text:
Can you measure plasma glucose with a regular glucose meter?
I'm wondering if plasma glucose can be measured with a regular glucose meter and strips like this. I know these meters are normally used to measure whole blood glucose, but can they measure plasma glucose levels as well?
Thanks.

What is blood: Mostly red blood cells, white blood cells and serum. So if you want to divide cells and serum, you should be able to measure the serum glucose levels with equipment like this as well.

ABSOLUTELY NOT - using those meters for measuring glucose in fluids besides blood is inaccurate and dangerous - you should never do that clinically or experimentally

Excellent question... "Can you measure plasma glucose with a blood glucose meter?"
Absolutely Not! In my experience, if you try to measure plasma glucose with a whole blood glucose meter the results are highly variable for a number of reasons (mentioned below). Using blood glucose meters to measure plasma glucose is dangerous. The meters are calibrated for whole blood and not plasma, which is chemically different and will yield different results. Depending on the clinical situation (or experimental situation), the results can be significantly different and non-linear across a huge spectrum of concentrations.
Here is a nice link from the University of Virginia demonstrating the basics of how one type of these meters works.
There are a number of types of glucose meters commercially available to the public as well as healthcare facilities. Most of these meters use varying solid-state chemistry techniques to drive the production of an electrical current that can be measured by the glucose meter. In other words, when the blood is taken up by the strip in the meter the glucose takes part in a redox chemical reaction that creates a small "electrical current" that is detected by the meter. The amount of glucose in the sample is proportional to the electrical current produced. However, there are a number of assumptions that the meters make (which can differ between meters). One of the most clinically significant assumptions is that the meter assumes that the hematocrit (i.e. the percentage of blood volume that is erythrocytes) is normal or approximately 45%. If you use these types of meters on plasma (which has no erythrocytes in it), the chemistry is inaccurate because the meter "thinks" all the glucose that it is detecting is actually dispersed within a pool of erythrocytes in a hematocrit of 45%. There are a number of other issues and important points discussed in this review.
When the clinical trials (e.g. NICE-SUGAR) began showing that intensive glucose control was associated with improved mortality, clinical practices changed from keeping blood glucose concentrations in critically ill patients between 150 and 250 mg/dl to a much lower concentrations (i.e. 80-120 mg/dl). As these new guidelines began rolling out, there were a number of subsequent studies that showed that intensive glucose control was actually associated with more frequent hypoglycemia episodes. There were likely a number of issues to explain this, but one of those was that if your meters were not correcting for differences in hematocrit the blood glucose meters would read spuriously higher than what the true measurement was (thus, you could be treating someone with insulin to lower their glucose that was 160 mg/dl - when in true the value was much, much lower).

I assume you mean that using the measurements is dangerous. There is nothing dangerous about doing the measurement, right?

Dangerous, if the patient is monitoring their blood glucose concentrations in order to maintain a safe bodily state. I.e. if the pateint has Type 2 diabetes. The incorrect reading could lead to incorrect administration.

@daniel yes - using the measurement is potentially very dangerous – that's what happened in some of the early intensive glucose control studies. Glucose was being monitored with glucose meters at the bedside and those meters were giving inaccurate results because the meters assume certain physiological parameters like hematocrit that were not normal. The patients were then getting treated with insulin who had normal blood glucose but high "measurements" – and then those patients were becoming hypoglycemic and having adverse events because of insulin they didn't actually need.

While I agree with the basic conclusion - that glucometers do not reflect plasma glucose, I think you're assertations can be misleading. Glucometers can be invaluable in predicting plasma glucose.  Also, this is a funny phrase "associated with improved mortality". Better death? Should that be "improved mortality rate" or something similar? This language is a bit loose.


text:
Convergent evolution of fruits
Many fruits are not homologous, originating from different parts of a plant. Yet they all have similar properties:

Ripe fruits all have yellow to dark red color
They all have a lot of water and sugars, even in dry climate where water is in shortage.
Besides sugars they usually have acids making them sour to sweet in taste

I understand that these possibly developed as a contract between the plants and the animals in that the plant would provide beneficial fruit tissue so that the animal to swallow the seed so to propagate it for longer distances.
But I wonder, why there are no fruits that would imitate the taste of meat, nuts, seeds,  foliage, grass, mushrooms, roots, milk and other food sources, common for the animals?
Why there are no salty fruits for instance or those rich in proteins rather than sugar and water, or having the smell of carrion?

I appreciate the intent of your question but I suggest you think more broadly about what are fruits. Coconuts are fruits. Dandelions produce fruits. Durian fruit smells terrible to most people. Look at samaras. Any seed-bearing structure on flowering plants is a fruit.

@3cat under fruits I explicitely mean those tissues intended to be eaten by animals. I am not interested in the other varieties. I ate durian, and as it was fresh I did not notice any distractiong smell. Do you claim it is not intended to be eaten? What's the purpose of it then?

Howe and Smallwood (1982) provide a nice review of the many methods of seed dispersal that have evolved in plants. The review is broad but they do have a section on frugivory.  They highlight hypotheses developed by McKey, and Howe and Estabrook (see Howe and Smallwood for citations) that suggest plants may use one of two strategies.
One strategy is the "high investment model." Plants invest lots of resources to produce large seeds and nutrient rich fruits. THe hypothesis is that these types of fruits tend to attract relatively few but specialized frugivores that are will to invest the energy necessary to find these types of fruits and their associated nutritional reward.
The second strategy is called the "low investment model." In this model, plants invest little in individuals seeds and fruits but produce an abundance of them. The hypothesis is that these types of fruits will be eaten by as many different potential seed dispersers as possible. These tend to be very small or starchy although they can still be colored as you describe.
Other factors also come into play. For example, tropical fruits tend to have large seeds and nutrient rich pulp while temperate fruits tend to be smaller and offer less nutritional reward.  All of this is placed in the context of the community diversity of frugivores. The Howe and Smallwood paper was an interesting read.
A paper by Gatier-Hion et al. (1985) looked at the characters of fruit choice and seed dispersal mechanisms by tropical forest vertebrates. The showed the relationships between fruit characteristics and the corresponding frugivores. They looked at 122 different fruit species and the frugivores that consumed them.  Their results showed that fruits tended to separate along one of three axes:

Heavy, indehiscent fruits with fibrous flesh and well protected
seeds vs light, dehiscent fruits with unprotected seeds. Many of
small fruits are red,
Lots of seeds produced (typically the the large indehiscent) vs few
seeds produced, and
Juicy and brightly colored fruits vs dry and dull-colored fruits.

Figure 2 from Gautier-Hion et al., shown here, shows the relationship between different frugivores and the fruit types.  Notice that small granivores, which are frugivores, don't eat large, juicy fruits. They consume lots of small green or brown grains that are easy to manipulate and produced in high quantities.  Squirrels are similar.

Thus, as you suspected, fruits and seeds have evolved in response to their frugivores but the fruits do not always have the traits you listed. I think, but do not know for certain, that the fruit traits you list are the result of selection being driving by the frugivores. The sugars provide lots of quick energy, which is necessary for active animals. The carbs probably provide a much greater nutritional reward than salts or proteins (which are present anyway). The colors may help the fruits to stand out against the green foliage (for organisms that are not red-green colorblind). These traits probably provide the greatest reward (lots of energy) with the lowest energy investment by the frugivore (easy to find).
Throughout, I've assumed natural conditions and not fruits modified by artificial selection for human consumption.
Literature Cited
Gautier-Hion, A., et al. 1985. Fruit characters as a basis of fruit choice and seed dispersal in a tropical forest vertebrate community. Oecologia 65: 324-337.
Howe, H.F. and J. Smallwood. 1982. Ecology of seed dispersal. Annual Reviews in Ecology and Systematics 13: 201-228.

Squirrels mostly eat nuts which are not intended to be eaten because their seeds are destructed in the process thus there is no surprise that nuts typically have no attractive color.

On the other hand, squirrels often take the nuts and bury them but do not later eat them. Dispersal from the plant's perspective has occurred.

How are you defining fruits? Because if you count any seed body of a flowering plant, you must include several items commonly described as vegetables, including pumpkins, zucchini, squash, cucumber, peppers, etc. And there are other colors of fruit, such as blue berries. These all serve similar functions for the plant, something eats the fruit, then deposits the seeds somewhere else.
If you define a fruit by what the average person calls fruit, then you've biased the population because humans have selected for juicy sweet tasting fruits over thousands of years of breeding. Humans like large sweet tasting fruits, so they selected for those traits, driving most fruits to have those traits. Wild fruits probably have much more diversity, and there would much less distinction between fruit and vegetable.

The most accurate way to define fruit is by using the botanical definition. Seeds are not fruits so nuts (in the sense of walnuts or nut mix that you buy at the store) are not fruits. Fruits are the seed-bearing part of the flowering plant.

I made an edit to remove the reference to nuts. By your definition many vegetables are still fruits.

Such as? Tomatos, widely perceived as vegetables, are fruits. Chili peppers (bell, jalapeno, habanero, etc.) are fruits. If it bears seeds, it is a fruit. Fruits, by botanical definition, bear seeds.

That's what I was getting at. I erroneously included nuts as fruits in my answer, and that reference is removed. Was trying to point out that fruits did not all go through the convergent evolution described in the question because not all fruits are sweet, many food items commonly considered vegetables are in fact fruits.

Cucumbers are green just because we eat not ripe cucumbers. Ripe cucumbers are yellow. Blue berries are just too dark red with a fungal film on the surface. I define fruits as the tissues intended by the plant to be eaten by the animals.

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text:
What's the purpose of colorful mushrooms' caps?
What's the purpose for many mushrooms to have colorful caps? Is not it is in their interest to hide as well as possible? Or there are mushrooms that propagate by being eaten, like fruits?
Why not all the mushrooms are poisonous?

Mushroom is actually the reproductive organ of the actual fungal body beneath the surface. It have a high surface area to disperse or spread the spores.
If the eating predators are low or dispersing is not an option, then it will need other organisms to attract to that they can be spread, so they are not toxic. Analogous to fruits, they uses different colors which are non-toxic to attract.$^1$
Whereas brightly colored mushrooms are less toxic, whereas, most toxic ones are either brown or white.$^2$
Edible Mushrooms

Toxic Mushrooms:

Source:

Why do mushrooms come in so many shapes and colors?
Mushroom poisoning

Image Source:
https://www.etsy.com/listing/93680839/antique-1900-edible-fungi-print

Are you claiming all color is due to toxins??? Then you have to explain why non-toxic Russula has the red cap https://en.wikipedia.org/wiki/Russula and why the most toxic species such as the Amanita phalloides are usually uncolored https://en.wikipedia.org/wiki/Amanita_phalloides

@Anixx: Thanks for the pointer! I hope it is correct now.

It's possible some colored nontoxic mushrooms could be mimicking toxic mushrooms. Very interesting, though, that in some cases it by more advantageous to attract herbivores/potential dispersers.

galerina are orange and highly toxic

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text:
Which turtle species was on board the Iranian Space Agency launch in 2010?
They are seen briefly in this video:
https://www.youtube.com/watch?v=nZoNdf6hlII
The launch made international news, but there was no mention of the species.
Here's the entirety of Wikipedia's description of the launch:

On February 3, 2010, ISA launched a Kavoshgar-3 (Explorer-3) rocket with one rodent, two turtles, and several worms into sub-orbital space and returned them to Earth alive. The rocket was enabled to transfer electronic data and live footage back to Earth. The Iranian Aerospace Organization (IAO) showed live video transmission of mini-environmental lab to enable further studies on the biological capsule. This was the first biological payload launched by Iran. Iran is the sixth country to send animals in space.

The Farsi language Wikipedia entry on the launch (کاوشگر ۳) does not appear to contain any more information on the species.
I've tried searching Google Scholar for papers, but my search turned up nothing. I also tried asking Reddit on the day of the launch, also without results.
Bounty Note: I appreciate all answers, especially from herpetologists. However, the bounty will only be awarded only for a reliable, third-party, published source (i.e. acceptable for use on Wikipedia).

We had this question here a while ago, it seems to be deleted. I looked for an answer back then and I wasn'T able to find one, so it has probably never been published.

Thanks for looking. It was deleted shortly after posting because it was cross-posted to Space (after a suggestion here), and then apparently you're not allowed cross-posting so the Biology one was deleted. It was only here for a short time. But it seems they couldn't find an answer so it's been sent back.

I apologize for the skepticism, but is there any indication this was a real turtle?

Can you try posting this on Skeptics SE?

Sorry, too big for comment!
It's actually hard to tell, as there is no official claim on this one.

Photo Link: http://youtu.be/nZoNdf6hlII?t=17s
Al I guess is, it can be:

Native breed of Iran like, Spur-Thighed Tortoise (Testudo graeca)

or something like this

(source: deserttortoise.org)
Trachemys scripta elegans

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text:
For how long can a person drink sea water?
How long could a person of lets say 18 years be able to drink sea water without getting too much into trouble ? Or can a person drink it without noticing that it is a very bad idea ? I don't mean in just 1 drink session but like can one manage a day or two ? Can one drink it and go to sleep and be still healthy (although very thirsty) in the morning ?
(this is just a hypothetical question, I'm not a scientist at all, I'm not sure what tags to use actually)

Additional brainstorming:

kidney failure
any other organ failure
dying of thirst
...

I don't remember were I read this. A shipwrecked man drank seawater to stay alive. He claimed that the seawater he decided to drink was to his surprise fresh water. He said that there was a pocket of fresh water floating about on the surface of the sea. Through a recent Google-scan I learned that saltwater is heavier than freshwater. After a a heavy downpour at sea the surface water would be less salty than the rest, wouldn't it? It was said in the article I read that sea water is 3.5 % salty and that the body can just deal with water that is less than 2% salty.

https://www.bbc.com/news/world-asia-45623130 This guy did it for 49 days involuntary .

It takes about 2 weeks under ideal conditions, and as little as a few hours under the worst conditions, dehydration is very strongly affected by things like environment and activity level. Your best bet is to just use information on dehydration as if they were not drinking anything and just use the shorter estimate since sea water is not helping at all.

(source: free.fr)
Alain Bombard
He is a french biologist who voluntarily tested how many days a man can survive drinking seawater and how?
Biologist point of view
Sea contains ~3.5% of salt$^1$. Our kidney separates the waste from water and excrete them in urine provided the salt content is less than ~2%.$^2$
So, it will take the water already present in the body. Causing excessive thirst and dehydration, eventually cause death.
Alain's Experiment

Just one spoon of seawater at 20 minute intervals, drinking very
  slowly and letting the saliva in your mouth reduce the saline in the
  water you have swallowed.

Though he survived 65 days (From and including: Sunday, 19 October 1952
to Tuesday, 23 December 1952, ~4,400km) of his journey and lost 25 kg of weight, this result is never successfully reproduced.
Source:

http://oceanservice.noaa.gov/facts/whysalty.html
http://paradise.docastaway.com/drinking-sea-water

The results of Bombard, are, nicely said, at least doubted.

@Chris I think it's more like no one in their right mind believes it....

@caseyr547 The accusations agains Bombard where that he was supported (also with food and water) by a ship during his time on the atlantic ocean.

Bombard had a rain harvesting system on his craft which he drank daily, he was NOT drinking only sea water. By his own admission without rain and fish fluids the sea water would have killed him, the media grossly exaggerates what he did.

After drinking 1 liter of seawater with 3.5% salt your kidneys need to excrete at least 1.5 liters of urine in order to maintain normal blood sodium levels, which leaves you with 0.5 liter of negative water balance. This occurs because the kidneys have a limited ability to concentrate urine; it's explained in more detail here.
When a negative water balance results in 1% loss of body weight (0.7 kg in a 70 kg person), which could occur after drinking of about 1 liter of seawater, you can already experience dehydration symptoms, starting with thirst, dry mouth, pounding heart and dark yellow urine, followed by fatigue, dizziness, nausea, headache and eventually coma and death, that can occur at about 10-15% loss of body weight (7-10.5 kg in a 70 kg person), which could occur after drinking 14-21 liters of seawater (Nature.com).
Death occurs due to acute kidney failure resulting in the accumulation of sodium, urea and other substances in the blood.
It is not time, but the amount of seawater that causes problems. One could drink 1 liter of water in the evening, need to urinate several times during the night, and be mildly dehydrated and otherwise "fine" in the morning. But what's the benefit of this?


text:
What is the name if this glittery fly seen in Pittsburgh?
I have photographed the following fly which is iridescent green in Pittsburgh, PA.
I guess it was about 0.5-1.5cm long.
Can you help me to identify it?

And here it is: https://commons.wikimedia.org/wiki/File:Lucilia-sericata.jpg

Gorgeous photo!

Thank you for making your photo available as Creative Commons. I use many CC-licensed photo in my classes. Perhaps I will one day use yours.

@moose Iridescent is probably the word you are looking for.

It's a blowfly. They sometimes ruin my compost heaps (the larvae).

This is the most annoying fly from all the commonly found flies!

Looks like a green bottle fly.
https://en.wikipedia.org/wiki/Green_bottle_fly
Might be a Common Green bottle fly.
https://en.wikipedia.org/wiki/Common_green_bottle_fly


text:
determine longest poly-purine tract
how to determine/ find the longest poly-purine tract in any genome  and this needs to be on the E. coli genome . is it to figure out the polypurine tract and then figure out the longest chain ? or is it to splice the introns and exons away from the DNA ? since E. coli's genome is 4.6 million BP long, i need some help in breaking this down ?

One comment: Bacteria have no intron/exons, only eukaryotes have them. Otherwise I don't understand your question. For what reason are you looking for the "longest poly-purine"?

i need to find out a longest poly-purine tract in a E.coli genome

Is a sequenced genome on the internet good enough, or do you need to take real cells, extract the DNA, and analyze it directly for polypurines?

yes sequenced genome on the internet is good enough

are you on windows, mac, or linux? Please say linux.

Code Golf!
This is my Python script, avoiding regex and not at all prettified.
def gettract(strand):
    #if strand is 1 then replace C with T and split on T
    #else replace A with G and split on G

    if strand==1:
        print 'top strand purine tracts:'
        aseq=seq.replace('C','T')
        tracts=aseq.split('T')
    elif strand==2:
        print 'top strand pyrimidine tracts:'
        aseq=seq.replace('A','G')
        tracts=aseq.split('G')
    sortedtracts=sorted(tracts,key=len,reverse=True)
    for i in range(5):
        print len(sortedtracts[i]), sortedtracts[i]

f=open('ec_dna.txt','r')
l=f.readlines()
print 'Sequence analysed is %s' % l[0][1:] #the header line
f.close()
seq=''.join([i.rstrip() for i in l[1:]])
print 'sequence length is %i' %len(seq)
print
gettract(1)
print
gettract(2)

And here is the output:

Sequence analysed is E. coli K-12 MG1655 U00096.2 (1 to 4639675 = 4639675 bp)
sequence length is 4639675
top strand purine tracts:
28 AGAGAGAAAAGAAGAAGAGAAAAGAAAA
22 GGGGGAGAAAGGGGGGAAAAGG
20 AAAGAGGAAAGGGGGGGGGG
20 GAAGAGGAAAAGAAAGAAGG
20 AAAAAAGAAGAGAAAAAAGA
top strand pyrimidine tracts:
29 TTTTTCTCTTTCCCTTTTCCCTTCCCTCT
22 CCCTCCTCTTCTCTCCCTCCCC
21 TTCTCCTCCTTCTCTTTTCTT
21 TTTTTCTTCTCTCTTTTCCTC
21 CTCCCCTTTTCCCTTTTCTCC

The longest purine tract is 29 bases long, and is on the bottom strand.
This script doesn't handle the problem that the E. coli genome is a circular molecule, so if the longest tract was split at the origin it would be missed - I leave that and obtaining the coordinates of the longest tract as an exercise.

Why do you need to do this?
This is pretty simple with the right computer tools and some knowledge of how to use regular expressions, but the fact that you are daunted by a 4.6 Mbase file suggests to me you don't  have that.
Using an old copy of E.coli DH10B, and Lasergene's SeqBuilder, I found a stretch of 29 Cs and T's, so in the reverse stand, that would be a poly-purine.  I don't see a longer stretch in my fasta.

thank you  for the reply . can you share your code or steps followed ? iam trying to use regular expressions . what are the recommend tools needed ?

Can I get the DNA sequence you used? I'd like to test it against my code.

I used commercial Windows software, just to get the answer fast.  If I was going to do it in Perl, I'd make sure newlines were stripped out, and just search for /[AG/{30}]/ and if I didn't find it, I'd keep dropping the number until it hit.  And the same for CT strings.  You might not be able to search the whole 4.6 million letter string at once, but cutting it into overlapping first 10k long pieces should work.  Grep in Unix might be able to handle the whole string at once.

I meant /[AG]{30}/ or /[CT]{30}/

search for /[AG/{30}]/ and if I didn't find it, I'd keep dropping the number until it hit... I like this method.. It is likely to be fast. But the issue is that it wont be able to find all instances- but a small modification in the code would fix it. Keep removing the part rightwards from the first match position and continue regex search. An awk example here

Since you said an internet sequence is good enough, I will propose a computer programming approach. The basic idea is to enter the sequence as a string of text and then have the program read the text, keeping track of the length of the current polypurine tract, and the longest encountered so far. When it's done, it reports the longest one. I'm not sure if you know any programming, so I'll attempt to write up an example in C++ and post it. There are probably other programs that can do this, but I don't know about them.
Here is the code:
main.cpp
#include <fstream>
#include <iostream>

// this program reads a DNA sequence from a text file and then looks for
// the longest polypurine sequence. Please make sure there isn't non DNA
// text in the text file. Please call your text file "DNA.txt" and place
// in the same folder as this program.

std::string base_complement(std::string in){
    std::string return_me = "";
    for(int i = 0; i < in.size(); i++){
        if(in.c_str()[i] == 'a' || in.c_str()[i] == 'a'){
            return_me += 'T';
        }
        if(in.c_str()[i] == 'g' || in.c_str()[i] == 'G'){
            return_me += 'C';
        }
        if(in.c_str()[i] == 't' || in.c_str()[i] == 'T'){
            return_me += 'A';
        }
        if(in.c_str()[i] == 'c' || in.c_str()[i] == 'C'){
            return_me += 'G';
        }
    }
    return return_me;
}

int main(){

    std::cout << "WELCOME TO POLYPURINE COUNTER" << std::endl;
    std::cout << "WRITTEN BY SAM CROWLEY, SAMUEL-CROWLEY@UIOWA.EDU" << std::endl;
    std::cout << "WILL READ THE DNA IN DNA.txt AND REPORT LONGEST PURINE STRETCH" << std::endl;
    std::cout << std::endl;
    // open the file and read the contents into the string
    std::string DNA;    // this string will hold the entire DNA sequence
    std::string line;   // this will hold one line of the file at a time
    std::ifstream text_file("DNA.txt");

    while(!text_file.eof()){        // read the file until we get to the end
        getline(text_file, line);   // get one line at a time in the line string
        DNA += line;                // add that line to the DNA string
    }

    //std::cout << DNA << std::endl;  // output the DNA string just to check

    int current_tract = 0;          // length of current tract
    int longest_tract = 0;          // length of longest tract so far
    // true = sense strand, false = opposite strand
    bool tract = (DNA.c_str()[0] == 'a' || DNA.c_str()[0] == 'g');
    char c = DNA.c_str()[0];
    std::string purine = "";
    std::string pyrimidine = "";
    std::string longest = "";
    if(c == 'a' || c == 'g' || c == 'A' ||c == 'G'){
        purine += c;
    }else{
        pyrimidine += c;
    }
    for(int i = 1; i < DNA.size(); i++){    // iterate through the DNA string
        if(c == 'a' || c == 'g' || c == 'A' || c == 'G'){
            if(DNA.c_str()[i] == 'a' || DNA.c_str()[i] == 'g' || DNA.c_str()[i] == 'A' || DNA.c_str()[i] == 'G'){
                purine += DNA.c_str()[i];
            }else{
                std::cout << purine << std::endl;
                if(purine.size() > longest.size()){
                    longest = purine;
                }
                purine = "";
                c = DNA.c_str()[i];
                pyrimidine += c;
            }
        }else{
           if(DNA.c_str()[i] == 't' || DNA.c_str()[i] == 'c' || DNA.c_str()[i] == 'T' || DNA.c_str()[i] == 'C'){
                pyrimidine += DNA.c_str()[i];
            }else{
                std::cout << pyrimidine << std::endl;
                if(pyrimidine.size() > longest.size()){
                    longest = pyrimidine;
                }
                pyrimidine = "";
                c = DNA.c_str()[i];
                purine += c;
            }
        }
    }
    if(purine.size() > 0){
        std::cout << purine << std::endl;
        if(purine.size() > longest.size()){
            longest = purine;
        }
    }
    if(pyrimidine.size() > 0){
        std::cout << pyrimidine << std::endl;
        if(pyrimidine.size() > longest.size()){
            longest = pyrimidine;
            longest = base_complement(longest);
        }
    }
    longest_tract = longest.size();
    std::cout << std::endl;
    std::cout << "LONGEST POLYPURINE STRETCH IS " << longest_tract << " BASES LONG." << std::endl;
    std::cout << "LONGEST STRETCH IS " << longest << std::endl;
}

If you're running linux put the file in a folder and use a terminal to go that folder, then run g++ main.cpp -o polypurine.exe Then run it with ./polypurine.exe
The DNA sequence goes in a file called DNA.txt in the same folder. Make sure it only contains a, t, g, c, so remove any header data or other annotations. If it contains an X, N, or other symbol to represent ambiguous bases I don't know what will happen, but the results may not be accurate. I forget which is used for purines and which for pyrimidines, but if you tell me I can modify the code to make it work with some ambiguous bases.
If you use windows or mac this same code should work but compiling it into a working program will be different. I don't program on those machines so I don't know how to make this work on them.
Also, I ran a test on the cDNA for bee venom PLA2 and got a longest purine tract of 17 bases. I think I can post that DNA here:
Bee Venom PLA2 cDNA
atgattatctatccgggtacactgtggtgtggtcatggtaataaaagcagcggtccgaacgaactgggtcgttttaaacataccgatgcatgttgtcgtacccatgatatgtgtccggatgttatgagtgccggtgaaagcaaacatggtctgaccaataccgcaagccatacccgtctgagctgtgattgtgatgataaattctatgattgcctgaaaaacagcgcagataccatcagcagctattttgttggcaaaatgtacttcaacctgatcgacaccaaatgctataaactggaacatccggttaccggttgtggtgaacgtaccgaaggtcgttgtctgcattataccgttgataaaagcaaaccgaaagtgtatcagtggtttgatctgcgcaaatatggatccatggataaagttttccggaattccgcaaaaaagaagagaaaggtagaagaccccaaggactttccttcagaattgctaagttttttgagtccaagcgcggccgca

If you use this program for publications or anything, let me know. I put it here so you can use it, but I'd at least like to know if it's used.

Just search for /[AG/{30}]/ and if I didn't find it, I'd keep dropping the number until it hit - swbarnes2

Code for swbarnes2's method (will work on Linux terminal, Mac Console and cygwin terminal)
Usually in a genome file a single fasta sequence will represent one chromosome. In E.coli there will be only one. You would need to pop the fasta header (first line) out when analyzing your sequence. (Assuming that you have done so).
This code below will find all polypurine tracts of a given length in the genome. Basically you have to keep dropping the part from the sequence start to the match location and redo the regex search.
cat ecoli_genome.fa | tr -d "\n" | awk '{for(i=30;i>=10;i--){
pp="[A|G]{"i"}"
s=$0
while (match(s,pp)){
       print substr(s, RSTART, RLENGTH)
       s=substr(s, RSTART+RLENGTH)
    }
 exit
}
}'

Regex searches of type /pattern{N}/ may not work on all versions of awk. It does work in gawk >=4.0 but doesn't work in mawk.
This will load the entire genome sequence in the RAM (this is not huge at all). If you have RAM limitations and the genome file is really huge then you can stream read letter by letter (but you can't do regex search in this case). Stream read and regex are two strong features of awk.


text:
What is the chemical process involved in human hairs changing colour after sun exposure?
After a day at the beach, my skin tans due to Melanin.
But I also observe the black hairs on my arm turn a blond colour.
My question is What is the chemical process involved in human hairs changing colour after sun exposure?

Melanin is the main compound responsible for the color in hair. It is synthesized from the amino acid tyrosine. The absorption of tyrosine is around 280nm, which is a shorter wavelength than humans can see. Tyrosine can not absorb or preferentially scatter visible light in order to appear colored. It appears colorless as it scatters visible light equivalently. After tyrosine is synthesized into melanin, a pigment is formed which can be seen. Melanin scatters and absorbs light preferentially, it appears non-white.

The absorption of melanin is in the visible spectrum. This means it can absorb and scatter light in the visible spectrum differentially.

As your hair is exposed to sunlight, melanin begins to break down into lower molecular weight compounds which have their own absorbance spectra. The different forms of melanin and carotenoids in your hair can be oxidized by sunlight, giving hair a spectrum of possible colors.
Pigment in bleached hair has been oxidized into products absorbing light primarily outside the visible spectrum. White hair appears so because it lacks compounds which preferentially scatter and absorb light in the visible spectrum.

There is an interesting paper on this topicChemical-and
photo-bleaching of brown and red hair.


text:
Potential evapotranspiration constant for trees in the area of London
I am trying to find the ET0 (Potential evapotranspiration) under the climate conditions of London (UK) and Coimbra (Portugal) for each month. From what I understand these data is available in the FAO's website but I was struggling to find it.


text:
Calculation of the bacterial growth rate from a spectrophotomer growth curve
Typically the microbial growth in liquid cultures is monitored by turbidity. Data is obtained with a spectrophotometer to measure optical density at 600nm. The slope of the bacterial kinetic curve in exponential phase is the growth rate.
But I have seen two ways of calculate the growth rate:

Growth rate = Maximum slope value of the Kinetic curve
$Log_{10}$ transformation of the growth data and then calculate the slope.

I think the second one is right if you want to calculate the generation time:
generation time = $\frac{ln(2)}{Growth rate}$.
What is the correct way to calculate the growth rate and then generation time?

This is a common experiment for microbiology courses and you can find instructions on the internet , here is an example from University of Wisconsin: http://inst.bact.wisc.edu/inst/index.php?module=Book&func=displayarticle&art_id=114
But the general method is measure optical density at regular intervals and plot them on a semilog graph, which has the normal linear scale on the X axis for time, but a base 10 log scale on the Y axis for optical density. You can set this up in microsoft excel or libreoffice calc by right clicking the y axis and going to format axis, there should be a logarithmic scale option somewhere depending on the version.
After you have the data plotted, the exponential growth phase should appear as a line with positive slope. The logarithmic scale on the Y axis will automatically transform the exponential curve into a straight line. To determine growth rate in terms of generation per hour, you need to get the optical density at time 0, which is the beginning of the exponential phase, and time t, which is just some other time on the exponential phase. Use this equation to determine growth rate: $k =\frac{log(X_t) - log(X_0)}{0.301t}$
Once you know the growth rate, you can determine the generation time with $t_{gen} = \frac{1}{k}$, which gives time for 1 generation in hours. To convert to minutes, just multiply by 60.
As a side note, remember to blank your spectrophotometer with sterile media. Also, if the optical density goes over 2 it won't be as accurate, so dilute the aliquots to make the optical density go below 2. Remember to record the dilution factor so you can multiply the density by the dilution and get back to the "original" optical density for plotting.


text:
Is an Eidetic Memory (or other unusual forms of memory) less susceptible to anterograde amnesia?
I'm a physicist, so as a fellow scientist I want to apologize because this question will be entirely based on anecdotal inferences and I am well aware how irritating that can be.
I have an eidetic memory and I've never experienced any of the common forms of anterograde amnesia. No blackouts from rapid consumption of alcohol (and believe me, I've tried. That was the fun part. But not for kids; then it's not fun), not from extreme fatigue, head trauma, I even went in for surgery once and the anesthetist said at one point "Well since you asked, the amnesiac should be setting in right about now" and I vividly recall another couple minutes of conversation while we waited for the general anesthetic to knock me out.
So, naturally, I just assumed it must have been because of my eidetic memory. But I've always had an interest in neuroscience and now my curiosity has gotten the better of me. Surely the memory systems of all people are similar enough that amnesiacs and the like should work on everyone. So I ask, are eidetic memories (or perfect, or photographic, or other unusual forms) actually less susceptible to anterograde amnesia? Or perhaps have I just been the victim of probability; this is more a matter of luck not neuroscience?
Please don't spare the gory details, neuroscience is cool (Neuroscientists are brainy guys. Sorry, I couldn't resist that pun). That said, I am physics, not biology; I'm probably under-specifying the question. Let me know if it's too broad and I'll try to focus.

If you have red hair you can expect a different reaction to anesthetic

This question is more of a medical question than one of the underlying mechanisms of biological function.
The formation of long term memories is related to long-term potentiation. There are multiple neurotransmitters involved in this process. Ethanol primarily affects NMDA receptors. Drugs used to specifically induce anterograde amnesia, like propofol, primarily affect other others, like GABAA.
The process of memory formation relies on a variety of factors including the orchestration of multiple neurotransmitters. Anterograde amnesia can be induced by many factors and does not have a single known mechanism of action. It is not possible to conclude any single person will react identically to all inducers of anterograde amnesia. It is often the case that people have unique responses to drugs within a distribution of possible reactions.
The individual nature of responding to drugs is why side effect lists are lengthy, and usually only a few out of this list are observed in any individual.
My hypothesis is, as a regular consumer of alcohol, your liver function is elevated and responsible for your high tolerance. The cytochrome p450 family of enzymes are responsible for much of the metabolism of drugs in the body.
Liver function tests are cheap and interesting, I find. You might have some blood work done at a local lab to check out those stats as well as your cholesterol, etc., if you have an interest in such things.

Hang on, that "might" explain amnesiac drugs (although an anesthetist should account for that), but blackouts from alcohol have more to do with the rate alcohol is consumed than the actual amount. So regardless of my tolerance I should still be able to experience it with a moderate amount. Plus that doesn't explain lack of fatigue or trauma related memory loss or that similarly regular consumers do experience this effect. That said, this definitely supports my "I'm probably wrong with my assumption" suspicions

Everyone reacts differently to drugs. There's nothing extraordinary about not suffering a few symptoms. Some people never have hangovers. You should ask a MD. These are all things that physicians specifically train to address. I think there's talk on StackExchange Area 51 on establishing a medical stack.


text:
why does blood when oxidized over time become bluish green?
Oxygenated blood is bright red and deoxygenated blood is dark red or brown.
If you take oxygenated blood and leave it in the air it will turn dark red, then brown, then finally a bluish green from exposure to atmospheric oxygen.
Why does it oxidize this far to get a copper oxide color to it after it has passed the phase where it is the same color as iron oxide? Why doesn't it stay at the iron oxide color?

green sounds like a copper compound, but I would have thought iron would be present in far higher levels than copper in the blood. Never seen blood turn green, but I don't have that much just laying around. How do you get it to turn green?

often during the last few days of my period it is extremely light bleeding and the blood is brown. After hours of extremely light bleeding it slowly goes from being reddish-brown like iron oxide to bluish-green like copper oxide. Because the 3rd stage of oxidation is so slow I don't see much green blood after 24 hours of extremely light bleeding but I do see more than I did in the few hours that it took to start that stage of oxidation.

Apparently there is a rare condition, sulfhemoglobinemia in which sulphide ions or H2S combine with the haem group in haemoglobin, causing a greenish colour. This can be related to certain drugs being present in the blood.
See here for an example in which surgeons discovered dark green blood in their patient.

well I think in the case of myself that I don't have H2S in the blood and it is a light bluish-green I get after hours of oxidation of reddish brown blood so atmospheric oxygen can slowly oxidize blood from the iron oxide color(that reddish brown) to a copper oxide color(the light bluish green). Thats what I notice during the end of my period where the bleeding is extremely light and sometimes not constant is slow oxidation to a bluish green

But the colour of oxidised blood (ferrihaemoglobin) is established, and there isn't another oxidation stage to go to in the context of the protein. If the Fe(II) is released from the protein it could form Fe(OH)2 which can oxidise to a greenish colour http://en.wikipedia.org/wiki/Iron(II)_hydroxide

so you think that is what it is is Iron hydroxide which gets further oxidised? Well than is it the formation of Iron Hydroxide(given that I have a pad on during that time which absorbs the blood) that is really slow or is it the oxidation of Iron Hydroxide that is really slow?


text:
Do identical twins have the same fingerprint?
When there is every thing same from their genes to their phenotype so then why they don't have same fingerprints?

This question is a near-duplicate of http://biology.stackexchange.com/questions/1054/what-causes-fingerprints-to-form-and-why-is-the-pattern-formed-unique

It's considered appropriate on biology.se that you present some of your reading/research with your question. Have you read anything about the formation of fingerprints? Otherwise it will be closed.

As @anongoodnurse says, previous research is required and you do not need THAT much of it ;) http://biology.stackexchange.com/questions/28352/why-do-human-eyes-glow-red-on-a-photo-and-dogs-eyes-green

I like the question a lot and the answer is also pretty awesome :) Voted to keep open. Background research = identical twins are clones (implicitly: same phenotype), why fingerprints different? Quite a legitimate question.

Identical twins have, despite the name, neither identic fingerprints nor identic genetic fingerprints.
Fingerprints: According to the papers listed below the fingerprints show higher similarities (the "structure" is the same), but they can be distinguished and are not the same.

On the similarity of identical twin fingerprints
Can identical twins be discriminated based on their fingerprints?

Genetic Fingerprint: Although identic (or monozygotic) twins share the same DNA, they are not the same and can still be distinguished with a DNA fingerprint, if enough regions are analyzed. The difference comes from small mutations (so called "single nucleotide polymorphisms", one base mutations) which occur in each of us individually. The other difference comes from epigenetic modifications of our genome (basically adding methyl groups to our DNA) which are also not the same between identic twins (there is an interesting video on this on Youtube). However, when using standard forensic kits it is usually not possible to discriminate between identical twins. Differences are detected with whole genome sequencing.
Have a look at these publications:

Identical Twins' Genes Are Not Identical
Finding the needle in the haystack: Differentiating “identical” twins
in paternity testing and forensics by ultra-deep next generation
sequencing
Epigenetic contributors to the discordance of monozygotic twins.

You might expect identical twins to have the same fingerprints as twins have virtually indistinguishable DNA. The distinguishing nature of physical characteristics of a person is due to both the inherent individual genetic diversity within the human population as well as the random processes affecting the development of the embryo. The same would then be true of clones of a person.

In the case of fingerprints, the genes determine the general characteristics of the pattern. Fingerprint formation is similar to the growth of capillaries and blood vessels in angiogenesis. The general characteristics of the fingerprint emerge as the skin on the fingertip begins to differentiate. However, the flow of amniotic fluids around the fetus and its position in the uterus changes during the differentiation process. Thus, the cells on the fingertip grow in a microenvironment that is slightly different from hand to hand and finger to finger. The finer details of the fingerprints are determined by this changing microenvironment. A small difference in microenvironment is amplified by the differentiation process of the cells. There are so many variations during the formation of fingerprints that it would be virtually impossible for two fingerprints to be alike.

Therefore, fingerprints aren't entirely a genetic characteristic. They are a part of a ‘phenotype’ which means they are determined by the interaction of an individual’s genes and the intrauterine environment.
Overall, identical twins’ fingerprints tend to be similar. Before genetic testing, the similarity of twins’ fingerprints was used to determine whether they were identical or fraternal. But there always will be subtle differences making even their fingerprints unique.
On the similarity of identical twin Fingerprints

Beautiful Answer! Very nice.


text:
Is the heterotroph hypothesis universally accepted?
I was wondering whether there are hypotheses that take a different approach that is contrary to the heterotroph hypothesis.
The heterotroph hypothesis states that autotrophs evolved from heterotrophs because of the lack of food.
Is this issue still debated by scientists or is the heterotroph universally accepted?

I would say the the topic is still very much under debate. This paper by Ferry and House (2006) briefly review the heterotrophic vs chemoautotrophic hypotheses. They include citations from proponents of each hypothesis. Interestingly, Ferry and House propose an "energy conservation" hypothesis that attempts to merge ideas from the other two hypotheses.  Overall, much work remains to be accomplished in this field before we have a clear understanding of the origins of life.
Literature Cited
Ferry, J.G. and C.H. House. 2006. The stepwise evolution of early life driven by energy conservation. Molecular Biology and Evolution 23: 1286-1292.


text:
Standard Process Identification of New Disease outbreak Causing Pathogen
Is the any standard procedure or protocol followed for the identification of cause of new disease outbreak(or new pathogen)? Is it different for different countries?

I am not sure if there is any standard method for this. You find a patient with an unknown disease. Than you try to find out, what is going on. Isolate body fluids, analyze them and so on. Depending on the reason the methods are different.

I won't post it as an answer because of the 'human-biology' tag but this paper describes the process by which Schmallenberg virus was recently(ish) detected in Europe: syndromic surveillance picked up the disease, and NGS identified the agent. http://wwwnc.cdc.gov/eid/article/18/3/11-1905_article

Pathogen identification procedure is not necessarily standardised due to differences in resources available to each country but there are certainly several characterised and accepted approaches used to identify a disease causing pathogen. The predominant techniques used to identify pathogens relies upon conventional clinical microbiology-based approaches, which has been highlighted in the comments above. However these conventional techniques such as standard culture and susceptibility tests have many drawbacks such as time-consuption and lack of scalability in addition to lack of direct characterisation of virulence factors. Most pathogen (except prions) logically carry a unique DNA or RNA signatures that differentiate it from other organisms, which provides the basis for disease causing pathogen characterisation. According to this page there are two approaches used to detect a pathogen, once sampling has taken place.
1) qPCR based pathogen detection: allowing sensitive and real-time detection of genetic signatures, which is not currently matched by sensors such as immune-assay techniques (lagging in detection time, logistics and costing) and optical techniques (lacking specificity).
2) Microarray based pathogen detection: allowing combination of nucleic acid amplification (offered by PCR based techniques) combined with massive screening capability of microarray technology, resulting in high level of sensitivity, specificity, and throughput.
These techniques are obviously combined with powerful software technologies required to sieve through the data and allow for easing of experimental burden, minimising assay development as well as operational costs. Now clearly these techniques including sensors and conventional microbiology are used concurrently/synergistically to more efficiently identify a disease causing pathogen and strategies a treatment/preventative measure. This review nicely illustrates the molecular basis for pathogen identification and discusses general considerations (in this case for fungus detection) such as DNA extraction methods, sampling preparations and strategies and goes on to highlight some other sequencing independent methods such as FISH and macroarray.
This paper writes about sequencing based strategies and using the BLAST (NCBI) tool and talks about identification of variant strains of known species, identification of non-cultivatable pathogens and more importantly related to this question, identification of new species using (rDNA) phylogenetic trees of bacterial 16S gene and the fungal 18S gene, commonly used for this type of analysis. This is done in order to determine the phylogenetic position of a the suspected new species compared to a closely known related species, which is useful when there is a <98% of the sequence similarity with known species.

I was first thinking of voting to close the question because it was too broad, but in reconsideration I think the answer of showing why it is too broad would constitute a proper answer in this case.
First of all, the term disease is one of the most general terms for a problem in medicine.  The only term that could be higher up is "medical condition."  It could be an infectious disease, genetic disease, induced disease (think chemicals, tobacco, etc), or [insert organ here, ie heart] disease (which are not necessarily genetic).  There are attempts to distinguish between "diseases" and "disorders," but the difference is not always clear.  The term "disorder" is growing in usage and scope because it is seen as having fewer negative connotations than disease (think disease of the mind vs. disorder of the mind).
Thus each field has it's own ways of identifying new diseases.  As a general trend new diseases are found now by identifying greater specificity within a previously general disease.  For example, a person could be said to have an "adrenal cancer," but now we would want to know if they have an adrenocortical carcinoma.  In an infectious setting, we could think of all the particular pneumonia being specified out of interstitial lung diseases.
Diseases caused by external agents (pathogens, toxins, etc) can sometimes be more uniquely novel, in that they can change into something unpredicted (new compound or virus made by man for example).  Perhaps you meant to ask if there were standard ways for identifying new viruses or microbes?

Can you change your answer now?

@DevashishDas. Sorry to be slow on this.  My participation in the site is very intermittent, and I'm not checking anywhere for notices.  I think Benz has a good awnser, with my only additional thoughts being arrays currently under development to gage if the host response is to a viral or bacterial infection.


text:
Percentage of mutations caused by radiation?
Consider a gamete in a typical human being. In the interest of being specific, let us say that we're talking about a typical ovum in a typical middle class woman living in a developed nation. What percentage, on the average, of the mutations in the genome of that ovum will have been caused by electromagnetic radiation?

May we also assume the person lives at sea level?  The sun will, by far, be the greatest source of radiation in an average person's life (in practically any location).  Elevation is likely to be a key variable in how much radiation she receives (doubles every 6k ft). Radon-222 probably deservers an honorable mention, but no matter what the radiation source, the answer is going to be a very, very low percentage.

@AtlLED, yes absolutely, and that is a very good point.

You might use the frequency of thymine-thymine dimers to extrapolate the rate of UV induced damage. This has been studied but I couldn't find a paper in human cell lines. It appears different cell lines have different susceptibilities to thymine-thymine dimers. The majority of DNA mutation in healthy people comes from endogenous sources, not radiation. Recombination during fertilization may also contribute significantly to changes in DNA sequence. Wikipedia nicely breaks down some of the different sources of mutation.
Manifestations of mutations from endogenous sources is measurable as our bodies become genetically more chimeric with time. Regions of our bodies become deferentially susceptible to disease due in largest part to errors in DNA repair and replication, unrelated to electromagnetic insult.
Damage due to UV radiation, like the creation of a thymine-thymine dimer, can be repaired readily by base excision and replacement. While DNA is dividing, it is cut many times to allow the molecule to unwind. Single strand breaks resulting from DNA damage have robust mechanisms for repair. For example, when a thymine-thymine dimer is excised or single strand break is otherwise introduced, enzymatic recognition makes identification of a template for repair possible. It is also very unlikely in a single strand break that another break will occur in the same location, decreasing the mutation effect of UV.
Double strand breaks and errors in DNA replication are intrinsically more permanent as a substituted base is chemically indistinguishable from any other of the same type. Much of the new genetic information introduced into any mammalian genome comes from endogenous sources, not the environment.

Error rate of human DNA polymerase
Deamination is a major contributor to mutation rate

The only problem with this, is that the germline should absolutely not be exposed to UV radiation.  One of the big things mammals got right was the whole "mama" thing.  In fact, the mother not getting enough UV exposure for vitamin production is more likely to be a problem.

Good point. Now I want to know the correlation between different products of DNA damage and energy of insulting light. Maybe the success of internal fertilization for animals with small litter sizes is related to protection from UV.


text:
Is there a more updated version of the book "Genome?"
I read the book Genome by Matt Ridley for my AP biology course. I found it fascinating, although it seems another book must have been written on the topic since 1999. Anything you can recommend?

How much science have you had sense AP bio?  It would effect my a recommendation.  More details are always nice for a question like this, so that an answer doesn't seem primarily opinion based.

Not much. I took it last school year, so I finished it last May. What I liked about Genome is that it didn't require a ton of understanding of genetics and explained many things without using advanced science jargon. That being said, I myself could probably take on something a bit more challenging with the help of Wikipedia and my science teacher.

What is AP biology?

@WYSIWYG Advanced Placement Biology. High school Biology course equivalent to a first semester college Bio course. The syllabus is defined by CollageBoard.


text:
Why are recombination rates increasing in mammals?
I have recently become fascinated with an awesome topic in biology and evolution that I feel is rarely covered in biology courses. That is, rates of meiotic recombination, or the the amount that an organism's genome is reshuffled before it is passed on to the next generation, varies across species! And no one really knows why.
A recent paper by Segura et al which gathered average recombination rates for males across a dozen or so mammals and showed that there is a trend of increasing recombination rate with mammalian divergence.
Why is recombination increasing through mammalian evolution? Is there any reason to believe that there is something special about placental mammals which would drive increased recombination?
There are some catches to this study such as low sampling of marsupials and monotremes and low power for most of species wide recombination rates, ie the average recombination rate of cells in a single individual. But I can see how getting samples from multiple tigers would be difficult.

If rates of meiotic recombination DIDN'T vary across species - THIS would require an explanation! After all, evolution creates diversity, not homogeneity.
I can only wonder that more recombination would allow for a faster diversification. The more DNA you shuffle, the more distinct each individual offspring may be (though I'm not 100% sure). The recombination rate has an energetic price, so not all animals recombine so much their DNA like later mammals. I.e. they needed a selective pressure to justify paying that price.
Perhaps it was useful for a group rapidly occupying the "vague niches" left by dinosaurs? This make sense, since the primary mammalian irradiation occured in the beginning of the Cenozoic era, right after the Cretaceous mass extinction that killed most big animals, including the biggest dinosaurs.
Unfortunately I have no references on the subject, it is just what makes sense to me, given evolutionary logic.

My logic would rather tend to predict that high recombination rate should rather be correlated with low speciation rate. Absence of recombination will lead chromosomes to diverge over time.

Yeah, it may be, though I'm not sure exactly how this divergence will happen? Can you explain it better? And is it chromosomic divergence the main genetic cause of speciation in mammals?

With low recombination chromosomes diverge following the same logic that makes two non-interbreeding population to diverge through time (just by the neutral processes of mutations and drift).

Does chromosomal divergence cause speciation? Intuitively, I'd say yes. Assuming that chromosomal divergence would yield to outbreeding depression (OD), then OD causes post-zygotic isolation which causes a selection pressure to increase the pre-zygotic isolation. I have absolutely no idea however of whether such mechanisms is an important factor to explain speciation in mammals and I might be wrong assuming that chromosomal divergence causes OD.

thanks for the input. After comparing rates across species, (which there are few), it seems to me that recombination rates maybe evolving too quickly to compare very deeply in phylogenetic trees.


text:
What is a good identification key for European mushrooms?
I live in the Netherlands, and I am looking for an identification key for mushrooms.
Are there any keys you could share?

1
2
3

There are various types of Mushroom identification Sites. you can take help from:

Mushroomexpert
Rogersmushrooms
MycoKey 4.0

Source: MycoKey 4.0


text:
Can the negative afterimage appear only if there is light or is it possible in darkness?
Reading the following paragraph:

After staring at the red and blue shamrock, you saw a green and
  yellow afterimage. Opponent-process theory proposes that as you stared
  at the red and blue shamrock, you were using the red and blue portions
  of the opponent-process cells. After a period of 60 to 90 seconds of
  continuous staring, you expended these cells' capacity to fire action
  potentials. In a sense, you temporarily "wore out" the red and blue
  portions of these cells. Then you looked at a blank sheet of white
  paper. Under normal conditions, the while light would excite all of
  the opponent-process cells. Recall that white light contains all
  colors of light. But, given the exhausted state of your
  opponent-process cells, only parts of them were capable of firing
  action potentials. In this example, the green and yellow parts of the
  cells were ready to fire. The light reflected off of the white paper
  could excite only the yellow and green parts of the cells, so you saw
  a green and yellow shamrock.
(Ellen Pastorino & Susann Doyle-Portillo, What Is Psychology? Essentials, 2010)

I've been wondering:
Can the negative afterimage appear only if there is light or is it possible in darkness?
In other words does the red color make the ganglion continue working even when there is no image and the afterimage appears green or is more light required in order for the afterimage to appear?

Glutamate release from photoreceptors is inhibited by incident photons (ref). During photobleaching, assume that the effect of an incident photon drops to zero. The implication then is that if all light is removed subsequent to selective photobleaching, there will be no difference in activation between bleached photoreceptors and unbleached photoreceptors. This observation suggests that no afterimage will be visible in darkness.
But there might be rebound effects or other effects of light adaptation that will result in a perceivable afterimage in darkness. Certainly there are hallucinatory visual patterns than can be generated cortically, suggesting that a cortical afterimage could be generated in darkness.


text:
positive and negative feedback
I want to know more about positive feedback in gene regulation and to know the similarity and differences between positive and negative feedbacks.

Do you have any specific genes in mind? The way you ask your question is really broad and hard tro answer.

I want to know about E.coli bacteria

Can you then edit your question and add the relevant information?

Positive and negative feedback are essential motifs that control transcriptional activity of genes. They may involve other genes, mRNA and/or proteins.
A classical pattern of negative feedback is where transcription of a gene results in mRNA and translation of this mRNA in a protein that represses the expression of the gene again. Feedback loops may involve much larger structures, e.g. if a gene codes for a hormone that stimulates the release of another hormone in a remote organ and if that other hormone represses the expression of the first gene again.
In general, negative feedback results in stable levels of certain products. Positive feedback leads to infinite growth (if not limited by a surrounding negative feedback loop or simply by lack of substrate).
It is easy to identify positive and negative feedback by counting the positive and negative correlations within the loop. Feedback loops are defined as positive or regenerative loops if there is at least one positive correlator and the number of negative correlators is even. If the number of negative correlators is odd than the loop is negative or degenerative.
See http://biomedicalcybernetics.wikia.com/wiki/Feedback for a more detailed explanation.

It is easy to identify positive and negative feedback by counting the positive and negative correlations within the loop.... Not that easy.. Correlations are not to be trusted blindly

A feedback loop is a network structure in which the gene is able to regulate itself via a single path.
$A\rightarrow B\rightarrow C\rightarrow A$
Interactions can be called positive or negative depending on their effect on the downstream gene. If a gene A represses another gene B, then it is a negative interaction; when it activates then the interaction is positive.
If you multiply the signs of all the interactions in the path from gene-A back to itself you will get the sign of the loop.
So a positive FBL will result (in the above example) if :

A activates (+) B; B activates (+) C; C activates (+) A
A represses (-) B; B activates (+) C; C represses (-) A
A activates (+) B; B represses (-) C; C represses (-) A
A represses (-) B; B represses (-) C; C activates (+) A

Any other combination of interaction will result in a negative feedback loop.
Differences are based on their properties. I'll mention two main unique properties of each.
PFBL

Switching circuits
Hysteresis

NFBL

Expression control (feedback control)
Oscillations

Similarity: well, nothing more that they both are called feedback loops and the topology is similar (just the nature of interaction is different).


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Why ml scale blood retrieval is required to run a blood test?
Substances found in blood are present at microscopic scale and tend to be invisible to the unaided eye. Why is a whole vial of blood (at ml scale) is required to assess the presence and concentration of substances, given that the modern equipments and testing is becoming more and more sensitive and efficient?

Can you please specify what kind of blood test you are talking about. And what is "so much blood"?

@Chris I would think that in any blood test you're looking for the presence of microscopic molecules, and thus you'd only need a very small drop of blood.

In fact a lot of tests are not done using a microscope. And besides that, you can not see molecules in the microscope. You can see cells. Typical amounts for blood tests are 4.5 or 9 ml which is not very much. Enough to handle and prepare the sample and to repeat it, if something goes wrong.

@Chris So is it a question of technology/affordability? Are we capable of obtaining the information from a very small drop of blood?

That depends on the type of test you want to do.

@Chris How is it that there exist tests that look for microscopic particles that can't be done with a drop of blood?

Because some of these tests need some amount of volume to properly work. (Automatic) Handling is also not getting easier when the volumes are getting very small. You want to have reliable and reproducable measurements.

@Chris What I'm asking is why these tests need some amount of volume to work.

It might be better to consider the sampling technology, economic and logistical issues with this question as well as the tech behind the tests.
First, some tests still will want a few milliliters of blood - e.g. cell counts for specific cell types.  Then there is the need to create and stock many different kinds of sample collection devices and train the collection centers to use them effectively- the industry won't be wanting to completely retool whenever the volume requirement for the assays changes.
Mainly, since the expense of collecting and shipping a few milliliters of blood is pretty much identical to doing so with a few microliters of blood, what has happened is that the tubes are used to do multiple assays with excess included in case an assay has to be redone.
Probably all this blood currently collected is not necessary at all.   I expect that the cost of changing all the blood collection systems and protocols is not worth the cost of collecting the exact minimum amount of blood needed.  The benefit to the patient or the lab between collecting 3-5 ml of blood and collecting 50 microliters of blood to be shipped off for lab analysis is probably close to zero.
Having more blood than you need does not hurt the lab either should they need to repeat the assay or when you need to use the sample for more than one different test.

So would it be possible to design a device that runs any blood test on a small drop of blood?

In many cases it would and people are working on that.  Microfluidics is taking the biomed world by storm.  That being said, there are potentially thousands of assays that are or will be devised for the market.  how many of them will be run out of a smartphone, time will tell.

Could you expand a little more on how blood tests work and why it's easier to do them with more blood?

Sorry i'm not being clear.  I've added one paragraph above to summarize...

Could you explain how blood tests actually work? Like do they look at it under a microscope or something? I think if I understood how they test blood it'd help me understand why it's useful to have more of it.

I have a doctor's order for a lab test here - there are scores of tests done with blood.  some of them stain cells and then count them under a microscope, others are chemical analysis of the plasma, others apply antibodies to cells in the blood, others sequence the DNA of cells in the blood.  There's really quite a variety - that sort of deserves its own question or may be too broad for a single question.  some require little or no sample tho.

One important point to be added here is that the tubes are usually vacuum / low pressure, to get the blood flowing into the tube.   This could be very hard to manufacture on a much smaller scale. And something else: many tests don't require too much sample, but standard equipment is built for a bit of excess volume (for example a HPLC accepts 1 mL tubes, while probably only 1-10 uL is actually injected). It's also efficient to use the same collection tube, whether you're doing one test or 20.

If they're collecting multiple tubes it's also mostly because different types of tests are done. https://www.bd.com/vacutainer/pdfs/plus_plastic_tubes_wallchart_tubeguide_VS5229.pdf

@shigeta brings some other interesting reasons, but I think the main problem with small draws is lack of representativity.
I suspect you are hoping that something Theranos "nanotainers" will replace today's blood draws. The fact is, the first drop of blood is not the most representative for the whole blood. For example, drops of blood collected from finger pricks are not very similar. if they differ between themselves, they are likely to differ from the rest of the blood. This variability is probably why Theranos tests were shown to be quite variable.
For some tests, it might not matter. Home fingerstick tests for blood sugar at home are generally acceptable, but even those come with a warning that results are somewhat inaccurate. For others, such variability cannot be tolerated. They may be too expensive or too urgent to allow repeats in case of a borderline result. They may be so scary that false positives must be avoided as much as possible. In all these cases, the tests must be run in the most representative conditions.
More blood collected is essentially averaging multiple drops. Many  tests are done on very small sample of blood - smaller than a drop. Drawing that sample from a bigger pool of blood makes the readings more representative for the rest of the blood.

The problem with Theranos is this they results are obviously not accurate and that they lost their testing licence over that.

@Chris I don't know what are you implying with your comment. I think I said just that, and suggested a reason why "results are obviously not accurate". Are you suggesting the problem is not caused by the tiny blood volume, but by something else?

From the few, which has been published about this, it seems like this. There are numerous reports of customers which say that by far more blood was drawn than announced (the "needle prick").

There are hundreds of tests that exist but many require different technologies so getting them all out of one drop is nigh impossible.
For a large fraction of your average chemistry/immunology blood tests, the blood has to be transported in a way that keeps the blood liquid so the collection tubes have anticoagulants in them. The analysis involves pipetting microliters of plasma into a cuvette where different reagents are added and the ensuing chemical reaction is monitored by a spectrophotometer which detects various chemical products by select wavelengths that are absorbed or emitted. This requires the red blood cells to be removed before the sample can be analyzed(they would block the light), so the collection tubes have a gel at the bottom and the sample is centrifuged before analysis so that the blood cells get buried in the gel and the analyzer probe can then extract just the clear plasma above it. Each assay has to be run in it's own cuvette otherwise the reactions would all be mixed up and it wouldn't be possible to quantify the assays separately. Using this approach we can currently run about 50 quantitative assays out of a ml or two of blood. Some assays require different kinds of tubes for various reasons so they may collect a red top and a green top tube when otherwise a single tube would do, and, as others have said, some excess is collected to enable reruns or add-on tests that your doctor may specify after seeing your initial results. If you only collected a small drop of blood (like is used in hand-held blood-glucose meters), you wouldn't be able to get it out of the collection tube and into the multiple reaction/measuring cuvettes.
There are technologies that detect e.g. DNA on a chip that could conceivably detect multiple viruses and things from a single drop of blood, but they fundamentally rely on some underlying chemistry/physics that would probably make them single use if connected to a phone.  While they are very specific, that tends to make them good for detecting things qualitatively (do you have HIV or HEP-C?) but probably won't make them good for quantitative test (how much potassium or glutamate do you have in your blood). And trying to combine that with e.g. counting red and white blood cells is unlikely at this point. But technology is constantly improving.

Hi Gary. It would be great if you can add some supporting references. Wikipedia links would also do but research articles/reviews would be the best.


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Why is high fructose corn syrup unhealthy?
I understand that high fructose corn syrup was found to have detrimental effects on peoples' health. Why is this so?

could you please reference this claim and what makes you think fructose is a contributing factor?

@Bez The OP may not know. I've heard this too, though, that corn syrup is bad for you, and I like the question.

One answer could be: because it's sugar.

High fructose diet cause many bad things: liver and kidney damage (oxidative stress, increased urate levels), insulin resistance (increased triglicerid and free fatty acid levels), atherosclerosis (low NO levels, high urate levels, high salt levels, high LDL/HDL ratio, high blood pressure, etc.), cancer (increased oxidative stress). So you should avoid foods rich in fructose and sucrose except fruits, vegetables and honey, because the polyphenols in them, can counteract with the fructose related problems.

@inf3rno could you provide sources for that please?

@user8669 Read Raoul's answer! Note that some antioxidants in fruits can render fructose harmless.

Besides a lot of propaganda there is not much evidence that high fructose corn syrup (HFCS) is more dangerous than normal sugar. Lets have a look at the sugar in detail:
HFCS is produced from corn and is originally a glucose syrup. Since fructose is obviously much sweeter, the glucose is converted enzymatically into fructose (see here for more details). Before the use in food production additional glucose is added to the syrup so that typical syrups contain 55% fructose and 42% glucose or 42% fructose and 53% glucose (the remaining % are water).
If you look at saccharose (which is our ordinary sugar) then this is a disaccherid which is build from one molecule of glucose and one molecule of fructose. The enzyme sucrase breaks this molecule up into one molecule of fructose and glucose each, so reaching a 50%:50% ratio between the sugars.
As the ratios are more or less the same, it doesn't matter for the human body, where the sugar come from meaning that in this context it is more too much sugar in the food than a problem with HFCS, as also this study suggests:

Straight talk about high-fructose corn syrup: what it is and what it
ain't.

Fructose itself is not without problems as this induces the production of fats in the liver, but again, it doesn't matter for the body, where this fructose comes from:

Fructose induced lipogenesis: from sugar to fat to insulin
resistance.

For further reading I can also recommend this article on Gizmodo:

Is High Fructose Corn Syrup Really Bad for You?

Clearly whoever named this substance "high fructose" corn syrup, while technically correct (regular corn syrup is almost entirely glucose), didn't understand marketing very well :)

Thank you for your answer. I am not sure I understand that it doesn't matter for the body that the ratios are 'more or less the same'. Any slight difference in structure or composition, can play a vital role in the effect on human health. In this case, however, I think that the way the HFCS is made plays a more important role than the percent composition of fructose and glucose in HFCS.

@user8669 The problem are the huge amounts of sugar which are consumed. And here fructose causes indeed problems since the glucose is used by all cells for making energy, while the fructose is used by the liver to produce fat and store energy, which promotes obesity when consumed in large amounts. What can also cause problems were contaminations from the production process, but I found sources saying that this problem is gone with todays production process which relies on the use of enzymes and not caustic soda anymore.

Moreover, fructose uptake is not regulated by insulin. And fructose can bypass a rate limiting regulatory step of glycolysis ( $F$-$1P \rightarrow F$-$1,6 BP$ ).

Just to clarify-- is there a difference between fructose in fruits and isolated fructose (such as the type that is converted enzymatically from glucose)?

Chemically? Not. Both have the same structure. They are not distinguishable.

You say that chemically there are no differences. Does this imply that there are differences in another way?

@user8669 Yes, fruits can contain other materials which counteract the diabetic effects of fructose and slow down the absorption, so they are much safer than sugar or fructose syrup. So it does matter where fructose comes from, but not by comparing fructose syrup and saccharose which both are bad...

Some reference about fruits: http://ajcn.nutrition.org/content/99/2/328.abstract

The following study abstract of "Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity" copied from http://www.ncbi.nlm.nih.gov/pubmed/15051594 seems to address your question.  I added a paragraph break; the second paragraph seems most relevant to me:

Obesity is a major epidemic, but its causes are still unclear. In this
  article, we investigate the relation between the intake of
  high-fructose corn syrup (HFCS) and the development of obesity. We
  analyzed food consumption patterns by using US Department of
  Agriculture food consumption tables from 1967 to 2000. The consumption
  of HFCS increased > 1000% between 1970 and 1990, far exceeding the
  changes in intake of any other food or food group. HFCS now represents
   40% of caloric sweeteners added to foods and beverages and is the sole caloric sweetener in soft drinks in the United States. Our most
  conservative estimate of the consumption of HFCS indicates a daily
  average of 132 kcal for all Americans aged > or = 2 y, and the top 20%
  of consumers of caloric sweeteners ingest 316 kcal from HFCS/d.
  The increased use of HFCS in the United States mirrors the rapid
  increase in obesity. The digestion, absorption, and metabolism of
  fructose differ from those of glucose. Hepatic metabolism of fructose
  favors de novo lipogenesis. In addition, unlike glucose, fructose does
  not stimulate insulin secretion or enhance leptin production. Because
  insulin and leptin act as key afferent signals in the regulation of
  food intake and body weight, this suggests that dietary fructose may
  contribute to increased energy intake and weight gain. Furthermore,
  calorically sweetened beverages may enhance caloric overconsumption.
  Thus, the increase in consumption of HFCS has a temporal relation to
  the epidemic of obesity, and the overconsumption of HFCS in
  calorically sweetened beverages may play a role in the epidemic of
  obesity.

Welcome to biology.stackexchange. If you cite sources, please mark the citations as those and make sure that you not only write answer which contain only of citations (in this case the abstract). Besides that: The paper shows that the problem is fructose in the food, not the HFCS.

It is also interesting to read the comments on this article, which can be found here and here. Especially the second is very clear about the Fructose and HFCS.

I've not read the study but I'm skeptical. During the same period, there was also a huge rise in obesity in the UK but we don't use HFCS.

Ah, but we do use [invert(ed) sugar syrup)[https://en.wikipedia.org/wiki/Invert_sugar_syrup] which is a 50/50 glucose/fructose mixture made by hydrolyzing sugar (typically beet or cane sugar in the UK). On the other hand, invert sugar syrup isn't nearly as widely used in the UK as HFCS is in the US.

Skimming through the article itself the authors seem to pick two trends, conclude their both rising and et volia, a causal relationship - not too strong of an argument. The title's "may" says it all.

@ChrisStronks This is not my answer.

@Chris - I know, the two "here"s are in your comment in this thread, it is not referring to your answer.

@ChrisStronks Ah, now I understand. I will see, if I can repost the second link.

Fructose has a special characteristic that other sugars do not have: its absorption in the human intestine is not regulated, as opposed to glucose, for example.
The important implication is that all the fructose you consume will end inside your organism, either used immediately or stored as fat. Other sugars will only be partly assimilated, or will require more energy to assimilate. If you take the example of glucose again, a glucose molecule requires active transport (meaning consumes ATP, the most basic fuel of your organism) to transit across the intestinal wall. Fructose is absorbed via free transport (i.e. no ATP consumption).
This claim can be verified by opening any human physiology book, and while it is debatable whether fructose itself is deleterious, increasing the sugar amount in an already sugar-saturated environment clearly does not seem a good idea to me.
I (inf3rno) appended the answer with further details:
Sucrose is split by digestive enzymes (sucrase, glycoside hydrolase) in the small intestine into fructose and glucose (1:1 ratio). By the high fructose corn syrup (HFCS hereafter) the fructose - glucose ratio is dependent on the HFCS type according to wikipedia. For example HFCS90 has 90% fructose, while HFCS42 has only 42% fructose (the rest is glucose).
Glucose is mainly transported by SGLT1 (active transport, which involves ATP), while fructose is mainly transported by GLUT5 (passive transport, does not involve ATP) into enterocytes in the intestines. After that the cells transport these sugars with GLUT2 (passive transport, not insulin dependent) into the blood. Fructose and glucose is transported to the liver (hepatocytes) from the blood, with GLUT2.
In the liver fructose is more dangerous than glucose, because it is transformed without any regulation. It uses the same pathways as glucose and mostly fatty acids are created from it, which increase the blood VLDL, LDL, FFA level and cause insulin resistance. The byproducts are urate and free radicals, which cause hyperuricaemia and oxidative stress. Hyperuricaemia cause decreased NO levels (by counteracting with eNOS and reacting with NO directly), which cause increased blood pressure due to vasoconstriction. Hyperuricaemia damages the liver and the kidney too. Too high urate levels enhance LDL oxidation as well, which cause atherosclerosis. The free radicals deplete the antioxidants of the body and probably cause cancer in long term.

High dietary fructose intake: Sweet or bitter life? -
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3158875/
A causal role for uric acid in fructose-induced metabolic syndrome -
http://ajprenal.physiology.org/content/290/3/F625
Gut microbial adaptation to dietary consumption of fructose,
artificial sweeteners and sugar alcohols: implications for
host–microbe interactions contributing to obesity -
http://www.drperlmutter.com/wp-content/uploads/2014/04/Payne-et-al-2012-Obesity-reviews.pdf
Early Life Exposure to Fructose and Offspring Phenotype: Implications
for Long Term Metabolic Homeostasis -
http://dx.doi.org/10.1155/2014/203474
Dietary fructose, salt absorption and hypertension in metabolic
syndrome: towards a new paradigm -
http://onlinelibrary.wiley.com/doi/10.1111/j.1748-1716.2010.02167.x/abstract?deniedAccessCustomisedMessage=&userIsAuthenticated=false
Toward a Unifying Hypothesis of Metabolic Syndrome -
http://pediatrics.aappublications.org/content/129/3/557.short
Uric acid transport and disease -
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877959/

@Chris: So summed up I think this is enough proof that HFCS with higher fructose - glucose ratio, than sucrose have a higher health risk.

It would be great if you added references to your response!

Thank you for your answer. I cannot understand, then, how it is healthy to eat fruits (which contain fructose). hi fructose in fruits absorbed differently by the body than other types of fructose?

@user8669 Where did you get the idea it was so healthy to eat fruits? ;-) No, the fructose in fruits is in no way different, and gets absorbed in the same way. In the wild, it used to be the best sugar-concentrated food around, which is most likely why its absorption is less regulated. However, diabetics for example are required to limit their intake of fruits to avoid hyperglycemia. So its a question of amount, and pure sugar used to be quite rare in the wild.

Yes, but according to your answer it would be better to eat something sweetened with sucrose than to eat naturally sweet fruits which contain fructose. Do I understand you correctly?

No, fruits are good for you and other sugars are ok too. However, fruits are nowadays good for your health because of all their other components (vitamins, etc.), because we already get high sugar loads from elsewhere (bread, etc.). If you were to limit your sugar intake to that of a wild animal, then fructose would become extremely valuable, while it is not so valuable to the civilized human.

In one comment you said "where did you get the idea that it was so healthy to eat fruits" and then you said "fruits are good for you". If I understand you correctly, fruits are good only because they contain vital nutrients, but the fructose that fruits contain is not as healthy as glucose or sucrose.

@user8669 Fructose is just as healthy as others. In a wildlife context sugar is difficult to come by, so fructose would be extremely valuable. Now that we get as much sugar as we want, it is no less nor no more healthy than other sugars. The point is that if you already eat too much sugar of whatever type, eating fructose will add more sugar to your organism than eating  an equal amount of another type, and in that way would become a less healthy option. It's not the fructose itself that is not healthy, but its relation to modern food.

But fructose's is not as regulated by our body as are glucose and sucrose. This does not play a role in the health factor?

@user8669 As I said above, in a wildlife setting this makes it extremely valuable. In a civilized setting, this makes it less healthy. If you want more info, get us into a chat room, 'cause it'll be easier than in commments


text:
What are the dimensions in angstrom of bacteria?
I'm going to take a picture of a bacteria but I am unsure how large it is. What are the dimensions in angstrom of bacteria?

It varies. Is there a specific species or genus you're studying?

Helicobacter pylori @canadianer

if you know in microns then you can convert it into angstrom. But why angstrom. It is a very small unit for cellular dimension

I agree with @WYSIWYG since as far as I have seen its use is for measuring how far apart two molecules such as fluorophores are from each other in experiments such as FRET

@WYSIWYG it's used in protein structure accuracy

Usually you know the scale of the micrograph and measure the size of the object in it to get its size, not the other way round ;)

What has changed about this question to warrant a reopen?

According to Wikipedia: 3 um long with a diameter of 0.5 um. That equates to a length of 30 000 A and a diameter of 5 000 A.
http://en.m.wikipedia.org/wiki/Helicobacter_pylori


text:
Why does replication require primers while transcription does not?
In transcription, there is no need for any primer. I guess the basic mechanism of DNA polymerase & RNA polymerase is the same. So why does replication have the need for a primer?

I read somewhere that the difference in catalytic activties of DNA ploymerase and RNA polymerase lies in the structure and geometry of theirbactive sites.But, i have studied in ' Lehninger principles of biochemistry' by Nelson and Cox that the active sites of both the enzymes contain highly conserved asp residues and they require magnesium ions for catalysis. Then why is a primer not required for RNA polymerase? waiting for a good,logical answer.

There are always two kind of answers to this sort of "why" question. One is mechanistic and simple — once you know the mechanism of action — they are built differently to work differently. The more fundamental question (and to me more interesting question) is why they got that way — why didn't DNA polymerase evolve the capacity to do what RNA polymerase does? I imagine nobody knows, but my conjecture is that it must be something to do with the replication evolved  from an RNA to a DNA world. Someone else must have thought about this before me, though.

I'm no expert at transcription but from what I can figure out here and here transcription requires a promoter region acting as a template-directed mechanism for allowing transcription, which presumably bear a certain sequence recognised by the RNA polymerase and associated complexes. However DNA polymerase requires primers to guide it to the correct location on DNA.
EDIT: In light of comments below, according to here and here, RNA polymerase is capable of de novo synthesis meaning it is capable of initiating synthesis of RNA without primers and this is done by RNA polymerase binding to two nucleotides rather than nascent RNA polymer and a single nucleotide. Initiating nucleotide hold RNA polymerase rigidly in place, facilitating chemical attack on the incoming nucleotide. For bacteriophage T7 RNA polymerase, transcription begins with a marked preference for GTP at the + 1 and + 2 positions. DNA polymerase cannot add primers, and therefore, needs primase to add the primer de novo.

The point of primers is that the DNA polymerase cannot make new chains de novo meaning it has to connect them to an existing strand. For RNA Polymerase II this is obviously different and the other general transcription factors present at the transcription initiation site seem to play an important role, too. I think it is also possible that RNA Pol II has primase activity itself and can make strands de novo. But I haven't found any details on this yet.

yes RNA polymerase has a primase activity itself. I don't know the structural basis of it; so I did not comment or answer.

@Chris I made an edit to the answer, which highlights the de novo aspect of RNA polymerase. Many thanks for the pointer!

thanks all of u....but i'm not fully satisfied.please give me more information

which subunit of RNA polymerase has primase activity? ..@WYSIWYH

@anamitraruj.. Primase is a type of RNA polymerase.. but as I said I haven't compared the structures.. I'll let you know in a while

Just thought if add that I was taught that the linker between regions 3 and 4 of the sigma factor helps orient the template strand so it's in the correct position for the first polymerization reaction.

The primer is an universal recruiter, for all DNA polymerases, bringing them to the DNA template. You must have both strands in place for a DNA polymerase to stop by. Moreover, the catalytic activity of all the polymerases requires a preexistent 3' end on the growing strand. You must have a 3' free end near a template, for a DNA polymerase to act. (A far longer description of the chemistry is at http://www.ncbi.nlm.nih.gov/books/NBK22374/ .) In contrast, RNA polymerases, including primase, are recruited to the template by DNA-binding proteins, such as ori-binding proteins, transcription factors etc., meaning there is no need for primers.
It may make some functional sense too. Once a cell decides to replicates, its ori-binding proteins are synthesized and/or activated. They bind the DNA template, and bring in the primase. Only after the primase does its job, DNA polymerase can take over. The cell needs stringent regulation only at the level of the ori-binding protein, because DNA polymerases are so strongly dependent on the preceding steps.
If we think in evolutionary terms, and we accept the RNA world hypothesis, the RNA polymerases (or at least their ancestors) should have evolved earlier than the DNA polymerases. In these conditions, the earliest DNA polymerase came in a world where double stranded RNA already existed, meaning it had access to a primed template. There was no immediate need for a primer-independent DNA polymerase, and no urgent need afterwards.
All these are speculations. There seems to be a primer-independent DNA polymerase in a thermophile bacterium (DOI: 10.1021/bi0489614). Its existence may be interpreted in two opposite ways: ancient mechanism, or recent evolution, forced by the special conditions where these bacteria live. The former will deny almost everything I wrote. "Why?" questions in biology are always tricky.

" You must have a 3' free end near a template," should not read "...of the template"? - That may have been it: RNA polymerase doesn't start at "ends", it's in the middle. Isn't promoter and primer basically i.e. funtially synonomous?

In replication you have 2 strands made.
In transcription you have 1 strand made.
Transcription uses ONLY the 3' → 5' DNA strand.
This eliminates the need for the Okazaki fragments seen in DNA replication (on the lagging strand).
And it removes the need for a RNA primer to initiate RNA synthesis, as is the case in DNA replication.
Edit; instead RNA Polymerase binds to Promoter region to initiate transcription, in replication (leading strand) DNA uses 1 Primer to initiate. And as AMR comment, RNA Polymerase dont need to add nucleotides to existing part.

Hi, welcome to Biology SE, thanks for answering - could you possibly add some supporting material (references to books, peer reviewed papers, reputable websites etc.)? This helps to maintain standards and helps users find good reading material on the subject which may help them further.

Actually that is not the reason. In order to polymerize a DNA daughter strand, the DNA-dependent DNA polymerase requires a free 3' hydroxyl group with which to catalyze the reaction. DNA-dependent RNA polymerase has no such requirement and therefore can catalyze the reaction without the need for a starting 3'-OH group.


text:
Compatibility drugs info
Let's suppose that I take a DrugA for ProblemA and then I got this ProblemB and started to take DrugB. Are there general rules I can look up to figure out whether I can take DrugA & DrugB simultaneously?
I mean drugs can cancel each other or vice versa increase effects of each other (in an extreme extend); or one of drugs has adverse effects that are bad for the other drug.

Can you rephrase your question? I think I understand what you are trying to ask but this is really unclear.

What about now? :)

Much better :-)

Yes.. if you look up drug info then they say which drugs are incompatible with it. I don't know of a standard database but sites like these are helpful. @Chris. are you going to sit in front of your comp on a nice saturday?? :P

@WYSIWYG Unfortunately, yes. bio.sx is nice for breaks inbetween. I got a load of work to be done until the end of next week.

If this question is not off topic I will explain some pharmacology to you but I think it is off

@caseyr547 Actually I was wondering about pharmacology in the first place, so that would be extremely useful.

@WYSIWYG is this off topic

@ctapobep i dont want to get in trouble so i will make sure its ok to post an answer first

I think you are referring to drug contraindications, which is a very large consideration and study in drug administration when multiple drugs are taken at a time. Many examples of drug-drug interactions can be found online such as here http://en.wikipedia.org/wiki/Drug_interaction

I would like to start by suggesting you talk to whoever prescribed you the drug or your pharmacist. They should be most up to date with interactions and there are some interactions which may only affect you more seriously because of your medical history or current conditions.
Here are some sites that you can check drug interactions in order of popularity:
Medscape
Drugs.com
Healthline
WebMD
RxList

Drugs.com provides good lists of side effects when combining drugs. Just type (drug) interactions into Google and it should come up. Then you can click on a given drug and see how dangerous the two are together/what they can cause. Of course, your doctor is always the best resource.