce this protein randomly, because if we do some math, the ADN is a base 4 code (there is 4 bases) and to produce an amino acid we will need 3 bases, so for 30 A.A protein we have only one chance in 4 power 90 without adding the random length and the random 3 dimensional structure, I know, even if there is billions of staphylococcus that will mutate all the time there will be nearly 0 chance to produce a protein that can action exactly with the prothrombin.
that's only for one protein.
I Know I have moderate knowledge in biology but I don't believe that errors in a code (mutations) can make it "better" or produce functioning mechanisms that can interact with other organisms, because if we say so, then we are just insulting our intelligence as human being, because we are saying that random process is making organisms that we, with our brain can't reproduce, the proof is we are still using antibiotics and didn't make our immune system more effective.

On a cellular level, Meiosis is the mechanism that creates genetic diversity in gametes.  Sexual reproduction, though, is the largest contributing factor to diversity and the catalyst of evolution.

Thank you for your comment MG_MD, I agree with you that  Meiosis and Sexual reproduction contribute to diversity. But not necessarily to evolution because we all know that these two processes use what's already existing of genetic material (from parent cells), but a new specie need new genetic code to evolve. so My question is, what  mechanism or structure that builds or generate this new code ?

The mechanism is simply random changes.  If the changes are neutral or beneficial, they stick around.  If they are seriously detrimental, the changed creature doesn't survive to pass on the changes.

It is one of those times when I would love to be allowed to down vote comments!

Evolutionary biology is a large field of research that investigate the mechanism that dictate evolutionary processes. There are hundreds of papers published each month on evolutionary biology and the question is therefore way too broad.

You might want to attend an introductory course to evolutionary biology such as the free online course Understanding Evolution by UC Berkeley. You seem to be particularly interested to mutations.

Okay so what I am interested in, are the insertion mutations (adding code to ADN) because they are the only mechanisms that can explain the new specie capabilities ex : from non flying to flying there must be new ADN fragments that will code for the wings and feather ...etc

First, I don't think that the code insertion that caused evolution was random.
For the simple reason that there is the Proofreading mechanism for the ADN (error-correcting processes). I mean a mutation (or billion of mutations) that happened randomly even for billions of years can't lead to produce something that prevents other future mutations.
if the evolution happened , then it happened outside of the ADN or ARN by inserting new code fragments to acquire new species features, so my question is what is and what caused this process ?

Not absolutely sure, but what you are asking for is mutation: the genetic code is altered by errors in replication. Some of those errors turn out to be beneficial. And,the first mutation in the direction of birds did certainly not enable them to fly, but gave an advantage (gliding) when jumping from one tree branch to another, or maybe only an insulation from clod (plumes) or, more basically, a way to dispose of nitrogen and phosphorus in a decent way, as feathers (unstructured at first).

@Allad1n Your questions are very very basic questions in evolutionary biology (no offense) and you will get all the info you need by following the links I gave you. It will take you a few hours and you will have a much better understanding of what evolution is about (and about the role of mutations in evolution). Your question for the moment is just too broad for a StackExchange post.

I think one of the elements you are missing is that many mutations do change the size of the genome. If you follow up with the references @Remi.b has provided you'll learn about insertions, deletions, translocations, aneuploidy, and mobile genetic elements. You may be familiar with conditions like Down's syndrome which is the duplication of an entire chromosome. Both replication and proofreading are imperfect processes, they are good enough to make changes very slow, but they don't entirely prevent change.

@Allad1n I added a small paragraph on mutations that increase/decrease the amount of DNA.

@Allad1n You say I Know I have moderate knowledge in biology but I don't believe that errors in a code (mutations) can make it "better" and it sounds extremely opinion based rather than evidence based. Do not believe! Investigate the question (Understanding Evolution UC Berkeley).

I strongly advice to have a look at an introductory source of information on evolutionary biology (such as Understanding Evolution by UC Berkeley). It will give you much more information.
Locus and Allele
Here are two definitions to start with:

A locus is a location on a chromosome. This location can be of any size. It can be a single nucleotide, a codon, a whole gene or even longer.
An allele is one variant at a given locus. When considering relatively short loci (say 1 nucleotide or 1 base pair (bp)), then the majority of loci have only one allele.

What is evolution?
Evolution is defined as any change in allele frequency in a population over time.
There are a number of "forces" that affect evolutionary processes. I picked the 3 most commonly considered: Mutations, Natural Selection and genetic drift
Natural Selection
Natural Selection is the process by which variants of genes called alleles are selected and therefore increase in frequency. This selection result from a differential reproductive success.
Natural selection occurs whenever the three following conditions are respected

Individuals in a population varies in terms of a given trait
This trait has some (additive) heritability. Here is one of the several posts that explain the concept of heritability. It might be slightly a post that is a bit advanced for you though but shortly speaking it means that offspring are more similar to their parents more than they are to other non-kin individuals in the population.
The fitness varies (not necessarily linearly) as the trait varies.

Simple example:

In a population, there are blue pens and red pens
Reproduction is asexual and blue pens create other blue pens while red pens create other red pens.
blue pens make more offspring than red pens.

In such situation natural selection occurs yielding the frequency of the blue pens to increase in the population while the frequency of red pens will decrease.
You may want to have a look at this post (although it might be too advanced) to understand the concept of heritability.
Mutations
In the broad sense mutation is any change in the DNA sequence. Some changes are more likely to happen that other but in any case the likeliness of these changes to happen is not dependent on the consequence they will have on the phenotype (shortly speaking, phenotype is how an individual looks like) and on the reproductive success. So mutations occur randomly and the specific mutation that would be needed in the population may not occur. Therefore saying, if a trait is needed (in the sense of "if a trait would be beneficial"), then a mutation will occur to make this trait existing is wrong. Note that most mutations are deleterious (decrease the reproductive success) while few of them are beneficial (increase the reproductive success) and those that are beneficial are more likely to raise in frequency in the population.
Mutations can be a simple a "small change" such as nucleotide substitution, an nucleotide insertion and deletion or can be a "bigger change" such as a chromosomal duplication/deletion, a whole genome duplication and the duplication/deletion of a long sequence.
Mutations create the genetic variance on which natural selection selects the best variants. As a consequence natural selection decreases the genetic variance while mutations increases genetic variance.
Genetic drift
If the change in frequency of mutations would depend exclusively on natural selection, then I would not have said before that a beneficial mutation is more likely to raise in frequency but I would have said that a beneficial mutation will raise in frequency deterministically. An intuitive explanation of what is genetic drift can be found on this post. It will also allow you to understand why small population undergo more random change in frequency of their genes than are big population.

source: Stack Exchange

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

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Why does HPV Infect Squamous Epithelial Cells and Not Others?
I've seen this question about HPV and the reference therein. The link states "Human papillomavirus (HPV) is a DNA virus that presents tropism for epithelial cells, causing infections of the skin and mucous membranes. Replication of HPV occurs in the nuclei of squamous cells and its life cycle is directly related to the differentiation program of the host cell. "
Why does HPV infect squamous epithelial cells and not others, what are the major differences? And why can't that difference be used to provide medication?

The answer usually lies in whether the cell of interest expresses the correct receptor.
Check this:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820467/
This excerpt from that review explains why:
"Although both the α6β4 and α6β1 heterodimer were capable of binding VLPs in vitro, only the former was supposed to function as a HPV receptor, which was concluded from the results that the α6 subunit associated preferentially with the β4 in epithelial cells [12], and the α6β4 complex was expressed exclusively in the basal cellular layer of the stratified squamous epithelium [13], which was presumably the only site of productive PV infection"

Given the question, does this mean how receptors are only expressed in squamous cells?

A receptor is usually a molecule that the cell uses for a particular function relevant to its extracellular context. In this case integrins mediate cell-cell and cell-matrix interactions with other cells and the extracellular matrix specific to squamous epithelial cells.

Just to clarify, whether a receptor is SOLELY expressed in one cell type is a reflection of its endogenous functions!

I understand all that. I'm just of the opinion the answer touches on the question, but doesn't answer it, given Why does HPV infect squamous epithelial cells and not others

The mechanistic reason of why HPV infects ONLY squamous epithelial cells is because its receptor is expressed ONLY on squamous epithelial cells.
From a virus advantage point of view, squamous epithelial cells are the outmost layer of epithelial cells, so perhaps the virus evolved that way because they are the first cells it reaches to from the outside. If it had let's say evolved to infect only a lower level epithelial layer then perhaps its virulence would be lower and would be @ risk of becoming extinct. Perhaps it has happened historically and we don't have record of it.

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


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What is this blue-green bioluminescent jellyfish I saw at Aquarium of the Pacific?
I took this picture of an animal in the bioluminescent section of Aquarium of the Pacific in Long Beach, California, but I neglected to write down what it was.  I've searched the Aquarium's web site, but it doesn't appear to have information about the individual species on exhibit.  (Or else I just can't find it.)  I've also looked at Wikipedia and Google Images, but can't seem to find a creature that looks like this one.
I suspected it could be a jellyfish, and the answer below confirms that.  But I'd like to know what species of jellyfish it is.  (Either common name or scientific name.)

After sifting through even more images on Google Images, I think I have finally identified this as the flower hat jelly, Olindias formosa.  (Wikipedia, Monterey Bay Aquarium)
The coloration looks different on those sites, but I think it's just a matter of lighting.

I think they probably have it under UV blacklight at the Aquarium of the Pacific. So it's probably not bioluminescence, but UV fluorescence,

Thanks for that tip!  I did some further research, and this article seems to confirm your hypothesis.

That is a Jellyfish! :D
Someone else took a picture of that same Jellyfish:
http://www.yelp.com/biz_photos/aquarium-of-the-pacific-long-beach?select=36BuiiqeN7OIFbowSDkPcw
Here is a picture from an article about the exhibit's jelly fish:

Source: New Jellies Exhibit at Aquarium of the Pacific Explores the Mysterious Lives of These Gelatinous Sea Creatures

Thanks!  I'd suspected it might be a jellyfish, but I wasn't sure.  I'd still like to know exactly what kind of jellyfish it is.  Unfortunately, the linked article doesn't have captions on its pictures.


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Brain wave and motor movement correlation
I am trying to better understand which brain waves are generated when the motor system (arms, legs, muscles of any kind) are activated.
According to Wikipedia, several types (Beta, Gamma, Mu) appear to be generated when motor movement is present, but it is not clear which muscle groups/movements/characteristics generate which types of waves.
Also, I see the certain waves (Alpha an Mu for instances) appear to have overlapping frequencies. If their frequencies are the same, then what makes them different?

EEG is a summation of all of the neural activity, and as such, it is difficult to attribute a certain wave type to something of the scope as activation of the movement center (primary motor cortex).   fMRI scans are much more valuable in a clinical setting (in conjunction with other methods).  It's a snapshot and sum of electrical activity.

I don't think that we know yet the exact answer of your question due to the reasons told by @MG_MD

Thanks @aayushsrivastav (+1) - so if I'm reading that correctly, if I am hooked up to an EEG that is monitoring ALL waves, and have been sitting completely still for ~10 mins (to establish a baseline) and then immediately start doing a repetitive movement (say, blinking my eyes or opening/closing my right hand, etc.), you're saying that ALL the types (Alphas, Deltas, etc.) will start changing, and not just one particular type (say, only Alpha or only Delta)? Can you confirm/deny? Thanks again!

@smeeb To put it in the simplest way possible, yes.  You would have a baseline, then when you started to do all of these things you mentioned there would be a marked increase in many wave forms.  You would be thinking about moving, actually moving, and perceiving the movement.  These affect different areas of the brain and as such, the electrical output would increase. That's why EEGs are commonly used in a resting state (like sleep studies).  Also depth comes into play when using EEG, as it is mainly superficial electronic activity, not deep within the brain.

Thanks @MG_MD (+1) - if you (or anyone else) can place this in an answer and provide citations that back up the claims, I will happily award you/them the check + bounty!

EEG signals can be broadly analyzed in two  domains; the time domain and the frequency domain.
EEGs are often analyzed in the frequency domain, where signals are subjected to spectral analysis, by methods such as FFT. This is a classic type of analysis and is still used widely today. As you rightfully state in your question, EEGs are often analyzed in terms of frequency bands. In terms of voluntary motor activity, one study reports activity in the 15 – 30 Hz range when subjects performed wrist extensions and flexions (Halliday et al. 1998). This frequency range corresponds to the alpha (8 - 15 Hz) and beta (16 - 31 Hz) frequency bands in the EEG. Beta activity in general is associated with an alert state, alpha activity generally with a more relaxed state. Both make sense because the subjects were actively engaged in a task (alert), but the task was simple and likely kind of boring (relaxed). The authors conclude that the frequency range over the motor cortex represents (Halliday et al. 1998):

[...] [R]hythmic oscillations in the sensorimotor cortex [...] associated with voluntary motor tasks involving maintained muscle activation, such as position holding.

In the time domain a relatively straightforward response to record motor activity in the brain is asking a subject to perform a certain action, for example finger flexions. These events generate certain synchronized neuronal responses in the brain that can be measured on the scalp with EEG. However, a voltage response to a single event is typically swamped in background noise. A way top enhance the signal-to-noise ration is to repeatedly record the EEG in response to the same event. By time-locking the event with the EEG and averaging the individual event-related EEGs, the random background noise will be reduced (stochastic noise) and the event-related potential (or ERP) can be extracted from the EEG (Woodman, 2010). An example of an ERP to repeated index finger flexions is shown in Fig. 1.

Fig. 1. ERP to voluntary index finger flexions. Motor activity was recorded from the motor area. Source: Ball et al. (1999)
References
- Ball et al. NeuroImage (1999); 10: 682–94
- Halliday et al., Neurosci Letters (1998); 241: 5–8
- Woodman, Atten Percept Psychophys (2010); 72(8): 10.3758

I think this is a part of the answer, not the full answer because the question is 'brain wave and motor movement co-relation', not 'how EEG works'.

@aayushsrivastav - have you read the answer at all? Both sections are on movement and motor cortex. And I don't know how my answer even touches upon the workings of EEG  O.o.

the only thing in your answer that seems to be answering this question is "Beta activity in general is associated with an alert state, alpha activity generally with a more relaxed state. Both make sense because the subjects were actively engaged in a task (alert), but the task was simple and likely kind of boring (relaxed)." Can you please tell how time domain and frequency domain tells anthing about brain wave and motor movement co-relation?

As said by MG_MD:

You would be thinking about moving, actually moving, and perceiving the movement. These affect different areas of the brain and as such, the electrical output would increase.

Also, it is very rare that the brain produces only one type of waves as it is continuously processing millions of information, though we know the basic functions of all of those types (from here).
As to how EEG works:

The billions of nerve cells in your brain produce very small electrical signals that form patterns called brain waves. During an EEG, small electrodes and wires are attached to your head. The electrodes detect your brain waves and the EEG machine amplifies the signals and records them in a wave pattern on graph paper or a computer screen.

Source

Source of image
If you look at the image, th EEG has captured many waves of different types at the same time, which proves the staement of MG_MD.
For the "overlapping frequencies..." part:

For example there is the “mu rhythm” (which is actually alpha activity in the relevant sensory and motor cortical areas that happens when the arms/hands are not doing anything)...

Source

Interesting points, @Christiaan (+1) - it's not too late to weigh in with your own answer!


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Are receptors integral membrane proteins or peripheral membrane proteins?
Integral membranes proteins serve as transporters. Peripheral proteins serve as cell adhesion molecules, antigens and enzymes. So what about receptors? Which proteins carry out the duty of receptors?

It may depend, but I know a detection system which has a receptor protein that is integral. Once it receives the signal it must somehow transmit that signal into the cell, which further suggests integral protein.

All the receptors I know about are integral, transmembrane proteins. It would certainly be possible for a receptor domain to exist on a peripheral protein that interacted with a transmembrane protein, but I don't know of any examples of this: an extracellular peripheral protein would tend to float away, which is a bit of a problem if they aren't intended for secretion.
There are certainly peripheral proteins that associate with the internal parts of transmembrane receptor proteins and may influence their function, but they are not themselves receptors.
I'm not sure about your question about "which proteins" - those proteins are most often named after their ligand followed by the word "receptor", or based on their function that is triggered by binding their ligand, or both (i.e., the AMPA receptor is a glutamate receptor that is also activated by AMPA; receptor tyrosine kinases are a family of receptors that are tyrosine kinases; the individual members of the family are typically known by their ligand).


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Is the male satin bowerbird's bower-building behavior innate?
The male satin bowerbird builds a stick structure, known as a bower (distinct from a nest), where courtship and mating take place.  They curiously decorate their bowers using blue or shiny objects.

(Image source: Wikimedia commons.)

When courting, the male satin bowerbird prances and struts around his bower. He offers the female items from his collection of blue objects, while making a series of hissing, chattering and scolding noises. Mating takes place in the avenue of the bower, and the male may mate with several females in a single season.  -- NSW Government Office Of Environment and Heritage

Question: Is the male satin bowerbird's bower-building behavior innate?
This is essentially a "nature vs. nurture" question.  E.g. If there were no other males around for him to learn it from, would he still build a bower?  If so, where did he get the idea from?  If there were no females around, would he still bother to build it?

Does your question allow for both possibilities simultaneously (nature and nurture)?

I guess it has to allow for both, as it could be the case.  (Mentioning nature vs. nurture was just to convey the spirit of the question; I'm not seriously suggesting these are the only two possibilities.)


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What is the probability of genetic reincarnation?
Parents pass on 23 chromosomes to their children, with a 50/50 chance for each chromosome. Considering that people of a families lived over millennia in the same region the abundance of some chromosomes in this region should be quite high. So if we for a moment neglect the occurrence of mutation the reincarnation of a genetic similar individual should just be a question of time. Therefore I asked myself how to actually calculate the probability and time span of this occurrence. (with and without mutation rates because of the complexity of the model)

And how would you define similar?

Looks more like a question for math.

Assume there is no mutation, leave enough time and the there will be no single living individual that will differ genetically from any other. If you really want to answer how much time it takes to have a probability of say $\frac{1}{2}$ that two individuals are exactly clones of each other in a population, we need to know the population size, the number of loci, the mating system, the population structure and the level of genetic diversity to start with.

Genetic clones are not "reincarnations" – there is much more to a person than their genes. For starters there are epigenetic and environmental factors.
Also, chromosomes are not passed on whole from one generation to the next. Genetic recombination occurs which means, for example, that a mother's egg contains chromosomes that are a mixture of her parents' chromosomes. As a result, chromosomes are generally not passed on identically from generation to generation. This means that it is therefore not true to say "Considering that people of a families lived over millennia in the same region the abundance of some chromosomes in this region should be quite high". The Y chromosome in males is an obvious exception to this rule (it is passed on down the paternal line mostly unchanged).
These points aside, the chances of two people having identical genomes is so infinitesimally small and genetic inheritance is so complex that I do not think there is a sensible model to calculate it.
If you really want a number you could simplistically say that the human genome is about 3 billion base pairs. Humans share about 99.5% of their DNA with everyone else, so let's just say that to be clones two people would have to match at that other 0.5% of the genome – 15,000,000 base pairs. For each base pair there are four options: A, T, C or G. The probability that someone would match on every single of these base pairs could thus be 1 in $15,000,000^4 = 5.1 \times 10^{28}$.
That's 1 in 51,000,000,000,000,000,000,000,000,000.
To put this in perspective, since time began there has been about 108,000,000,000 people who have lived, so humanity would have to repeat it's history several billion billion times to make this remotely likely.
Calculating this number make more assumptions than I care to count. You might take off a few zeros if you are considering a highly inbred population.
It is theoretically possible that an accidental genetic clone of a person could occur, but the point is it's just not going to happen.


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How are 6 "fixed" CO2 molecules joined toegther as glucose?
When we study calvin cycle, we study it with 6 molecules so as to form 1 glucose in a single cycle as:
6 RuBP + 6 CO2 => 12 3-PGAL => 1 Glucose + 6 RuMP
But if we look deep, then we know that the molecules are synthesized one-by-one & 6 cycles give 1 glucose, but:
1 RuBP + 1 CO2 => ... => 1/6 Glucose + 1 RuMP
My question: What is actually this 1/6 glucose (organic carbon fixed from inorganic carbon and how are such 6 molecules joined together?

See https://en.wikipedia.org/wiki/C3_carbon_fixation

Okay, now I understand that I need to change my question a bit because its actually drastically misleading.

It's not really possible to break it down this way. The CO2 fixated by the RUBISCO enzyme generates two phosphoglycerate (2 x 3C) molecules from one ribulose bisphophate molecule (5C), while the rest of the Calvin cycle serves to regenerate 3 ribulose bisphophate from 5 phosphoglycerate. Hence, one 3-carbon sugar (glyceraldehyde phosphate or dihydroxyacetone phosphate) can exit the cycle for every 3 CO3 captured. The regeneration of ribulose bisphosphate involves several enzymes, and the stoichiometry is rather complicated; it would take an entire essay to describe it all. I suggest you look the calvin cycle in the metacyc database, it's a nice interactive resource where you can explore all the details of the reactions. Wikipedia also provides some details on these reactions.
The glyceraldehyde phosphate produced by the Calvin cycle is then converted to glucose and other sugars by the enzymes of gluconeogenesis. The key enzyme is fructose diphosphate aldolase (or simply "aldolase") which condenses glyceraldehyde phosphate and dihydroxyacetone phosphate to one fructose-1,6-diphosphate. A chart of the pathway leading to other sugars is found here.

Glucose (and other hexoses) are not products of the Calvin cycle. Glyceraldehyde-phosphate (a triose) is the immediate product the cycle; 2 of these can be condensed to fructose-2,6-biphophate by aldolase, and from there on to other hexoses, like glucose.

You were asking about the "1/6 of glucose" and how it derives from CO2; this is via glyceraldehyde-phosphate. No, I did not imply that 2 CO2 makes 1 glucose, that's obviously not correct; but 2 glyceraldehyde-phosphate makes 1 glucose. And for net production of 1 triose, 3 CO2 must be captured. I don't think it makes much sense to talk about "turns" of the cycle, I hear this often about metabolic cycles, but I think it's better to just look at the stoichiometry of the reactions. (It's not actually a wheel :)  I will extend the answer with the aldolase part.


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Is Asteraceae and Compositae the same family?
I'm wondering what taxonomic family sunflowers (Helianthus) belong to. Although it's mentioned it belongs to family Asteraceae it is also a composite flower. So it belongs to Asteraceae or Compositae or both?
And do they refer to the same family or to different families?

https://en.wikipedia.org/wiki/Asteraceae#Etymology not the most scientific source, but they seem to be synonyms.

There are a number of plant families that, for historical reasons, have two accepted family names. In addition to Asteraceae/Compositae, there's also Fabaceae/Leguminosae, Poaceae/Gramineae, and others.

They are either treated or even declared to be synonyms in all the texts using both of the terms that I have ever read.
Just one reference: the nearest Flora on my desk, G. Marconi, F. Corbetta, Flora della Pianura Padana e dell'Appennino Settentrionale, uses the notation Compositae = Asteraceae.
It is worth to note that Compositae, 'composite ones' in Latin, refers to the their typical capitulum inflorescence, while Asteraceae comes from Aster, a genus belonging to the family, meaning 'star' in Latin, which represents an allusion to the shape of the inflorescence of Aster, and of many other species, which is supposed to look like a star whose rays are represented by the ligules of the ligulate tiny flowers of the capitulum. Nevertheless, there also are species of the family having no ligulate flowers, for ex. Tanacetum vulgare.


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Is eye colour of Drosophila a polygenic trait or an X-linked trait?
I have seen examples of various eye colours in Drosophila and they have been described both as "X-linked" and "polygenic". I thought these were mutually exclusive. Is Drosophila eye colour polygenic or X-linked?

A trait can be X-linked and polygenic. It is not contradictory. Can you please link to your references?

I don't think this question is unclear, the user didn't understand the terms X-linked and polygenic properly. I have voted for reopening. @SanjuktaGhosh could you add sources to this showing where it says they are x-linked/polygenic?

Polygenic and X-linked are not mutually exclusive; a trait can be polygenic, X-linked, neither, or both.
Polygenic traits are those affected by many genes. According to Conner and Hartl, "Traits that are affected by many gene loci are often called polygenic traits." For example, childhood intelligence is affected by many genes throughout the genome. Monogenic traits are relatively rare, but are linked to some diseases, and occur when a single gene affects the trait; most traits are affected by multiple genes.
X-linked traits are affected by genes (only) situated on the X. If a trait is monogenic, it is very easy to describe it as being, or not being, X-linked. If the gene is on the X, it is X-linked. If it is on the Y, it is Y-linked. If it is in the autosomes, it is autosomally linked. If all of the genes affecting a trait are found on the X then that trait is X-linked. A gene on the X is X-linked, but I would only call a trait X-linked if all genes were on the X. If there was a mix of X-linked and autosomal genetic variation I would describe the trait as having some X-linked genes.
For polygenic traits it is less likely that the genes would be all X-linked, so it is less likely that the trait is X-linked. Imagine a trait affected by 10 genes, and those 10 genes are randomly spread across the genome. It is unlikely that all 10 would be on the X. However, if some were on the X, then we could describe the trait as having X-linked variation. Many highly polygenic traits will have some X-linked variation.
Having more genes affecting the trait further increases the probability that some genes will be on the sex chromosomes. For example, lifespan is expected to be a highly polygenic trait, and genetic variation in lifepsan can be attributed to the Y chromosome in Drosophila melanogaster, despite the Y carrying just a tiny fraction of the genes.
Many eye colour traits in Drosophila can be attributed to single genes, and White in the image below is X-linked. However, one can also produce a white-eyed fly using multiple genes; in this paper one of the lines used has white eyes as a result of combining genes (T(2;3) rdgC st pp bwD) which are on the autosomes.


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How prevalent is sexual dimorphism?
I'm writing a lab on sexual dimorphism (sex differences in phenotypic traits) and I want to include a sentence in the abstract that states how prevalent sexual dimorphism is. However, I can't find any figures that pertain to organisms generally (or even for a clade).
How prevalent is sexual dimorphism in nature? How frequent is sexual dimorphism beyond primary sexual traits (gonads, gametes etc.)?

Ubiquitous to all anisogamous species - gametes (eggs and sperm) at least are sexually dimorphic

You need to clarify exactly what kind of sexual dimorphisms you are thinking about (or define 'sexual dimorphism'). One common reason that sexual dimorphisms occur is sexual selection - which by definition is affecting reproduction - so to say that sexual dimorphisms are sex differences that don't affect reproduction doesn't make much sense to me.

@fileunderwater all dimorphisms outside of the sex organs.

You might consider the possibility that all species have sexual dimorphisms, even if they aren't readily apparent to our limited and prejudiced by anthropomorphism perceptions, since males and females are able to tell each other apart.

I hope something comes up, but without a clear definition this is a matter of opinion.

I would say that anisogamy, the different gametes such as sperm and eggs, is itself, a form of sexual dimorphism. However, you've since stipulated that you want to know the prevalence of sexual dimorphism beyond sex organs/gametes.
Sexual dimorphism occurs in a vast plethora of traits, at a variety of levels, and in almost all known dioecious species. It occurs even at the level of gene expression in, for example, mice, birds, mosquitoes, fruit flies, nematode worms, humans, and much more. Sexual dimorphism is prevalent and obvious in morphology such as peafowl, red deer, mallards, humans, guppies, fruit flies, horned flour beetles, and much more. It also occurs in physiology, behaviour, and life history traits (e.g. lifespan, ageing).
Simply put, sexual dimorphism is extremely common. It is hard to put a number on it, any studies of sexual dimorphism are likely to be focussed on sexually dimorphic traits (so a meta analysis will likely suffer from publication bias), and not all traits can be easily measured. However, gene expression is a good place to look because many traits (expression level of each gene is a trait) can be sampled simultaneously. This study found that 18% of genes were significantly sex-biased in any one tissue, while this suggests that at various developmental stages it was between approximately (based on table 1) 13% and 61%. Note again, there's not much literature which actually puts numbers on the general frequency and extent of sexual dimorphism. That is generally because, in the relevant research community, the gonads and gametes are included as sexual dimorphisms.*
Also, despite the frequency of sexual dimorphism, it is thought that the evolution of sexual dimorphism is severely constrained by the sexes working from the same genome (links: 1, 2, 3, 4, 5, 6, 7) and sexually antagonistic selection could readily favour further evolution of sexual dimorphism.
In terms of your report, I don't think you would need firm numbers or a citation; it's a well accepted fact that sexual dimorphism is common.* You would be more than fine to say something along the lines of:

"Sexual dimorphism is extremely prevalent in nature, found in a
  range of taxa, and found in a variety of traits."

* These points are based on my experience, I did my phd thesis on the evolution of sexual dimorphism so I've read quite a substantial component of the relevant literature.

I second the comment. Any species that reproduces sexually presents dimorphism. Even S.caerevisiae produces haploid spores with MatA and MatAlpha. Although otherwise indistinguishable, they are dimorphic from a molecular point of view (the expression of the receptor).
Here is a set of figures:
https://en.wikipedia.org/wiki/Mating_of_yeast
"The MATα allele of MAT encodes the α1 and α2 genes, which in haploids direct the transcription of the α-specific transcriptional program (such as expressing STE3, repressing STE2) which causes the cell to be an α cell."

This needs work to be considered as an answer. It's more suited to a comment as it does not attempt to answer the question.

It does as "Any species that reproduces sexually presents dimorphism" and I also mentioned that it traces back to S.caerevisiae, which is one of the simplest model organisms.

The user specified that they want sex differences beyond primary sex traits (gametes, gonads etc.)


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Why are there different species of bacteria?
The usual (high school or intro to bio) explanation for diversification of species comes from multicellular, usually sexually reproducing organisms, and seems to be closely tied to the biological species concept.  It is that once organisms are different enough, they will be unable to exchange genes and therefore gradually become more distantly related.
This is not really applicable to species of bacteria which can exchange genes through horizontal gene transfer (obviously not all can, but many can).  It seems to me that if HGT rates are low relative to mutation rates, the same process of diversification could take place.  However if they are high (and random), it seems like either species would not exist as discrete entities or would exist only because the environment was only favorable to specific collections of genes.
Is there a commonly accepted reason why species should exist among species which have horizontal gene transfers (ie is there a reason to expect that HGT rates will usually be very low), rather than bacteria existing as a continuous gradient?

Yes. HGTs rates are likely to be low because the restriction system digests foreign DNA. Therefore you can note that each bacteria has a unique set of restriction enzymes. Your question seems to consist of two parts 1. How correct is the common definition of a species and 2. Why does HGT not cause all bacteria to coalesce into a single "species". I think it is the second question that you are interested in; am I right?

Restriction system is not the only factor, though. I have to look up on this.

HGT is not very different from sexual reproduction when it comes to speciation - in fact, it's often considered a kind of sexual reproduction. Just as organisms with sexual reproduction (e.g. most animals or plants) form species and not a continuum, bacteria can form species too.


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What type of point mutation and chromosomal mutation cause Albinism in humans?
First of all, I know that OCA1 (Oculocutaneous Albinism Type 1) is autosomal recessive which means that both parents-who are unaffected-have to pass down one copy of a mutated gene in order to activate the mutation (in this case it is Albinism). Based on the following link, "TYR (The TYR gene provides instructions for making an enzyme called tyrosinase. This enzyme is located in melanocytes, which are specialized cells that produce a pigment called melanin) is the only gene in which mutations are known to cause oculocutaneous albinism type 1." Also, there is a table on the website but it does not justify the exact point mutation that causes OCA1...unless I'm wrong.
----> http://www.ncbi.nlm.nih.gov/books/NBK1166/
What type of point mutation and chromosomal mutation?
Point Mutations:
http://www.britannica.com/science/point-mutation
Chromosomal Mutations:
There is good insight on Chromosomal mutations at http://biology.about.com/od/genetics/ss/chromosome-mutation.htm
I would really like help, this information is for my biology project!

I suspect albinism in general due to pigment deficiency is due to polygenic(quantitative) inheritance, that is to say, recessive for all three (?) pigmentation determining genes. Not really a point mutation. However, PKU, as it is due to tyrosinase deficiency, also causes albinism.


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Why is it not advisable for humans to drink distilled water?
Distilled water is pure and it does not contain any minerals, so may not be advisable for drinking.
Although laboratory made distilled water is completely pure, industry made water may still contain harmful impurities.
Also there is some probability of exosmosis into body tissues which may lead to swelling.

What is your question?

If your question is about how to avoid contaminated drinking water by use of distilled water: 1) you can re-mineralize the distilled water or, better 2) use other (cheaper) methods to decontaminate drinking water, depended on the type of suspected contamination.

As you said, distilled water is completly out of minerals/ions. The principle of diffusion is that reagents diffuse from high-concentrated to low concentrated places to reach an equilibrium. So normally, ions from the erythrocytes would diffuse into the plasma to reach that equilibrium. However, it is quite difficult for ions to pass the cell membrane which is not the case for water. So what finally happens is that the distilled water wants to dilute the ions in your erythrocytes, passes the cell membrane and the cells explode because they are too full. As consequence, you die because there is no oxygen transport anymore.

The scenario of erys exploding would necessitate substituting substantial amounts of blood plasma with demin. water.


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Does sickle cell anaemia protect a victim against malaria?
My biology textbook says that a person with sickle cell anaemia is less prone to malaria. Why is that so?
I'm guessing that its because the malarial parasite needs human RBCs for completing its life cycle. So are the sickle-shaped RBCs inhospitable to the parasite? In what way exactly?

The answer to the question of which mine seems to be a duplicate has the following paragraph "Individuals which are heterozygous for HbS alele (which in homozygous state causes sickle-cell anaemia) can catch the parasite, but the chances are bigger, that the infected cells will be phagocytized by macrophages and the parasite will be unable to reproduce in them."

So I do not understand why chances are greater that the infected cells will be phagocytosed by macrophages. I agree that my query is quite similar, but I am unable to fully comprehend the posted answer.

Cells only with HbS (Form of hemoglobin responsible for sickle cell anaemia) have limited lifespan , have changes in shape (due to HbS polymerisation) AND consequently are phagocyted. The heterozygots for HbS have some concentrations of this protein in their RBC, these cells have a bit shortened lifespan, but otherwise can function normally. After infection of such RBC by parasite however, cell has an increased chance of sickling.Sickle cell will probably be phagocytized. Therefore the parazite won't be able to reproduce. Look on an illustration in the original answer, and its article for ref.


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Why is ab initio protein secondary structure prediction less reliable than alternatives?
To predict secondary structure of proteins three types of Algorithms are used Ab initio, homology based and neural networks. Among these neural networks prove to be more accurate and give good results as compared to ab initio, especially when multiple sequence alignment and neural networks are combined the accuracy of results reach almost to 75%. My query is that what actually lacks in ab initio methods which reduced their sensitivity and specificity and lacks the ability to predict reliable secondary structures? (Some of ab initio based softwares that I have studied are Chau Fasman and GOR Method)

Why do you mention specifically GOR methods and Chou Fasman?

Because I studied and used them thats why I have mentioned them as an example, only.

This article may be outdated but they outline three major problems in ab initio modeling that include energy functions, conformational search engines and model selection scheme. Open access.

Preamble
In the comments @CMosychuk linked the most comprehensive text on ab initio I have seen this side of the year 2000 (Lee et al., 2009). It agrees that you've raised a good point.

It is important to acknowledge that ab initio prediction methods
  solely based on the physicochemical principles of interaction are
  currently far behind, in terms of their modelling speed and accuracy,
  compared with the methods utilizing bioinfor- matics and
  knowledge-based information.

This is a good real life example of different philosophical approaches of inductive reasoning and deductive reasoning (AKA top-down logic) behaving as one might expect. Each specific software has it's own problems and advantages and may not fit into the below categories. I'll grossly simplify each approach in crude categories and then broadly explain why errors crop up in them.
Below, we'll discuss ab initio and why it goes wrong and then the alternatives including why they're currently generally more reliable. We'll round up with how ab initio is probably going to become realistically involved in reliable protein predictions.
Ab intio.

Figure showing the broad pipeline difference between ab initio and homology modelling.Nara Institute of Science and Technology.
Ab initio often works on the premise that physical laws can be applied universally in biology. As you are most probably aware, biochemistry is far messier than chemistry and often those physical laws appear bent if not completely broken. The goal of ab initio is therefore to combine physical properties with some fudge factors to account for a complex system. Due to the complexity of the system never being fully modelled, ab initio predictions are limited to what your input is. There are also limitations pointed out in the 2009 article:

potential energy functions.
conformational search engines
model selection scheme

What you can see now is that ab initio is missing something that the others have: biological experimental empiricism. Without that inductive reasoning ab initio modelling is very vulnerable to assuming far too much and oversimplifying the system (This xkcd springs to mind).
Although perfect ab initio prediction is the "Holy Grail" of protein structure prediction, currently if there is homology which provides an experimentally known structure then that is often more reliable.
Ab initio is not completely without merit. For relatively short proteins (100 residues) the accuracy has improved over the last decade (Lee et al., 2009). From the above mentioned article:

...the physics-based atomic potentials have proven to be useful in
  refining the detailed packing of the side chain atoms and the peptide
  backbones.

Homology modelling.
This type of modelling is a safe bet provided that the MSA is available and reliable. The premise here is that if two proteins look similar enough at a sequence level, and you know the structure of one, then probably there is structural conservation as well. The problem is that obviously, those small changes in sequence, or other contextual differences like post translational modifications, localised pH differences etc. might mean that the protein folds differently.
Machine Learning.
Neural networks are a form of machine learning. Conceptually, these use the same assumptions as homology modelling, but on a larger more sophisticated scale (not necessarily an advantage). A good example of “machine learning” winning out in terms of homology clustering and secondary structure prediction is that of HHpred. An algorithm will make subsets of "if" statements. If a protein has a certain combination of "ifs" and "nots" then it's safe to assume other proteins with the same "ifs" and "nots" have similar structures.
You need to know a lot of information about the dataset that you put in, and also one needs to know which of that information is relevant. If these conditions aren't thoroughly complied with the categorisation results will just be amplified errors, arbitrary categorisations, missing categories, or a combination of those three.
It's worth pointing out at this point that most modern secondary structure predictors use a combination of homology and machine learning.
A reasonable ab initio approach.
More recently iterative optimisation based on vague experimental data has become the standard practice shifting ab initio from a top down approach to something more inductive. Kulic et al., 2012 is an interesting example of such a modern holistic approach. It involves an iterative optimisation of ab initio protein structures based on experimentally derived structures.
Another excerpt from the 2009 article.

Thus, developing composite methods using both knowledge-based and
  physics-based energy terms may represent a promising approach to the
  problem of ab initio modelling.


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How does a seed determine when to start germination?
I'm sure there are many different ways for seeds of different species, but what is a general rule? Is it some kind of ideal temperature & wetness that triggers a chemical reaction? What factors stimulate seeds to germinate?

Dormancy breaking (no article on wikipedia?!?) is sure related. As far a I heard, a cherry pit does not germinate unless it had experienced some very cold temperature.

Temperature and humidity are factors. Germination is also controlled by some hormones including Abscissic acid (ABA) and Cytokinins. With sufficient humidity ABA is dissolved and washed away and germination pathway is de-repressed. I had read this long-long time back; I'll verify this and post an actual answer.

Certain conditions are necessary for seed germination:

Moisture — seeds dry out during dispersal, but at germination the cells need to absorb water in order to rehydrate so that metabolic reactions can take place, which will eventually lead to the growth of the embryo tops and shoot. Furthermore, some seeds contain a hormone that inhibits germination and water is needed in order to wash it out of the seed. The water needed for these processes is absorbed by the micropyle.
Warmth —  many of the metabolic events of germination use enzymes, and these are sensitive to temperatures. Temperature will often be used as a trigger for germination.
Oxygen — many of the metabolic events that occur during germination use energy. This energy is produced by aerobic respiration.

Many metabolic processes take place at the start of germination, such as the synthesis  of giberrellin, this is a plant hormone that stimulates mitosis and cell division in the embryo. Other plant hormones include Abscisic acid (ABA), which regulates seed dormancy and germination. It has been found to stop germination once it has been placed in the soil, it causes the seed to enter a period of dormancy. This allows the seed to remain dormant until when the conditions are more favorable for the seed to grow.


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How did dolphins acquire their dorsal fin?
I had been thinking bout atavism when I saw a picture of a dolphin. I had seen it before, but suddenly the dorsal fin startled me.
How did this dorsal fin evolve? Is it some atavism from eons ago, a revived feature, or a new development altogether? (Strong evidence of the former would be if the genes ruling dorsal fins in fish and dolphins would be similar.)
I've seen this How and why did mammals go back to the oceans?, but it doesn't ask nor explain about the dorsal fin.

Short answer
I reckon that the dorsal fin of sea-faring mammals are a new development altogether.
Background
The presence of a dorsal fin is one of the defining characteristics of fishes like sharks. Mammals that returned to the sea generally lack a dorsal fin.
However, killer whales and dolphins, while being mammals, indeed do have dorsal fins. In contrast to the dorsal fin in fish, these structures do not have bones (Fig. 1). Instead, the dorsal fins of mammals are made up of dense tissue, somewhat like a ridge of thick, folded skin. Hence, it is not a 'revived structure' that was 'activated' from a latent state in mammals.
Hence, given that mammals returned to sea later in evolution and lacked a dorsal fin on land, I would deduce from these data that dorsal fins are an example of convergent evolution where analogous structures with a similar function (like in fishes, the dorsal fin acts as a stabilizer or a rudder in mammals (source: The National Marine Life Center) develop from unrelated bodily structures. Hence the genes involved may, and likely are, different.

Fig. 1. Dorsal fins of a killer whale (left) and in a fish (a redhorse on the right). sources: Sea World and Mosxostoma

This paper here sums up cetacean evolution very well and also explains the dorsal fin: https://doi.org/10.1016/j.ympev.2012.10.012

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


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Am I a lobe-finned fish?
I really wish this question only contained the title and tags, but the website forces me to write some text.

Yes. All tetrapods are descendents of lobe-finned fish. (https://en.wikipedia.org/wiki/Tetrapod)

@Gyro How does that make him a lobe-finned fish? I've never met lolmaus-Andrey Mikhaylov, so you could be right, in which case I'd be intrigued to know how he used his little fins to type this post.

(My half-finished comment somehow got lost on my browser). I take the question a little broader.  He, (and me, don't know about you(?!)) is a descendent of lobe-finned fish. And, of course, I'm not my mother nor my father.  He's a lobe-finned fish in version 42k (call it that way) with shrinked dorsal fins, several times re-designed lungs and skeleton, uncountable changes on immune system and many other amendments,

The answer depends on whether you want to know in the common sense or in the modern scientific sense.  The phrasing of the question suggests you want to know in the common sense, but the choice of the phylogenetics tag indicates you want a scientific answer.
In modern biology, the term lobe-finned fish would be formally taken as (an imprecise) convenient term for the clade Sarcopterygii.  Presuming you are not an alien or computer but are human, yes, you are a lobe-finned fish (a member of the class Sarcopterygii).
In the common sense, no, you are not a fish, lobe-finned or otherwise. This would also be the answer under the old tradition of zoological taxonomy, which was based on taximetrics (measurement of an organism's form) rather on the modern phylogenetic (evolutionary relationship) basis for biological taxonomy.

I would add "ecological sense" to "common sense". Ecologically, humans are not lobe-finned fish: they do not live in water, and don't use fins for swimming. But their body structures are inherited from animals that did so.

@mgkrebbs, thank you for your answer. It explicitly covers my short question. ♂

@bli So? Beavers live in water and have flappy tails. Does it make them fish? Medieval monks believed beavers to be fish, which was a loophole allowing eating meat during fasting. Very convenient, but meaningless otherwise.

@lolmaus-AndreyMikhaylov That's a very good illustration of the fact that classifications may have a purely practical goal!

A practical goal of fabricating a rule by neglecting the true nature of things?


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How to Download the broadpeak files from the encode chip-seq experiment matrix?
I have tried the SqlDatabase of Encode opened it trough R ,i have tried other packages in R, i have tried the ENCODExplorer package but none of them seems to do what i want. I have an app that asks the user which cell type and which antibody factor wants to choose in Shiny. These cell types and antibody targets are drawn from chip-seq matrix here https://genome.ucsc.edu/ENCODE/dataMatrix/encodeChipMatrixHuman.html. I want to download the .broadpeak file from the experiment that was made using the two selections of the user . I cant find where the data from this matrix are stored and for sure they are not stored in the new website database of ENCODE.
Does anyone has an idea ??
These are some notes not all  from a what i searched

1)https://www.bioconductor.org/packages/3.3/bioc/vignettes/ENCODExplorer/inst/doc/ENCODExplorer.html
New portal of ENCODE https://www.encodeproject.org/
#Load the ENCODExplorer
suppressMessages(library(ENCODExplorer))
#Find all the files from the experiment with biosample from A549 human cell using H2AFZ as antibody target
query_results <- searchEncode("a549 chip-seq homo sapiens h2afz") or
search_results <- searchEncode(searchTerm = "a549 chip-seq h2afz", limit = "all")
//downloadEncode(resultSet = search_results, resultOrigin = "searchEncode", format = "bed_broadPeak")
cant find any broadpeak files

2)Connect to an Oracle database(Encode sql Database) using R
http://rprogramming.net/connect-to-database-in-r/
channel <- odbcConnect("genome-mysql.cse.ucsc.edu", uid="genomep", pwd="password", believeNRows=FALSE)
http://stackoverflow.com/questions/15420999/rodbc-odbcdriverconnect-connection-error
#Database schema
install.packages("RMySQL")
library(RMySQL)
drv = dbDriver("MySQL")
con = dbConnect(drv,host="genome-mysql.cse.ucsc.edu",user="genomep",pass="password")
album = dbGetQuery(con,statement="show tables")
Tables_in_hgcentral
1          blatServers
2                clade
3                 dbDb
4             dbDbArch
5            defaultDb
6               gbNode
7          genomeClade
8            geoIpNode
9            hubPublic
10           jorgetest
11       liftOverChain
12       liftOver_bkup
13           sessionDb
14   tableDescriptions
15            targetDb
16              userDb
17           wikiTrack
3)Not working-->https://www.simple-talk.com/sql/reporting-services/making-data-analytics-simpler-sql-server-and-r/

There is an FTP link from where you can download the data (I had downloaded it from there). In any case this question is off-topic because it is not at all about the bioinformatics aspect of the data.

http://hgdownload.cse.ucsc.edu/goldenPath/hg19/encodeDCC/wgEncodeRegTfbsClustered/

I'm putting this question on hold because it is not about biological or bioinformatics principles.


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What is the reason for fear induced defecation?
I started to handle mice for my job and noticed that they tend to defecate and/or urinate when they are scared. The fear is induced by me, because I need a long time (due to inexperience) to grab the mice and then move them from one cage to a new one. My question is why?
I tried to look up literature for this behavior and there are different fear behaviors for different animals some shake in fear, some play dead but I could not find something for fear induced defecation. Therefore my question: What is the reason behind the "Fear induced defecation"?
I am especially interested into the neuroscience pathway behind it.

Just a guess - but this could be a mechanism to try to deter their attacker, the smell of urine and faeces may ruin the meal

Just to share, if I'm nervous or am afraid, I feel like saying Hello to the bathroom.

Even if you're a pro, handling certain strains of mice for any length of time will cause them to void. It's not just you :)

If your mice are stressed or scared during those manipulations, as we can expect them to be, defecation can be a consequence of the "Fight-or-Flight response": in this situation, the organism try to focus its energy to act quickly, and a wave of specific neurotransmitters (noradrenaline in particular) is released. In consequence, mice's bladders relaxe, which cause them to urinate, the digestion stops, but the transit of the faeces in the colon is accelerated: they defecate.
This is all controlled by the activity of the sympathetic nervous system, which secrets acethylcholine and noradrenaline.


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Why doesn't hair grow all over your face?
Why doesn't hair grow all over your face?
Surely hair on a face would have blocked the sun and kept it warm.
Or perhaps through natural selection we opted for hairless faces over hairy ones?

Why doesn't hair grow on the face- because there are no hair follicles in that region of the skin. Actually, in males the hair does grow all over the face except the eye region and forehead. Hair in those regions would block the vision.

Actually, we do have hair over most of our faces - it's just mostly vellus hair and not as visible.


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Is there one centomere for the two chromatids in a dyad?
I have no explanation for this. It is all I have to ask.
Thank you

Each chromatid has a centRomere. A chromosome is a pair of sister chromatids (general term)... also known as a dyad in meiosis. Tetrads are the precursors to separated dyads in meiosis. Having centromeres is super important for being able to pass down genetic information in eukaryotic cells. Prokaryotes and archaea have similar structures to physically keep track of their DNA.


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Is it possible for two creature in the same order and have odd haploid chromosome species to reproduce
Take the degu and the rat for example.
The degu has 29 chromosome pairs
Rats have 21 chromosome pairs.
They are only share the same order ( Rodentia )
Would it be possible for them to reproduce?
( also , before someone says " they're not the same species , so obviously not" allow me to remind you of the mule , and the europeans have 1 - 4 percent Neanderthal )

On the side of the question, there are a few words on the concept and definition of species that you might like to read.

What point are you trying to make about having odd number of chromosome pairs? What difference does it make?


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Where can I find SSR and/or SNPs that locate RC1 genes in Soybean?
Where should I look to find SSR and/or SNPs that locate RC1 genes in Soybean?

SoyBase has Illumina SoySNP50K iSelect BeadChip and they've identified soy SNVs. You could find them in dbSNP - identifiers starts with 'ss'.


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Prediction of transmembrane beta barrels?
I studied that prediction of transmembrane alpha helices is more easy and accurate and also good algorithms are available for their prediction. But when we move towards prediction of transmembrane beta barrels (cylindrical structure composed of anti parallel beta-sheets) then for their prediction only a small number of algorithms are present which also don't give reliable results.
My query is that Why it so? Why the prediction of transmembrane beta barrels is difficult and why developers can't develop reliable algorithms for this purpose?

This might just be me being cynical, but isn't it predominantly to do with them being a lot more rare than TMH? Less cynically I would also say that the hydrophobic signal for a TMH is usually very strong. Perhaps TM beta barrel is more nuanced when compared to non-TM beta barrels?

I could tell only from my pretty poor experience.
I had all PDB entries processed with DSSP and then I've tried to find any trends in amino acid preferences. I did not find any except the pretty obvious absence of proline in double (i.e. with two neighbours) strands. Also, negative charged amino acids (I, L, V) were slightly more frequent in parallel strands. After that, I tried a sort of naive Bayes classifier for the amino acid and it's neighbours in two neighbour strands and +/-2 amino acids up/downstream. For single\double parallel\antiparallel strands, the prediction precision was about 60%.


text:
Why do the vines change their spinning direction?

Look at the vines holding onto the lattice. The "vine springs" change their spinning direction in the middle. Why? And how do they achieve this?
(By the way, what's the name for this plant? Is is correct to call these "springs" vines?)
Edit: I notice that some vines fail to get in touch with the lattice, in such case they still change direction.

I believe what you are referring to are tendrils, the positively thigmotactic curly things that help some vines attach and climb. That sure looks like a cucumber to me, certainly a cucurbit anyway.


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Can exhaustive algorithms produce MSAs that are suitable for 3D structure modelling?
While predicting 3D structure of a protein through homology modelling, the most important step is Multiple Sequence Alignment of template sequences with the target protein whose 3D model is to be predicted. At this step according to my book for Multiple Sequence Alignment, the either T-coffee or Praline software is used; these programs are heuristic in nature and based on a progressive alignment method. There are always concerns regarding the sensitivity and specificity of heuristic  algorithms.
To avoid that problem I imagine one option is to use exhaustive algorithms. During this alignment step, which is very critical in 3D modelling, can we use exhaustive algorithms to yield good models?

Which exhaustive algorithms are you talking about? Finding the right homolog is, AKAIK, an NP-complete problem and that's why heuristic methods are used.

I am talking about Dynamic programming modeling as it is exhaustive.

@WYSIWYG can you explain your answer please, so that I can develop better understanding.

Heuristic/greedy algorithms are faster than DP. I am not an expert in computer science to explain this in detail. You can have a look at this SO post.

No.
Methods for multiple sequence alignment (MSA) like T-coffee, which you mention, and Clustal (http://www.clustal.org), which is also widely used, employ heuristics for the alignment for the very good reason that exhaustive algorithms to do this are NP-complete.
You mention the dynamic programing algorithm as exhaustive in your comment. Alignment of two sequences by dynamic programming has an order of time complexity (big O) of $n^2$ and may take a few minutes depending on sequence length etc. Alignment of three has a big O of $n^3$ and can be done if you have lots of time on your hands, but it should be obvious that that's the limit to the number of sequences that can be aligned using dynamic programming.
There's no shame in heuristics. Perhaps the most widely used bioinformatics program in the world, BLAST, employs a heuristic. (And your brain makes decisions that your life depends on every day using heuristics.)
The methods that use heuristics for MSA have been successively modified to deal with known factors that can cause problems, so often they perform very well. How can you tell? What you need to do in using MSA programs is to perform a "sanity check" on any alignment that the programs produce — does it look reasonable, has it matched up similar regions well or are there vast gaps introduced or obvious regions of homology missed. And if you are doing 3D modeling and you don't get an alignment that looks good, then your modelling isn't likely to work.
Finally you always have to consider the possibility that there aren't any proteins of known structure that are similar to the one you want to model so you'll never get a good MSA.


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What is the speed of blood?
The speed of blood may vary from one place to another and may be quite low in the tiniest vessels compared to the biggest one. What is the speed of blood while exiting a normal human heart?

This question could be read in a more interesting way: given an injection in the veins or my left arm, how long would it take to reach my brain, heart, liver? Or, if some organ sheds some hormone, what time will it take to reach other organs?

@GyroGearloose For the round time there is an old paper which I can add later. They injected substances into the arm and measured when they could find them again.

http://biology.stackexchange.com/q/43360/21844 asks at least part of my followup question.

As you note yourself, this depends strongly on the vessel that you are studying. I found this table in reference 1:

It lists speeds between 34 and 45 cm/sec for the inferior vena cava and 12 to 16 cm/sec for the superior vena cava.
For the capillaries I found this table in reference 2, which measured the blood velocity in cats. Nevertheless I think this approach is also useful for an approximation for humans since the capillary system should be comparable:

It lists velocities between 0,2 and 2,7 mm/sec.
References:

Velocity of blood flow in normal human venae cavae.
Regulation of blood flow in single capillaries.


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Is an athlete's heart rate after exercise greater than a non-athlete
I was just wondering
And if it is greater or lower how does this benefit an athlete
Also what is the averaged number of heart beats per minute

Do you mean for example a) if a trained 5 k runner and a regular person both ran 5 k in the same time, or b) if a trained athlete and a regular person both exercised as hard as they can. For your second part, do you mean are people with lower natural heart rates more/less able to become athletes? Also for your third part, do you mean resting heart rate?

If they both ran througsame distance

For second part if persons with a lower heart rate better abled to become athletes and for the third part the resting heart rate

The answer is that resting heart rates vary a lot.  Typical rates can be found with Google.  For an active person or athlete, capacity increases with training (that's what training is FOR), so (all else being equal) doing the same distance/time causes less increase in pulse rate.

@ user21887- The Heart can only endure a certain amount of pumps and then it fails, So speeding up the limited amount of pumps just for exercise is only shorting your life expectancy in reality.

@ user21887- Look into how many deaths occur in Soccer from heart failure, Those guys were in absolute great shape, How did they have a heart attack? They used up there limited heart pumps from years of extreme exercise and died a rather premature death in my eyes. If only they knew it was self involuntary.

Whilst exercising, the heartbeat of a non-athletic individual is faster than that of an athletic individual. The untrained heart beats faster, but less efficiently than that of an athlete. Both the maximum, and the resting heart rate of an athletic individual are lower than the average heartbeat. In a non-athletic individual, the heart rate when resting is about 60 to 90 beats per minute, whilst in athletes it can drop below 40 beats per minute.

When you exercise, the heart works harder when other muscles in the body pump more blood back to the heart. The major muscles of the legs have large veins that will fill during the relaxation stage of the movement, and the muscle contraction in the active movement pushes the blood back into the circulatory system. Increasing blood flow triggers a faster heartbeat. Because the heart muscle of conditioned athletes enlarges and strengthens, the hearts of athletes pump more blood per beat. 1


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Infer type of nucleic acid based on number of nucleosides
Let's say we analysed a nucleic acid and found out that it had 20% adenosine, 25% guanosine, 40% thymidine and 15% cytidine. We know that A always pairs with T and G with C.
So, based on these numbers, could we infer that the nucleic acid must've been single-stranded? Or could it be that it was a double-stranded DNA, but just not perfectly matched? Is it even possible for DNA to not perfectly match? Say like a zipper that is shifted?

There's 10% of your nucleic acid that's not A, T, G or C - you may have made a major discovery!

@HarryVervet Haha. Sorry, those were arbitrary numbers. Edited.

Though base pair mismatching is very common and is the basis of evolution, such a big violation of Charagaff's rule (in DNA where just 1% would mean thousands/millions of B.P.s) would only prove that it is ssDNA.

@aayushsrivastav Awesome! Haven't heard of Charagaff's rule before. That would explain the assumption then.

I'd say it depends on how you 'analyzed it'. You can also have a mixture dsDNA and ssDNA, for instance 20% polyT oligos and 10% polyG oligos.


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Protein tertiary Structure formation
As we know that coils and loops are evolutionary variable regions where mutations,deletions, and insertions frequently occur. So does it mean that they don't have much role in the structure of protein? If it so then what are the factors for the protein core structure formation?

I think it would be useful in this case to look into instrinsic disordered proteins. Not to say that coil or loop regions have no role in the structure of a protein, but in avoiding the expression of a completely broken construct, protein domains including disordered or linker regions can tolerate mutations of specific types that don't 100% inactivate a critical region. For example, amphipathic residue substitution to another amphipathic residue. The reason we don't see functional valine -> lysine mutations, for example, is they seriously mess up the protein, even from a coil domain.

This is a really big question. Are you asking specifically "How and why do disordered loop regions pack the way they do in protein structure"?

Firstly, is important to remember that protein structures are dynamic due to the torsion angles between the N-terminal and C-terminal bonds. There are different conformations to expose different sequences to the outside of the protein to react/catalyze. So there is no one perfect conformation for a protein in a biological system.
The best models we have are taken through x-ray crystallography of the crystalized protein structure. This static portrayal of the protein may be inaccurate, because the biological system will expose the protein to different hydrophobic/hydrophilic interactions than the affect of the protein to itself.
Anfinsen's experiments were able to definitively prove the a proteins structure is coded by its amino acid sequence. To answer your question, this sequence is primarily responsible for a protein's core structure formation.
It is still incredibly difficult to predict the structure of a protein using its amino acid sequence. The tertiary structure is a product of salt bridges, hydrogen bonds, hydrophobic forces  and polar attractive forces within the molecule  (disregarding a proteins possible quaternary structure ). Scientists  (from what I believe is Yale, but I may be incorrect), have been trying to find a pattern using computing software for years. As of right now, we cannot purely use amino acid sequence to determine a protein's dynamic structure.
Loops and coils on the outside of proteins because they tend to compose of polar or charged amino acids. Hydrophobic amino acids tend to get pushed towards the center of the protein structure. This occurs because polar residues do not affect affect the entropy of water molecules as much as the nonpolar residues (in the system).
Many deletions/insertions occur during specific transition states that the protein is in. Enzymes actually target specific conformations of a protein that best produces the P product. See image:

Hi and welcome to Bio.SE :) You hit on a really important point about the amino acids fundamentally determine structure. Could you expand on that a little?

Hi James. I edited my post to elaborate more on amino acid sequence and protein structure. This is still an area of continuing research, so I can not provide a definate answer without the risk of being incorrect.

Solving the 3D structure of a protein is complex problem. There are multiple layer of informations that come into play.
The first level of organization comes from secondary structure, which is in turn dictated by the AminoAcid sequence. There are common secondary structure motifs such as alpha-elices and beta-sheets. The combination of several 2nd structure motifs will give rise to more complex motifs and eventually to a local 3d structure. This local 3D structure is called a "domain" and is a minimal independent functional unit of a protein, which means it can often be cut out from the rest and retain its function.
Given this overview, the first layer of selection comes from creating 2nd structures which depends on the charge and size of amino acidic residues.
Mutations that destroy the creation of these secondary structure motifs will ultimately have an effect on the final 3d structure.
Loops in a way connect these more rigid motifs and therefore they are less likely to be subjected to evolutionary selection.
However in the end it all ties down to function. If you have a loop within a catalytic site inside a protein, the sequence in the loop will be greatly preserved because size and charge will strongly dictate its interaction with substrates.
Hope this helps.