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Is 100% antibacterial resistance possible?
The quest to develop antibacterial and antibiotic substances has often been described as an arms-race, as bacterial life develops resistance, requiring us to develop novel agents which can effectively kill said microbes.
My question is: is it at all possible for a single microorganism to develop resistance to everything we can possibly develop?
There is only so much information-capacity in microorganism DNA to encode the means of resistance to various substances. If we climb the arms-race ladder high enough would a highly-advanced bacteria somehow "forget" how to defend against penicillin, for example?
...or are we utterly boned?

If there is no advantage for a MO to be resistant to a certain antibiotic, it will very likely loose the resistance over time. Problem is we need to collectively not only stop using penicillin, but likely the whole class of penicillin-derived antibiotics for that to happen. No easy task.

When you look at individual bacteria, they would forget how to defend against particular types of antibiotics. Growing in the absence of penicillin, most of them would throw away the resistant genes. The problem is that even very small population among them still carries the resistant genes and they would become dominant when they met penicillin.

This is a theoretical question, which I can't answer, because genetics is not my favorite topic. In practice we only have about a dozen antibiotic classes. There are already panresistant bacterias, which are resistant (as far as I know) all of these classes of antibiotics, so we have already lost.
The causes of our defeat is more interesting I think:

Pharmaceutical industry does not have enough interest in the antibiotics research, since it is not as profitable as for example cholesterol reducers. Antibiotics are cheap, and you usually heal after the first treatment, while the research and the clinical trials are really expensive, it is hard to find working chemicals, which do not have severe side effects.

“We  need  to  shift  from  the  concept  of  the  pharmacy  as  a
  ‘shop’  and  build  a  culture  of  pharmaceutical services. This is
  already happening  in some countries, but we need to make it  the
  rule  everywhere,”  says  Zsuzsanna  Jakab,  WHO  Reg ional  Director
  for  Europe.  “As  pharmacists  dispense  medicines  to  patients,they
  are   important  allies  in  our  fight  against  antibiotic
  resistance.  As  such,  they  need  to  be  ena bled  to  deliver
  accurate  information  and  counselling on proper antibiotic use.”
Over  40%  of  antibiotic  prescriptions  are  inappropri ate,  recent
  studies  found.  This  relates  especiallyto antibiotics prescribed
  for the common  cold and sore throat; these most oftenresult  from
  viral infections,on  which antibiotics have no  effect. Further, in
  some countries, there is  atendency towards self-medication.
  Inappropriate an tibiotic use is the major driver of growing
  antibiotic resistance.

Pharmacists have decisive role in combating antibiotic resistance, says new WHO European survey
People with Mycobacter infections does not always do the treatment long enough, so Mycobacters can become resistant to antibiotics.

Most people with TB are cured by a strictly followed, six-month drug
  regimen that is provided to patients with support and supervision.
  Inappropriate or incorrect use of antimicrobial drugs, or use of
  ineffective formulations of drugs (e.g. use of single drugs, poor
  quality medicines or bad storage conditions), and premature treatment
  interruption can cause drug resistance, which can then be transmitted,
  especially in crowded settings such as prisons and hospitals.

http://www.who.int/features/qa/79/en/
There is no global regulation of how to use antibiotics, so in some countries you can buy them without consulting a doctor and get a prescription. On top of this you can buy antibiotics without prescription on the internet if you want. This leads to overuse of antibiotics, and overusage leads to resistance.

Self-medication is more common in developing countries due to factors
  such as ready availability of antibiotics without prescription, the
  unrestricted access to antibiotics,lack of regulation over drugs, and
  physicians and pharmacists prescribing and dispensing antibiotics
  without regard to the cause of infection

http://article.sapub.org/10.5923.j.cmd.20110101.02.html#Sec3.3.4

We found 138 unique vendors selling antibiotics without a
  prescription. Of those vendors, 36.2% sold antibiotics without a
  prescription, and 63.8% provided an online prescription. Penicillins
  were available on 94.2% of the sites, macrolides on 96.4%,
  fluoroquinolones on 61.6%, and cephalosporins on 56.5%. Nearly all,
  98.6%, ship to the United States.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746509/

These results demonstrate that, although illegal, the sale of
  antibiotics without a prescription continues in Spain.

http://cid.oxfordjournals.org/content/48/10/1345.full
Some of the antibiocstics are used by agriculture industry, which leads to antibiotics resistance as well.

They identified bacteria able to shrug off the drug of last resort -
  colistin - in patients and livestock in China.
It is likely resistance emerged after colistin was overused in farm
  animals.

http://www.bbc.com/news/health-34857015

Nutritive and therapeutic treatment of farm animals with antibiotics,
  amounting to half of the world's antibiotic output, has selected for
  resistant bacteria that may contaminate the food produced.
  Antibiotic-resistant enterococci and staphylococci from animals are
  found in food when they survive the production processes, as in raw
  cured sausages and raw milk cheeses1. The broad host ranges of some
  plasmids and the action of transposons in many bacteria allow
  antibiotic-resistance genes to be communicated by conjugation between
  different species and genera2,3. A multi-antibiotic resistance plasmid
  from a lactococcus found in cheese provides a historical record of
  such events.

http://www.nature.com/nature/journal/v389/n6653/abs/389801b0.html

About 2/3 of the antibiotics are used in animals.

https://youtu.be/iLJAleLjJv8?t=3m47s

So the problem is with not enough motivation in development and the lack of proper regulation of usage. Regulation is the business of the politicians, so its their fault as always. :D

A lot of theorizing about motivation makes for conspiracy-theory-like thinking (Big Pharma, etc.) Some sources to back this up might be nice.

@anongoodnurse I did not add the sources, because it is hard to find in the browser history, but if you really need it, I'll update my post.

@anongoodnurse I still cannot find the documentary about the "big pharma" I wanted to link. :S According to some comments I watched it in march 2015.

I think this is a better answer now; had already upvoted, so can't do so again. I know documentaries can be pretty convincing, but they are not always truthful (honest.) I saw one on a cardiology issue which was so convincing that had I not known for a fact that it was false, I would have had serious doubts about my profession. As it is, I don't know why the makers haven't been sued, but ?

@anongoodnurse It contained reports with pharmaceutical engineers and managers from different pharma companies. They claimed, that they stopped antibiotics research because it was not profitable enough. Currently some countries try to make a difference by giving some money for the clinical trials, so it is certainly not fake.

I won't say anymore after this, but I think you have to be almost as careful about  what you believe in the media as on the internet. Now I sound like a conspiracy theorist!

@anongoodnurse :-)

I can't really give hope because a video is not a good reference. But towards the end this video claims that bacteria cannot be immune to both both bacteriophages and antibiotics at the same time. So bacteriophages might help us win provided they don't cause some other disease. https://pubmed.ncbi.nlm.nih.gov/24619620/

@anongoodnurse

My question is: is it at all possible for a single microorganism to develop resistance to everything we can possibly develop?

If you are only discussing antibiotics, the answer is, yes, it's theoretically possible but very highly unlikely, as different classes of bacteria have different characteristics that allow resistance to certain antibiotics to develop.
For example, if a bacteria doesn't have penicillin-binding proteins -  allowing cross-linking and stabilization of the bacterial cell wall - then resistance to this antibiotic which makes susceptible bacteria unable to synthesize their cell walls - is meaningless, so unlikely to happen (except through sharing of useless genetic material, which does have limiting factors.)
If you're discussing all antimicrobials (and you consider something like bleach an antimicrobial), the answer is "no".
The danger isn't that a microbe will be resistant to every antibiotic. The danger is that it will be resistant to enough of them to cause a significant problem. It takes time to test for antibiotic sensitivity; in the meantime, a person with an infection that needs antibiotic treatment is getting sicker. Labs start testing for antibiotic sensitivity with antibiotics that the identified organism is usually sensitive to. If that fails to reveal sensitivity to an antibiotic at acceptable levels - one option is to increase the amount of antibiotic given - new tests need to be carried out, taking even more time (for antibiotic combinations or "atypical" antibiotics). It's possible that an antibiotic (or combination) will be ascertained only after that person's death.
Staph aureus has lived closely with man for I don't know how many hundreds of thousands of years. Most of the time, it's presence is benign. It's only when it becomes invasive that antibacterial resistance is a factor in dealing with it.
Antimicrobial Resistance Learning Site Although this is a veterinary site, it's clear and informative, and, though most people are unaware, use of antibiotics in feed animals - which falls under veterinary medicine - is a major contributor to development and spread of antibiotic resistance.

A 100% antibacterial resistance is a very dangerous situation, which would mean that the age of antibiotics will be over. To achieve a total resistance the microorganisms would have developed new ways of mutation, transferring genes between them, rapid cell damage repair. It would mark a new step in the evolutionary process. There has been many questions as to whether the age of antibiotics have come to its end or not, but the demand has never been this high. its a very scary scenario, a ticking time bomb.

The age of antibiotics will never be over. There will be new antibiotics, and there will be fading resistance. But a lot of people will die from once-treatable infections. That's different


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Difference between various evolutionary terms
Could someone kindly explain me the difference between Phylogeny, Phylogenetic Tree, Evolutionary Trees, Phylotype, Clusters, OTU (Open Taxonomic Units). Or if possible please do suggest me a beginner's book on that said topics.

Any evolutionary biology textbook should cover this, e.g. Futuyma's Evolution. To me, your question is too open-ended and broad, and it reads as unresearched homework.

Source of information
Understanding Evolution is a free online introductory course of evolutionary biology that will probably answer these questions.
Wikipedia will also make a decent job at answering your questions.
Any introductory book to evolutionary biology would do it.
To answer your question

phylogeny = phylogenetic tree = evolutionary tree: evolutionary relationship between lineages
phylotype: An observed morphological similarity that is used to classify a group of organisms.
OTU: An observed genetic similarity that is used to classify a group of organisms.

Both OTU and phylotype are often used for asexual lineages where the concept of species poorly apply. See more info on the concept of species here.

source: Stack Exchange

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text:
What is the lifecycle of hanging woody vines?
In the first ten seconds of this video, you can see a vine that appears to have started its life 60 feet up in a tree and has now grown down almost close enough to touch the ground. I have seen similar vines that do make it to the ground and start curling around, but don't sink roots. Why do they create this long woody stem? Or do they start at the bottom, grow up the tree, and then release their roots somehow so they can swing free? They're sometimes not wrapped around the trunk at all, just hanging from the very upper branches, as if their seeds found purchase there and started stealing nutrients to grow. Is that possible?
I have swung from these in several locations in Wisconsin and Iowa. They're very tightly attached.

There are no epiphytic vines in the US. Most likely, if it's sturdy  enough that you can swing from it, it's the vine of a wild grape. (The vine in the video is classic wild grape.)
They grow like most other flowering plants: they start innocently enough with a seed that takes root in the ground. They are initially tender and small stemmed.

From there, they grow along the ground, sending out tendrils. If they find something growing vertically, they cling to it (a shrub, tree trunk, or a low hanging branch) and grow upwards towards the light. If they have enough light (they are shade intolerant), they continue to grow, branch, and elongate. because they can become quite heavy, they break canopy branches of their supporting tree and fall in long loops toward the ground.

If the loop breaks for some reason, you have one swinging vine. But if you diligently follow it back, you'll find either the continuation of the vine near the canopy (the part after the break) or the trunk growing from the ground alongside of a nearby tree.
Though cool-looking, they are very destructive, bringing down not only branches but often entire trees (plural. They intertwine different tree branches, and if they bring down one tree, others fall in a domino-effect.)

Imagine that SOB hanging onto your upper arms for support (not the guy, the grapevine).
Smaller vines (which can also be destructive) that climb up the sides of trees are Oriental Bittersweet, Poison Ivy, Virginia Creeper, etc. (Probably Kudzu as well, but we don't have that here yet.) But these aren't likely to become large or sturdy enough to swing from if they come loose from the tree.

This is a photo of two common offenders: a wild grape (dark shreddy bark, about 2.5 inches in diameter) being slowly strangled by an oriental bittersweet (lighter bark), both climbing this large oak. If you look carefully, the base (roots) of both these vines are behind the tree (about five feet), one on either side. (You might have to take my word for it...)
Wild Grape

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text:
Is it possible to have raw ngs data to practice
I'm looking for raw human ngs data to practice in bioinformatics. Better if it is from different machines (illumina, roche, pacsbio, etc). Panels, exomes and genomes.
Anyone knows something?

Yeah. Look at GEO and SRA.. You'll find tons of data.

You can also find it in the supplemental data sections of papers you're interested in.

yes, thank you. But there I found mostly trimmed and refined data. I'm looking for very raw data, meaning as the files exit from the sequencer. I want to practice with bioinformatics and so I need file as much raw as I can obtain.

Like fastq formatted files originating from the different technologies... on NCBI/EBI there are files, but their identifier is not the original from the machines.

This question was asked somewhere and nicely answered. You might find lot of examples of .bam files. see https://www.biostars.org/p/45320/

At least PacBio do provide some example datasets on their DevNet resource. You should be able to get a lot of different Illumina data from the public data in BaseSpace. I am not sure where to look for official samples from Roche 454, but I wouldn't bother too much as it is discontinued anyway. Rather go for MinIon or IonTorrent data, if you want more.


text:
results of FgenesH and GenScan
Why FgenesH and Genscan don't give good results as I have prdicted number of genes of Chromosome 16 which according to NCBI are 86 but the results I have obtained are 57 genes predicted by FgenesH and only 47 genes predicted by GenScan. why they have done missed predictions. Kindly help me to know the reason?

You would be mistaken to assume that a computer program that is predicting, or classifying, the biological features in a nucleic acid or protein sequence is infallible.
Different programs use different algorithms and will have different parameters for their models of what a gene looks like. Typically they are tested on a learning or training set of features, and optimized to yield the highest score on that training set.  Then when you feed in your novel sequence and ask the program to predict where the genes are it will hopefully give you a list of predictions along with an estimated probability of the confidence of that prediction. However there will always be outliers, actual protein-coding genes that have atypical features not contained in the training set.
In other words, each program is only as reliable as its underlying model, and nobody has a perfect model.

Ok i get it that these methods are not reliable but my problem is that I was using Chicken Chromosome 16 for which FgenesH is trained so my question is that if its parameter is trained for chicken then why don't it give me missed prediction?


text:
In what two ways is ATP used in coupled reactions?
I already have down "A coupled reaction is when leftover energy from a reaction fuels a reaction that needs more energy. ATP can break apart to transform into something new and use the energy created by breaking a bond to fuel a reaction in need of more energy" I think that is one use but I am not sure and I still need another

A coupled reaction is where a catabolic reaction drives an anabolic reaction, usually with ATP as an intermediary. The energy released from the first reaction allows for the formation of ATP from ADP and P. The second reaction is then driven by the hydrolysis (breakdown) of ATP, which releases energy.

So the answer to your question is: In a coupled reaction, ATP is first used to store energy from a catabolic reaction and then used to release energy for an anabolic reaction.

Another use of ATP is phosphorylation of different substrates including proteins.


text:
What is this species of tree?

In my city, there is a unique tree, with thorns all over it. I would like to know - what species is this?

Which city is it?

If you google the name of the place where this tree is found you might well found information.

Thank you, but this is a unique tree, there are not many trees like this in the area. Also, there is not that much information about this city's flora in google.

Can you please give us the name of the city?

Modii'n Maccabim Reut, Israel.

would be Ceiba sp of bombacaceae

I am not a botanist but looking at the flower in the second picture and the thorny trunk and pods it is likely to be part of the Ceiba genus. I cannot however be sure of the exact species.

Found it! The tree is Ceiba insignis, כוריזיה בקבוקית, planted in many cities in Israel. Its origin is from South America, and it grows to a height of 10-15 meters.


text:
How do burrowing animals get enough oxygen?
Tree borers make a small hole in a tree. At the end of it, they chew on wood to elongate the tunnel. They digest food and grow. All this takes oxygen.
The entrance to the tunnel is generally small. Some borers plug the entrance. Even without that, air circulation must be non-existent. How do they breathe?
It just seems off hand that tree borers might be an extreme case. But I have the same question about all kinds of burrows. How do worms do it? Rodents? Ants?
Do burrowers have any special behaviors or adaptations to help them cope?

Thank you all for your answers and comments. But I suspect there is more to it than that. I doubt enough oxygen diffuses down the length of the burrow to keep an insect alive under bark.
A tree died in my yard recently. The bark now comes off easily. When a tree is stressed or diseased, insect often attack. They finish off the tree if the original problem doesn't. Clearly that has happened here. They have eaten almost the entire layer under the bark. No wonder the bark is peeling off. There is almost nothing left of the wood it was attached to.

Most of the burrows are long and narrow. The insects carefully leave a small strip of wood between adjacent tunnels.
Here is a close up of two burrows from the bottom of the previous picture. It was taken before I pulled off all the bark. You can see they started at the bottom, and grew as they climbed.

Here is the bark that covered the burrows. When insects chew the wood, the wood does not disappear. At the bottom you can see a portion of the sawdust that packed the burrow. Most of it fell out when I peeled off the bark. I have seen other pieces of bark where it clearly filled the entire burrow.
At the top, you can see the holes where they dug out.

Now that the tree is dead, the bark is falling off. But it wasn't when they started. Trees do not make it easy for insects to eat them. I expect the bark was well attached. I doubt it was porous enough for air to penetrate. I doubt there was damage, such as the long crack you can see along one burrow.
Sometimes wood can be surprisingly porous. You can literally blow smoke lengthwise through a plank of red oak. But that is cut and dried wood. Live wood is full of sap.
I expect that insects do not make holes in the tunnel. They make it hard for predators to get it.
And yet enough oxygen does get in.

A year later, I still think about this off and on. While having a small mass reduces oxygen needs, oxygen is needed to chew a tunnel in wood and grow. I cannot believe that enough oxygen diffuses down a long narrow tunnel packed solid with sawdust.
Here is a photo from when I burned a log from the tree. You can see the surface is covered with burrows. There are also holes into the interior.

Here I have split the log. You can see the holes continue deep into the tree and lead to chambers. These burrows are almost entirely free of sawdust.

Here is a detail view.

I expect they are kept clear because insects need to crawl down them. One reason would be they need air.
Yet the surface burrows are packed. It seems likely an insect that can chew tunnels in wood can poke holes in bark. Does anyone know if they do this?
One last thought. I heat my home with wood. When I carry firewood home, I store it under this tree. People tell me you can transport insects in firewood...

Well it helps that insects and worms are cold-blooded, which means they have a slower metabolism and lower oxygen demand. How burrowing mammals handle air flow and oxygen could be different.

Oxygen is a small molecule, and can pass into that hole a million abreast!

@anongoodnurse We should look up the physical chemistry equations to estimate diffusion rate of O2 in and CO2 out. It might be interesting to see just how deep you have to go before it becomes a problem.

Many of these organisms are evolved to have low metabolic rates (oxygen consumption) and tolerance to high CO₂ levels. I know that this is the case with the naked mole rat.

Your question focuses mostly on insects, but there are cases of special adaptations by larger burrowing animals. The naked mole rat has a special kind of hemoglobin, and is also capable of surviving for about 10-20 minutes without any oxygen at all by switching from glucose metabolism to fructose.
See http://www.npr.org/sections/thetwo-way/2017/04/20/524511231/researchers-find-yet-another-reason-why-naked-mole-rats-are-just-weird

As the body mass of an organism decreases, their volume decreases with direct proportionality, so their metabolic needs are also reduced. The result is that small organisms like worms and insects have a much larger surface area to body mass ratio, which lets them passively transfer oxygen into their bodies much more easily.
I am by no means an entomologist but most species of insects are able to exchange gases with the environment without any active respiration at all. Due to their small size, gases can passively diffuse through the trachea and spiracles directly to their internal fluids/muscles.
That said, insects simply have much much lower basal metabolic rates compared to even small vertebrates. Lower metabolic rates mean lower oxygen needs, so that's why its not uncommon to see insects surviving in cracks and crevices that don't have a lot of air circulation. The little air circulation that does occur in the temperatures that insects thrive in is more than enough to support their oxygen needs.

As the body mass of an organism decreases, their volume decreases exponentially This is a misuse of "exponentially." The dependence of the volume on the mass is a direct proportionality, not an exponential dependence. Direct proportionality is $y\propto x$, exponential is $y\propto b^x$.

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Death from too little salt?
I know that sodium deficiency can be deadly. But why is it deadly? Is it because of your muscles getting so rigid that you can't get something with salt in it? Is it because of your brain not able to send signals? Is it because of excess urination to try to get the sodium levels right? Is it because of anemia leaving red blood cell ghosts(the membranes of rbcs) in your bloodstream? Is it a combination of all these factors?

Can you define "sodium deficiency"? Hyponatremia (not enough sodium in the blood) is usually not caused by insufficient sodium intake. If you eat, you'll get enough sodium.

As @anongoodnurse said hyponatremia causes a lot of very bad things to happen to the human body. Also, as anongoodnurse said, I have never heard of it from lack of consumption. I have only heard of it when people have consumed too much water causing electrolyte imbalance and is basically just a function of osmosis. Remember that cells have aquaporins, so water is exchanged freely. This seems to be an issue during marathons. Now not consuming enough iodine can be a problem, but that is different than hyponatremia.

I mean too little sodium in the whole body when I say sodium deficiency. In other words not only is the blood affected but everything else that needs sodium(muscles, neurons, blood cells(leading to anemia), and kidneys(leading to dehydration) just to name a few. I don't mean too much water intake(mild water toxicity)

What you are suggesting pretty much will not happen. Because of osmoregulation, your kidneys recirculates the sodium to keep levels constant. It is only in cases of extremes such as water poisoning, extreme exertion, or severe gastric distress that fatal electrolyte imbalance results. On average a serving of rice and fish will give you about 410mg of sodium (a typical meal for large portions of the world). The RDA in the US is no greater than 2300mg per day, but that is the upper limit. An average serving of vegetables gives 32mg, so as @anongoodnurse said if you eat, you'll get enough.

But if, for arguments sake, you could have too little salt, then the result would likely be exactly the same as death by hypernatremia or cholera.

But in order to get the sodium concentration right the urine becomes much more dilute and that leads to dehydration. Muscles need sodium and calcium to contract and without that, they get very rigid. Neurons need enough sodium to send a signal. If it is too low it won't send a signal. And with low salt in the blood and high amounts in rbcs the water rushes into the rbcs and potentially bursts them which leads to even more dehydration as well as high blood sodium levels which can lead to high bp. It also leads to anemia which can lead to cyanosis from low oxygen.

Basically with too little sodium, it goes from bad to worse until the heart and lungs are affected and the person dies.

@AMR - drugs, SIADH, and a host of other things cause (chronic) hyponatremia as well. That doesn't mean you're incorrect about what you've stated, though.

Part of this depends on the exact nature of "salt depletion" you're referring to. I have never actually heard of a case of hyponatremia being caused by low consumption of salt. We don't need to consume NaCl. It's present in the foods we eat in adequate amounts. We may want to salt our food, but it's not necessary for life.
Hyponatremia is an electrolyte imbalance, be it due to excess intake of H2O, inappropriate H2O retention, excess Na+ loss, hyperglygemia or other osmotic force, or other cause. For ease of explanation, I'll address acute hyponatremia, as it leads to death more rapidly. Hyponatremia kills because of the difference in the concentration of sodium across cell membranes.
Normal serum Sodium (Na+) is ~140mEq/L. Acute severe hyponatremia occurs when serum Na+ falls rapidly below 120 mEq/l (some authors use 125mEq/L) in less than 48 hours.
Water accounts for 60% of total body weight, with approximately two-thirds being intracellular and one-third extracellular; of that extracellular water, ~75% is in the fluid between/surrounding cells, and 25% is in blood vessels. Distribution of water/Na+ throughout the body is very tightly regulated.
When serum sodium falls too low, free water moves from areas of lower concentration to higher (into the cells). Tissue becomes edematous.  While this isn't a great problem for some tissues, it is for the brain.
The brain is enclosed in a rigid compartment (the skull) with a small amount of fluid (cerebrospinal fluid, or CSF) surrounding it. Inferiorly, there is an small opening called the foramen magmun, where the brainstem leads to the spinal cord.

When water moves from the blood into the cells of the brain attempting to establish osmotic equilibrium, the brain compensates for the increase in volume by forcing CSF out. This buys some time, but not enough; there is headache and nausea. As the brain continues to expand, intercellular fluid is forced out into CSF (which is being displaced by the brain.) This causes hyperexcitability which leads to seizures. In the meantime, astrocytes swell. Blood flow to the brain is reduced because of increased intracranial pressure, which further damages the cells, increases cellular edema and coma ensues.
If this isn't bad enough (it is; it's an almost irreparable  cascade of events), the edema can actually "push" the lower part of the brain down through the foramen magnum resulting in brain stem compression and respiratory arrest. At this point, few people make it back intact with even the best help.
You say,

Basically with too little sodium, it goes from bad to worse until the heart and lungs are affected and the person dies.

Not really. In acute hyponatremia, the brain goes before the rest. Once the brain goes, so follows the body.
in layman's terms
not layman's terms but still easily understandable

It is a big problem for the rbcs as well. Water rushes into the rbcs and they burst leaving behind their cell membranes. This helps balance the sodium levels but it leads to anemia. Anemia then leads to less oxygen transport. Less oxygen transport leads to faster heart rate. This eventually isn't enough to raise oxygen transport because it makes atherosclerosis related heart problems more likely and widespread.

Um... no. I don't think you're prioritizing the effects of hyponatremia. Hemolysis isn't one of the major players in morbidity and mortality from hyponatremia. The red blood cells have leeway. The brain does not. If you already have strong opinions about all this stuff, why are you asking this question?

I am talking about chronic here, not acute. In chronic sodium deficiency it is mainly urination, blood, and the heart and lungs that are affected as well as neurons and muscles

@Caters- I really think you should post your own answer with references. I'm always up for learning new stuff!


text:
Yew seed dormancy reduction
Yew seeds have very long dormancy when artificially planted.
They are also adapted to passage through digestive systems of animals that eat/transport them.
But could the dormancy be shorter (or the viability higher) if the seed passes through a birds digestive tract first? (An explanation: the seed's outer layers can get worn down that way, signalling that it is ready to start the process leading to germination.)
That would imply that the dormancy could also be artificially shortened by eg. dipping the seeds in acid and then alkaline solutions, which would be great.


text:
How body loses more fat in CO2 form than in sweating form?
Yesterday, I saw TV Game Show.
There is question like this: Body loses more fat in which form?
It gave 4 options:
1) CO2
2) sweating
3) xxx
4) xyz
sorry i didn't remember 3 & 4 options.
so right answer is CO2. anchor explaining the reason behind it, suddenly my brother switch the channel. all gone.....
Everybody thinks sweating is right answer, i have reason for it, if we work out our body whole fat comes out in sweating form.

Sweat is the release of water that evaporates, allowing the body to cool itself under exertion. When fats are converted to energy, they are used as an input into the Citric acid cycle. The molecules are eventually broken up and the byproduct is CO2.

Fatty Acid Metabolism and The Citric Acid Cycle. And for perspiration

This is a curious case of a rather poorly stated question that actually has something pretty interesting underneath --- where does the atoms from fatty acid oxidation go? CO2? Water? Now I don't know how to vote :)

If you exercise heavily, you can sweat enough where you have to drink to replace it. But on a normal day, you don't sweat all that much.
On the other hand, when you metabolize food, you essentially burn it. According to the Merck Manual,

Carbohydrates, proteins, and fats supply 90% of the dry weight of the diet and 100% of its energy. All three provide energy (measured in calories), but the amount of energy in 1 gram (1/28 ounce) differs:
4 calories in a gram of carbohydrate or protein

9 calories in a gram of fat

A typical diet is 2000 calories per day. If you get 50% of your calories from fat (shame on you!), that is 1000 calories of carbohydrate or protein, or 250 grams. It is 1000 calories of fat, or 111 grams. 361 grams total.
We will simplify. CH bonds contain little energy compared to CC bonds. H weighs little compared to C. We don't change much by ignoring H. There is some O and other stuff, but we will ignore that too. It will still be roughly right. So you burn about 361 grams of C.
For every C atoms you metabolize, you must breathe in 2 O atoms, and breathe out all 3 atoms as CO2. C atoms have an atomic weight of 12. O is 16. So CO2 is 44. Every 12 grams of C becomes 44 grams of CO2. So to burn 261 g of C, you breathe out 1324 g of CO2.
1324 g of water would be 1.324 liters. It is easily possible to sweat that much in a day, but you typically don't. You typically breathe out more CO2 than you sweat water.

I think this is rather misleading. The CO2 produced in fatty acid oxidation is not derived from O2 but from water, via hydration reactions. O2 is the terminal electron acceptor in the respiratory chain. You must take this into account when estimating water production. Also, C-H bonds are as important as C-C; many high energy electrons are extracted in fatty acid oxidation by replacing C-H with C-O bonds.

@Roland - I am sorry. I did not see this until today when someone upvoted. I thought I was supposed to be notified. You clearly know more than I about this. How should I improve the energy estimate of CO2 production? The O in CO2 can originate from water in a hydration reaction, but C cannot. Also this was about sweating, not the total water produced by metabolism. Some water is breathed out, some goes in urine.

Yeah the questions was pretty vague to being with. I would just ignore the effect of oxygen since it doesn't originate from fat anyway, and say that since fat is mostly (CH2) units with mass ~14, then by mass 12/14 = 85% of fat is exhaled as CO2 and 2/14 = 15% leaves as water.  Of course we're tallying up parts of molecules here but it's the way the question was posed I think. The energy yield is not relevant I think.


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Are there species that occupy several roles in the food hierarchy?
Are there species that occupy several roles in the food hierarchy?
By role, I am referring to producer, primary consumer, secondary consumer, tertiary consumer, quaternary consumer and so on.
Examples of more specific questions

Are there species that are both primary and secondary consumer?
Are there species that are primary consumer, secondary consumer and a tertiary consumer?
Are there species that are both producer and primary consumer?

I greatly modified the question to generalize and clarify it. Please do not hesitate to roll back if you preferred the original version for any reason.

I thought I remembered answering a very similar question here before, but it turned out to be on Worldbuilding.SE instead.

Food hierarchy and food web
Ecological trophic interactions are better represented by food webs rather than simple hierarchical relationships. As a consequence, the concepts of primary/secondary/tertiary/... consumers sometimes poorly apply to reality.
Obligate and Optional
Many species are able to feed on a various source of nutrients. As a consequence, a species can be a primary consumer under one environmental condition and be a secondary consumer under another. Such species might eventually almost never be both a primary and a secondary consumer at the same time and it renders the classification of species into one or another category a little more arbitrary.
How much does one need to eat to belong to a given category?
Note also that species like the cat, for example, are generally considered as being just carnivorous while in reality they often eat a very small amount of plant material. They also indirectly consume plant materials that are present within the gut of their preys. Such cases make the categorization more arbitrary again
Examples
Primary, secondary and tertiary consumer
This one is pretty easy. Humans, pigs, bears, corvids and catfish are all examples of species that are primary, secondary and tertiary consumer all in the same time. In other words, humans are omnivorous.
I am currently preparing a stew for tonight $\ddot \smile$. There are a number of vegetables and a little bit of pork (which itself is omnivorous). Tomorrow, I'll make some salmon (which is a secondary consumer as it mainly feeds on zooplankton).
Producer and secondary consumer
Carnivorous plants are able to photosynthesize and to capture animals. Most animals they capture are often best described as a primary consumer but some carnivorous plants small fish that feed on phytoplankton or even mice and frogs according to this video.
Producer and primary consumer
Parasitic plants (such as the common holly) are able to both photosynthesize and parasitize other primary consumers (it therefore also is a primary consumer if we equate parasitism to consumerism).
The eastern emerald elysia (a sea slug) feed on algae and is able to photosynthesize (using the chloroplasts of its preys).
Producer, primary consumer and secondary consumer
I cannot think of any examples right now but I would bet that it exists (eventually in a chemoautotroph species and eventually in a species that has a various life cycle).

so can you also be a primary and secondary consumer and a teritary consumer?

Nice answer, but i would argue that parasitism is not equivalent to consumerism

Perhaps you can add a note on whether these food habits are obligate or optional. For example humans can be either secondary or tertiary consumer (I am not sure if humans can totally avoid plant food as meat cannot provide all nutrients). The carnivorous and parasitic plants are strictly both producers and consumers because they cannot produce all the nutrients needed by them and therefore resort to carnivory/parasitism.

Thank you for the comments. I think I addressed them in my edits.

First of all, apart from primary producers, it can sometimes be difficult to assign an exact position or role to organisms in a tropic web or net since trophic levels might be diffuse or tangled. Most obviously, omnivorism is defined as organisms that eat from different food types, which in practice often means they eat from several trophic levels. Besides what is mentioned in the other answers, you also need to add species that shift their trophic role over their life history, which is e.g. the case for many species of fish, where juveniles are primary consumers (of e.g. plancton), while adults are secondary or tertiary consumers. The same situation is found in frogs (tadpoles vs adults) and many other organism groups. The basis for these shifts is often a change in body size (so trophic position is partially a function of body size), and these shifts are often discussed under the label ontogenetic niche shifts (see Werner & Gilliam, 1984). Functionally, such trophic shifts also means that the species can exploit widely different food sources over its life course, which will decrease the amount of intraspecific competition.
Another example of life-history shifts in the feeding hierarchy are species that change their trophic level when they change habitat. This is the case for salmon that migrate between marine and freshwater habitats. A third example is species that have intra-species predation (see e.g. Polis, 1981), which is also called cannibalism. This is, for instance, common in perch (Persson et al, 2000).
See this as a complement to Remi.b's answer.

To follow up with Remi.b's answer, there is an example of an organism that is a combination of  producer + primary consumer + secondary consumer:
Bladderwort (Utricularia spp.) is a carnivorous plant that photosynthesizes and is known to eat insects, fish and tadpoles. In addition, research by Marianne Peroutka suggests these plants also eat algae. (see here and here).
Others have also noticed other carnivorous  plants ingesting plant parts, possibly suggesting that more than one genera of plant fits this combo of trophic roles.


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"Signal Advance": Unsure of meaning or contextual use
I am reading through Recombinant DNA; Genes and Genomes - A Short Course - Third Edition by James D. Watson, et. al. and I came across this paragraph in the discussion about discrete factors of inheritance in Mendelian genetics:

The character shown by a plant depends on the pair of factors it receives from its parents. If both factors it receives are the same, that is, two dominant (yellow seed) or two recessive (green seed), then the plant exhibits those traits - yellow seeds for the former and green seeds for the latter. If one factor is dominant and the other recessive, then the dominant character is expressed; in this case, a plant with a factor for yellow seed and one for green seed will show the dominant trait, yellow seed. But the factor for green seed persists, even if the plant is yellow, and can reappear unchanged in later generations. This was a signal advance. In the 19th century it was believed that the traits of parents were blended in their offspring and, once mixed, the contributing traits could not be recovered. At the time, this was a severe problem for Charles Darwin's theory of evolution through natural selection. His critics pointed to that any favorable variation arising in an individual would have no long-term effect, because it would immediately be lost by blending.

Note: Added emphasis is mine.
I have done both Google and Google Scholar searches for

Signal Advance
Signal Advance Biology
Signal Advance Genetics
Signal Advance Science

and I have not had much success finding a definition for the use in this context.
One article, Plant biology: Signal advance for abscisic acid was one of the only relevant references I could find that used the words in combination, however they were only used in the title.
I am not sure of the context that it is being used in Recombinant DNA or in the plant biology article.
Are they saying that the signal advance marked a change in thinking on the subject, the way we would use the terms paradigm shift or quantum leap?
Or are they instead using the term in the sense of the recessive gene being maintained in the genome and was able to be expressed in future generations?
I have not come across the use of the term signal advance before, and it is difficult to work out from the context as the first half of the paragraph speaks about the genetics and then the second paragraph discusses how it provided evidence to change the hypothesis of the day.
There is a similar problem with the plant biology news and views as it talks about six new papers on a topic that had been elusive, but as it happens to be about a signaling pathway; I am left wondering the context here as well.
If anyone has come across this before and can help to clarify it for me, I would appreciate it. Thank you.

I almost wonder if this isn't a typo for 'singular'. I have no idea but I am curious.

@Resonating I do not think that they meant singular. Your question made me think about the grammatical structure of the Watson sentence, and it seems to be Signal as adjective and Advance as noun. When I looked at the definition of Signal as an adjective, there is this unusual; notable; outstanding: I think that both authors may be using it in this regard, but I still want to see if there might me a biological perspective to it.

@AMR you are essentially correct in your interpretation. "Signal" is a Britishism meaning key or important or groundbreaking. I think it's a bit old-fashioned, as I haven't really seen it much in contemporary literature, but I may be wrong on that part (I'm 'Murican, after all...).

@MattDMo Hmm... That would make sense, something that Watson picked up at Cambridge.... Also one of the co-authors, Jan A. Witkowski may be British as he was educated in England.

I found it in another context and would agree.  I don't see anything in the paragraph that would mean it had anything to do with the more common meaning of signalling.


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How do we predict the lifespan of dinosaurs?
Of course, they are fossils now. I found a link here which states that herbivors lived far longer than carnivores. The example being a T-Rex being "old" at 29, and a herbivorous Bothriospondylus having not reached half it's adult size at 43 years old.
But, is there any evidence that can indicate their life spans, or life spans of at least one kind of the dinosaurs?
An additional brief question is are their lifespans comparable with modern day descendants?

@questionhang: The general technique with dinosaurs is to count the rings in bones, although there are limitations to the method. Most notably, the technique gives an estimate of how old an individual was at death, not how long a member of the species could survive per se. Nevertheless, see https://books.google.com.au/books?id=9zRMBAAAQBAJ&pg=PA107&lpg=PA107&dq=ageing+dinosaurs+by+bone+rings&source=bl&ots=jOlKtu8vsK&sig=BjNoZxlMkPwF763PdWSUqYjEigI&hl=en&sa=X&ved=0ahUKEwi82dKSitvJAhUkGqYKHTneCeAQ6AEIITAB#v=onepage&q=ageing%20dinosaurs%20by%20bone%20rings&f=false

The question is unclear. 1) Are you talking about dinosaurs or mammals? 2) What dinosaur are you talking about? 3) Are you interested in estimates of age or description of the methods to find these ages (as suggested in the comments). Note also that you end sentences who are not questions with question marks which is quite confusing.

@Remi.b The description is better now?

I have made some major edits to the question and retracted my close vote. In it's current state the question is very answerable since the question is now asking about a general technique (hinted at by @bshane's comment).

I also don't find the question particularly unclear in its current form - voting to keep open.


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How can I generate a random DNA sequence?
I've found this paper which involves the construction of 19-bp random DNA sequences, but I don't know enough biology to understand how this method works.  Could someone explain it to someone who is highly technical, but has knowledge of only introductory, undergraduate biology?  How do the authors know that their resultant sequence is truly random?

If you want to synthesize a specific DNA sequence chemically, you start by attaching your first nucleotide (one letter in your DNA) to a solid phase. You can then continue adding individual letters to it. Because it is bound to a solid support material, you can wash the whole thing without washing your growing DNA away.
So if you want to synthesize AGC, you would first only add A to your reaction and then wash away all the A that hasn't reacted. Then you'd add G, which binds to your previous A, and again wash away all the G that hasn't reacted. Then you'd add C, and do the whole thing again.
If you want to create a random or semi-random sequence, you simply add multiple letters at once. If you always add all four letters in each step, you'll get a completely random sequence. You can also randomize only specific positions, and only there add all letters.
The result is random, but I don't think it is as random as e.g. a cryptographically secure pseudorandom number generator. There are various factors that can affect the randomness, variations in the concentrations of your nucleotides, variations in the quality or composition of your reactants and probably a lot more.
See also Oligonucleotide synthesis on Wikipedia

They say that the maximum sequences is 4¹⁹ which means every permutation. So I am not sure if they really synthesized random bases per each position or just synthesized all possible variants by allowing equimolar mixture of nucleotides at every step. This is what you also describe but the result IMO cannot be called random. It is expected to yield all permutations.

@WYSIWYG I'll have to look at the paper again, I though I had read them indicating that they were using chemical synthesis like I described, but it looks like I read that into their description

This is what is written in the M&M: "Random sequences were synthesized with equimolar mixtures of phosphoramidites." This is exactly what you said but I am not sure if that can be called random, in the sense of RNG.

@WYSIWYG Each individual coupling is random, and if you get to a length of DNA where you don't have enough molecules for all permutations, it gets truly random as well.

Sure. In fact all chemical reactions are essentially stochastic. I would however interpret "random primers" as set of n primers generated using a random number toss for a nucleotide at each position for all n primers. At n→∞ all possible permutations can be obtained.

For practical purposes, IDT offers randomized oligos. Saves a lot of trouble.Other companies probably offer this too.

As far I know, the way that Mad Scientist describes it is how random oligos are generated. There may be more advanced methods that the synthetic DNA providers like IDT use these days, but in principle that was how it was done around the time of the publication date of the paper.

@AMR Fundamentally it's the same chemistry, but IDT has it very well optimized, at the chemistry and synthesizer level. I've seen their plant a couple times and it's amazing how they can turn out so many oligos in a day from some nondescript building next to the walmart. Their shipping department is probably the best nonviral DNA delivery group in the world.


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Insertion of synthetic DNA sequence
If I have some synthetic DNA sequence (<=20 bp long), is there a way for me to reliably insert this sequence next to some n-bp motif?  I'd like for this to be possible in humans.  If so, are there any restrictions on the size of n?
I have explored the use of CRISPR/Cas9 for this end, but it is limited in the sense that the gRNA target sequence must be adjacent to a PAM sequence.  Attempts have been made to solve this problem (http://www.nature.com/nature/journal/v523/n7561/full/nature14592.html#affil-auth), but they fall short of full generality for n.  Are there any better approaches?

How big is the n (size of one/both flanks)? Also have a look at this post.

Just use something not restricted by PAM site, such as Zinc Finger nucleases or TALENs. But NOTHING about DNA insertion is reliable. The most likely repair route would be nonhomologous end joining, but you're looking for homology directed repair based on your 19 base template. Also 20 bases is way too short for good homology. You might be able to improve insertion rates by using a single-stranded template though.

gRNA is just for the targeting of the cut in order to engage site directed homologous recombination. You need to insert your synthetic sequence in between homology arms to get it to incorporate.


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Which part of the reflex arc takes the longest time?
The reflex arc is composed of 5 parts:
sensory receptors, afferent neuron(s), synapses within the central integrating station, efferent neuron(s) and the effector (includes transmission across the neuro-muscular junction and contractile mechanism - Assuming this is a myotatic reflex).
Which part takes the longest time & why?

I am providing this answer considering myotatic reflex arc (as you have specified in the question).
There are so many factors on which it depends...I have listed as many as I could -
Here the sensory receptor is intrafusal muscle fibres. Afferent neurons are type Ia or type II. Central processing may involve mono- or poly- synaptic junction(s). Efferent neuron is alpha or gamma motoneurons. Effector is intra- or extra- fusal muscle spindle.
Considering the human or animal to be of normal health and condition (absence of hypoxia, pyrexia, high or low pressure and anesthesia) sensory receptor takes the shortest time in reflex arc. Central synaptic junction may be mono- or poly- synaptic. Poly-synaptic junctions take longer time, but still it is shorter than neuro-muscular transmission.
So the competition now is between neurons and neuro-muscular junction. In case of neurons it mainly depends on the length, diameter and myelination (provided the above mentioned conditions about the sample is "normal"). Neuro-muscular transmission speed depends on the length of synaptic cleft, body calcium and chloride level, type of muscle fiber innervated and the type of reflex arc (alpha-gamma co-activation, reciprocal innervation etc) to name a few. So, it can be said that longest time would depend on the reflex arc you are considering, as this will decide the speed of transmission through the afferent and efferent neurons and neuro-muscular junction.

The answer to this question depends which reflex arc was activated, without knowing the exact reflex arc one should assume the answer as multifactorial and relate to this (or similar) table:

(Source: Fundamental Neuroscience for Basic and Clinical Applications,  by Duane E. Haines)

This provides only information on the conduction velocities. Thing is that peripheral sensory transduction, synaptic delays in the reflex arc and in the neuromuscular junction may add considerable amounts of time too, and not to forget the time it takes for the muscle to contract. Conduction velocities are just part of the equation.

@Christiaan In other words, this question could not be answered.

Then why did you O.o ?

@Christiaan I gave a direction... Sometimes it is better than exact answer.

The nerves in the gray matter would expect to conduct slower. Also synaptic transmission is generally slower than saltatory conduction.


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How do plants get their O₂ for respiration during the night?
If I am not mistaken the stomata are closed during the night. As a result I have a hard time to imagine how the plant can get the O2 it needs for respiration during the night. I thought the plant could produce the O2 internally through some chemical reaction. Such reaction might include splitting H2O absorbed through the roots in two. Or maybe the O2 diffuses well enough through the plant tissues.
How do plants get their O2 for respiration during the night?

Welcome to Biology.SE. I edited the question. Feel free to roll back if you don't like the edit. Here are a few notes on the format of your question. 1) Your title is too uninformative 2) You could use MathJax to write $O_2$ 3) No need to thank and sign at the end 4) Avoid double question marks.

Not all plants have their stomata closed during the night. A notable exception are Crassulacean acid metabolism(CAM) plants that keep their stomata closed during the day and open it during the night. This is a common evolutionary strategy with Xerophytes.
There are also 2 other types of metabolic pathways namely C3 and C4. As a consequence we get what is called a C3 and C4 plant, which aptly represent the predominant metabolic pathway it employs.
Additionally plant cells, like all life, can produce energy without oxygen by Glycolysis. Furthermore, when stomata is closed, oxygen respiration is restricted, not blocked entirely. Finally it might be important to note that plant metabolism is reduced during the night.
Full disclosure, I am not a botanist. Please let me know if there are any glaring errors.

The problem here lies in your assumption:

Stomata are closed during the night.

Despite the fact that most (C3) plants do indeed close their stomata during the night and open them when detect blue light in the morning, the stomata are not completely closed, that is, they are not closed to the point of not allowing any conductance.
According to Snyder (2003):

It is generally accepted that for C3 and C4 plants stomatal closure minimizes transpirational water loss (E) at night when there is no opportunity for carbon gain. However, there is increasing evidence that some species maintain substantial stomatal conductance (g) and E at night. Arabidopsis, Betula, Brassica, Chrysothamnus, Fraxinus, Picea, Rosa, Sarcobatus, and Tilia all have substantial night‐time g, based on gas exchange measurements.

Thus, these plants do absorb O2 at night.
Source:

Snyder, K. (2003). Night-time conductance in C3 and C4 species: do plants lose water at night?. Journal of Experimental Botany, 54(383), pp.861-865.

You are not wrong. Plants can use the oxygen obtained from the photolysis (light breaking) of water to drive cellular respiration. For every 1 $C_6H_{12}O_6$ (glucose) produced, 6 $CO_2$ and 12 $H_2O$ are consumed. In addition, 6 $H_2O$ and 6 $O_2$ are produced as well. But the primary way plants receive oxygen is the same way in which they receive carbon dioxide – through their stomata.

However, I do want to emphasize on Niobe's point of CAM plants. CAM plants have adapted to hot, arid conditions by closing their stomata during the day and opening them during the night to collect $CO_2$.

"Plants use the oxygen obtained from the photolysis (light breaking) of water to drive cellular respiration." any reference?

Well, plants provide oxygen as a byproduct of light-dependent reactions. Organisms, including photosynthetic organisms, use this oxygen as an oxidizing agent in cellular respiration.

I would like to add that plants perform cellular respiration throughout the day and night; and the way they do it is by storing oxygen during the day.

Plants lack proteins to accumulate oxygen. How are they supposed to "store oxygen during the day"? I'm not saying this is impossible, but the statement definitely requires a reference.


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How many genes does D. melanogaster have?
Obviously there is no 100% exact number, but I came across this on flybase, the gold standard for annotation. I am confused now. "Genes located to the genome", is that what I am looking for? If so, what does "Genes not located to the genome" mean?

I guess that the genes not located to the genome are the ones which cannot be mapped to a particular chromosome but are a part of some unmapped contig. You can see that from the GTF file but the figure does not match the stats shown here. In fact the stats page reports a total of 32078 genes records but the GTF only has 17716 (which is same as the genes located to the genome including unmapped contigs and mitochondria). So I guess the other genes are just present in the transcriptome assembly and are not mapped to any genome contig

@WYSIWYG it is related to genes and phenotypes from literature prior to having the sequenced genome.

EDIT
Personal correspondence to representative at FlyBase.org

In FlyBase we have been gathering information about genes and phenotypes for over 20 years including information from papers and resources older than that.  We annotate gene models on the Drosophila melanogaster genome assembly and when possible associate those annotations with other information (eg. phenotype, function etc) that is known about the gene.  However, in some cases, especially for genes and phenotypes that were described in the older literature before the genome was sequenced we still have some information about those genes but have been unable to associate that information with a genome annotation.   Those are what we call unlocalized genes (i.e. those without a annotation on the genome).


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Can we predict a person's tolerance to cold exposure during excercise?
Being an amateur athlete and student of anatomy I've always wanted to know if there is a formula for determining an unconditioned body's tolerance to cold temperatures while exercising.
I know the factors of age,weight, gender, humid versus dry weather etc. are going to make it tough to determine.
Has there been any research into formulaicly describing a persons cold temperature tolerance?

Hi and welcome to Bio.SE! The original question invited homebrew formulas which could be opinion based. I've made an edit that asks for a more established method. Feel free to role back on the edit!

The first thing I'd look for is some kind of acclimatization index.  Even if all the other factors mentioned are the same, people living at different heights or different biomes (desert v tundra) will have different cold temp tolerance.


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Why does our mouth "water"?
Whenever we see something delicious, rapid salivation starts in our mouth. Also, it doesn't happen for all other food, which we eat regularly.
So, Is there any particular use of "rapid salivation"? and why doesn't it happen for everyday foods?

Basic biology: saliva in digestion is used to digest starches and fats.  It also lubricates food so that it is easier to move down the esophagus.  It is the first response your body has to food entering your digestive system and occurs in advance of food arrival. Pavlov's dog is a demonstration of this.
Rapid salivation occurs most often in two cases.  The easy example is seeing or smelling something like cake or pie, though this applies to any highly desirable food to the individual.  The case we think less of is that of starvation or even deep hunger.  In this case, even "everyday foods" cause rapid salivation as the body needs any calories it can get.


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Do evergreen trees have higher densities of stomata to compensate for retaining leaves?
According to literature (Walls-Thumma), evergreen trees have less stomata on their leaves (than deciduous trees) to limit water evaporation.
Does this mean they have less less stomata in total, or do they have stomata on the adaxial surface that compensates for the smaller amount of the abaxial surface (in comparison to deciduous trees?).
Thanks!


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Machine-readable APG III trees?
Does anyone know where I can find a machine-readable version of the phylogenetic trees from APG III?  I'm looking for something that contains the full tree structure, including unnamed branches.  (i.e. not merely a list of which families are contained in which orders.)
The trees at the APG III site are graphic images -- not easy to turn into a data structure.

Just email the curators. peter.stevens@mobot.org (Missouri Botanical Garden), or stevensp@umsl.edu (University of Missouri, St Louis)


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What are these two fruit flies doing?
When taking some pictures I accidentally captured two fruit flies doing this:

The photos are unfortunately blurry, but from what I can tell, one fly approaches the other from behind, and something is then retracted/pulled into the front fly's body. I'm guessing it has to do with reproduction, but it doesn't look like the fruit fly mating I've seen before.
Here are some stills from the sequence:

From what I can tell, the one that flies away is a male while the subject is a female correct? That also leads me to believe this has something to do with reproduction. My guess. Curious to see an answer.

I've been working on fruit flies now for 7-8 years, including a lot of large mating and courtship assays. I believe what you are seeing is the male (identifiable by the black end of the abdomen and different shape) approaching a female. Judging by the extension of the male's right wing in the second still image, he is making a brief courtship attempt, but its very difficult to be certain of that from these images. The female then extends her ovipositor.
I believe that this could be one of two things:

A mate rejection behaviour by females - she actively made the movement to stop the males advances
The female was simply preparing herself for oviposition - the male just happened to approach her

I've seen it happen enough times both with females subject to courtship and females not subject to courtship to think that either of those is plausible for what is happening in your clip. Given the possible courtship by the male and the following text & videos from a recent paper I would say it is option 1, a mate rejection.

"Recently mated females reject courting males through a variety of actions such as decamping, flicking their wings, kicking the approaching male, or extrusion of the ovipositor [8]. Thus, copulation switches female behavior from acceptance to rejection." - Kimura et al. 2015

and

"Under natural conditions, the recently mated female occasionally extends the ovipositor straight along her body axis (anterior-posterior axis) toward the courting male (Fig 1A, S1 Movie), who usually positions himself behind the female [21]. During the ovipositor extension, the female abdomen was width-compressed throughout its entire length. We refer to the ovipositor extension as mating-type extrusion when it was protruded horizontally along the female body axis. A mated female that has found a suitable site for oviposition will lower and bend her abdomen downward and insert the ovipositor into the substrate before performing movements to expel an egg that is inserted into the substrate (Fig 1B, S2 Movie) [9]. Unlike the extrusion for rejection, the female narrowed the abdomen only at its posterior part." - Kimura et al. 2015

In figures S1 and S2 you can see those two behaviours very clearly in videos.
Note, I came to my answer before finding this Kimura paper so that's two lines of independent evidence (my experience and their paper). I hope it answers your question.


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What are the known energy capturing processes in biological systems?
I am not a biologist. I am aware that photosynthesis is the main process for capturing electromagnetic energy from the Sun. Also, I am aware that some bacteria can capture energy from boiling water and others from certain chemicals.

What are the known energy capturing processes in biological systems other than photosynthesis? I am looking for references or a good survey of all known mechanisms.
Is there an explanation for the ingenuity of evolution in solving the energy capturing (transforming) problem via multitude of mechanisms?

Apart from phototrophy, there is only chemotrophy (obtaining energy from redox reactions of chemical substances) and radiotrophy (obtaining energy from ionizing radiation such as gamma rays). However, radiotrophy as of now is only known to be a supplemental mode of energy and not a primary one.
Diversity is a central theme of evolution. It would be interesting if there was a single common mechanism for all modes of energy-nutrition which is perhaps true for the case of the chemiosmotic energy generating mechanism (ATP-synthase like systems which generate energy from chemical gradients). Otherwise, diversity is expected as the organisms evolve to survive in different environments.

Nice answer. Can you provide an example organism for each mechanism under chemotrophy and raditrophy?

@MohammadAl-Turkistany The link to the article gives the example of radiotrophic fungi. You can also check the other linked post. There are several chemotrophic bacteria. See the wikipedia link.

1:
The only two sources of energy that I could find (not that there aren't any others that I couldn't find or that haven't been discovered) are from light (plants) and "abiological compounds" (some bacteria).
Reference
http://link.springer.com/chapter/10.1007%2F10825622_4#page-1
It seems you have to buy this book, but the website does provide a preview containing the answer to your question (in the first paragraph).
2:
The likely explanation for having a multitude of ways of capturing energy is adaptive radiation. Having a different method of gathering energy would place the organism in a different ecological niche, which would have been otherwise unoccupied. This allows the organism to flourish. For example, heterotrophs evolved to metabolize a variety of compounds. Some digest mainly glucose, while others evolve to break down cellulose, amylose, protein, etc.
Further Reading
http://www.jstor.org/stable/2463047?seq=1#page_scan_tab_contents
https://en.wikipedia.org/wiki/Adaptive_radiation


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Is it worth to experiment with pro-biotics at home?
Let's assume that Joe has done some investigation on Internet and wants to see, if pro-biotics would help him. Now he goes to amazon.com and buys a pro-biotic product with excellent average rating. Note that not all of the reviews are from  "Amazon Verified Purchaser" for the specific product, but you got the point that it sound convincing that other people claim to benefit from the product.
So validity of Joe's pro-biotic experiment starts from pro-biotic supply chain. What are the steps in his pro-biotic experiment where experiment could go wrong; and what are the precautions he can take to make his experiment successful - either prove or disprove their benefits?
In the answer I seek something between lines (feel free to reuse these points to make your answer whole):

Joe should be confident that seller is selling the real thing and not  candies. Are there any regulations that ensure that there is no fraud going on at this step from Over-the-Counter seller? How common is such fraud by sellers? Have there been any studies?
The bacteria might die during shipping before Joe actually received his pro-biotics, for example, because of temperature changes. Obviously responsible seller should know how his merchandise should be shipped.
Joe should probably not take pro-biotics together with other drugs or even together with other pro-biotics, because they might kill each other.
There already could be some bacteria living in Joe's body that immediately kills "good bacteria" in pro-biotics without even making it.
And most important - The initial hypothesis found by Joe on Internet about "good bacteria" in pro-biotics was wrong in the first place. Is there a website that I can check with convincing research that has studied how each bacteria affects our body as a whole?

Also, would it be worth to grow culture of pro-biotics at home to make sure that there is bacteria in the first place? How hard that would be? We have microscope at home.
The reason I am asking this is because a person very close to me is super excited about pro-biotics so that it starts to affect my life. I just want to get opinion from people in the biology field on how skeptical they are about DIY people doing such pro-biotic experiments at home. I am not sure yet whether I should support this person or try to talk out of this. It seems that this person has been reading a lot on Internet about this subject so it is not easy for me to argue back.

The supplement market in the United States is regulated by the Food and Drug Administration, however, they are not required to prove that their products work as they are usually sold as a food supplement and not as a medicine. As such, their clinical studies, if done, come under little scrutiny. Also there is a very small number of the species that make up the human microbiome that can be cultured outside of the human GI tract. A healthy diet is likely a better solution, unless of course "Joe" has a medical condition such as IBD and can find a Doctor willing to perform a fecal transplant.

@AMR With "Also there is a very small number of the species that make up the human microbiome that can be cultured outside of the human GI tract." did you try to imply that it is impossible to make pro-biotic supplements in the first place, because most species of good-bacteria would die right away once packed in pro-biotic capsules? I.E. suggesting that pro-biotic suppelement claims for that kind of bacteria would be scam? Is there somewhere a catalog of bacteria that would identify these kind of bacteria that can't be transferred via capsules?

"Studies of Segmented Filamentous Bacteria biology have been hampered by the current absence of ex-vivo culture methods." -Ivanov II, Littman DR. Segmented filamentous bacteria take the stage. Mucosal Immunol. 2010;3(3):209-212 Nothing in science is ever impossible it is just a question of feasibility and whether someone has accomplished it. Obviously the ones in yogurt can be cultured, but many of the ones that they find genomes for in samples have not bet cultured, yet. The question of whether they can be ingested in capsule form and populate the colon is up for debate.

If you look at my answer here http://biology.stackexchange.com/questions/41478/can-an-argument-be-made-that-humans-are-90-bacterial and here http://biology.stackexchange.com/questions/41415/do-intestinal-flora-have-the-same-dna-as-their-host/41429#41429 I have provided a lot of details about the microbiome and there are many references linked that you can research for yourself.

This is a list of the 539 journal articles that have been published as a result of the Human Microbiome Project. https://commonfund.nih.gov/publications?pid=16

Statistics-wise the sample size is too ridiculous to call this an experiment, because you can't control any random effects if your sample consists of a single person.

I agree with Eli, unless you have a lab and a moderate amount of microbiological training/skill, you're not going to know the answer to any of those questions.  When it fails, you'd have no way of knowing where.


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Why does uniprot sometimes not label single-pass transmembrane proteins as "anchors"?
Currently, section 3a) of unitprot TRANSMEM reference page divides single-pass transmembrane proteins into 4 types: I, II, III, IV. I is not explicitly labelled as an "anchor" whereas the others are. What criteria need to be made for a single-pass protein not to be classed as an anchor?

A membrane anchor is close to the end (N-terminus or C-terminus) of a protein. For "Single-pass type I membrane proteins" the transmembrane region is not necessarily close to N- or C-terminus, which is why single-pass type I membrane domain are not labeled as anchors.
Instead, relevant entries usually have a signal peptide annotated.
Note that we have replaced the example for single-pass type I membrane protein by http://www.uniprot.org/uniprot/P14778#subcellular_location which is more relevant (the modified version of the documentation will be available with release 2016_01).


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Can brain damage caused by physical injury affect the social behaviour of a person?
Can a physical injury to the brain, resulting from an accident, and not the result of a diagnosed mental illness, affect a person's social behavior?

If sociability wouldn't have anything to do with the brain, by what other mechanisms would the exposure to the world shape future behaviour?

I didn't say that sociability isn't due to brain. I asked whether brain injury can affect social life or not. :)

So you should edit your question cause now title and first sentence are terrible

oh, sorry about that.. I changed it.. :)

Socialization is a cognitive and executive brain based function that requires higher level thinking mechanisms usually dependent on the prefrontal coretex. A lot of social cues we obtain from our environment when we are young can shape our brains during its developmental growth (infancy-post puberty) and cause our brains to develop social habits and access specific social functions.
A great text book example of altered social behavior due to brain injury is Phineas Gage. He had a metal rod shot through the prefrontal cortex and it caused a severe change in his behavior. He no longer cared about social cues and people often referred to his behavior as becoming "rude" and "out of context." There are many subtle aspects of behavior that are regulated by brain functions and there are many books on the topic.
Source: Wikipedia page on Phineas Gage and
Pyschopharmacology, book by:  Meyer and Quenzer
DSM-5, text book on clinical psychology
Further Reading on Phineas Gage
- What were the symptoms of Phineas Gage after suffering his brain injury?

I was going to suggest that we migrate this question to cogsci, but this answer kept it neatly on topic.

Thanks! I think both sections intermingle nicely sometimes.

Great answer and +1 for including a reference other than Wikipedia. @James - This question is on topic on both sites, regardless the answer.

@Christiaan I don't think it was off-topic, but from the question I thought a better quality cogsci answer would emerge than what our community might provide, but this answer showed me wrong. Cross posting might still be interesting with this question.

Despise the tasteless title, I find this case really interesting: Brain tumour causes uncontrollable paedophilia


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What is the difference between stomata in evergreen broadleaf trees and deciduous broadleaf trees?
They must have some difference in their stomatal density /whether they are hypostomatous or amphistomatous/whatever, mustn't they?

@Christiaan - Evergreen have needles. Broadleaf have broader leaves, which are generally larger than needles. It is not unreasonable that two trees of similar size need a similar number of stomata. So the question is how do the stomata of the two types of leaf differ? Do needles have a higher density? My first thought would be that evergreen trees must have more needles than broadleaf trees have leaves.


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Is there a free software for manual sequence annotation?
I'm looking for a software that would allow me to make a quick graphical annotation of the structural features of a sequence. Something that would look like what you get in jalview, with your sequence on top and tracks at the bottom that highlight which part is an alpha helix or a beta sheet.
My final annotated sequence would look like this:

Benchling is free for academics and makes sequence annotation really easy. Check out an example sequence I annotated here: https://benchling.com/s/1m8QllV2/edit It's all on the web, so you can sign up at https://benchling.com :)

You might find some success with using WebApollo or JBrowse
WebApollo allows you to perform many manual annotation functions for your genes, such as editing exon boundaries, fixing coding sequences, and merging or splitting gene predictions, which looks like what might have been done in the UCA-At2g42245. It can also be used for adding various attributes, GO terms, pubmed info, or generic attributes. WebApollo actually uses JBrowse, but JBrowse itself has very flexible options for displaying annotations. The part about highlighting the alpha helix/beta sheets is not built in, but JBrowse can be configured to do lots of different renderings, and I could provide more details if you are interested. Disclaimer: I'm a WebApollo developer/JBrowse contributor.


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Is addiction adaptive?
Addiction and addictive traits seem common amongst animals.  A pubmed query shows it's been studied in everything from humans to worms.

My personal favorite of these is: "Individual Consistency of Feather Pecking Behavior in Laying Hens: Once a Feather Pecker Always a Feather Pecker?"

Is there/was there something adaptive about addictive behaviour?
Alternatively, how it is that addictive behaviour survived/persists if it is not adaptive?

First, I think you are mixing up obsessive compulsive behavior with addiction, which isn't exactly the same. From a strictly biological perspective, addiction generally has to do with the reward pathways. What usually happens is the chemical that the organism becomes addicted to binds irreversibly to a receptor on a neuron. In order to stop the signal, the cell pulls down the receptor, as there are less receptors, more of the chemical is needed to induce the same response. Also the body tends to develop a physical need for that chemical and without it there are severe withdrawal consequences.

See this related ? Here.  http://biology.stackexchange.com/q/36620/6061

Albeit used in the keywords of the paper, feather pecking is not an addiction, but normal behavior turned pathological in artificial (overcrowded) environments.
Addiction typically arises through overstimulation of reward centers in the brain, most notably the dopaminergic pathways involving the nucleus accumbens. Massive dopamine release, e.g. through cocaïne or meth intake, results in euphoria (Wise & Bozarth, 1985). When the drug's effects wear off it is followed by the 'crash', characterized by dysphoria and a longing for more drugs (CSAT, 1999). Gambling addiction works much in the same way.
Addiction develops because of an interplay of dependence and tolerance. Dependence is caused by downregulation of dopaminergic responses in the reward centers. Notably, dopamine receptors are downregulated when dopamine agonists like stimulant drugs of abuse are chronically administered. Downregulation of dopaminergic responses causes the physiology of the reward pathway to adapt to the presence of dopamine agonists. While the drug is in the system, everything is OK. However, once the levels of the dopamine agonist wears off, the body enters a state of lack of dopaminergic responses, causing dysphoria and depression. Tolerance develops as the liver and other tissues start breaking down the drug more efficiently due to upregulation of the necessary catabolic enzymes. Hence, more of the drug is needed, and the user becomes more and more tolerant. The interplay of dependence and tolerance form the dreaded vicious, downward spiral of addiction.
The reward centers have been crucial in evolution, as they provide motivation to vital acts of life, including eating and sex (University of Colorado, Boulder). Without a proper reward system, why eat or reproduce? However, drugs and other addictive acts such as gambling also activate the reward system.
Highly purified drugs such as crystal meth and cocaïne result in massive dopamine release that is unparalleled by normal physiologic processes such as eating. Before the occurrence of stimulants and things like gambling, the reward system was nothing but essential to life and evolution. Now, things are different and man needs to adapt to these novel, artificial pleasures in life.
References
- Treatment Improvement Protocol (TIP) Series, No. 33. Center for Substance Abuse Treatment. Rockville (MD); 1999
- Wise & Bozarth, Psychiatr Med (1985); 3(4): 445-60

Although addiction as a coping mechanism may help in the short term. Ie.preventing a depressed person from killing themselves through temporary relief of symptoms. In the long run addiction causes many more problems then it solves. The type of addiction also needs to be considered. Many alcoholics can go years before health and financial problems begin to cause trouble. Enough time to raise a family. Possibly the reason addiction genes haven't been removed from the pool. If you look at possibility the most extreme form of addiction, wires directly into the pleasure center of the brain. You see how completely maladaptive it can be. The monkeys will sit and press the button over and over. They neglect grooming behavior, other external stimulation,food and water. Loosing interest in anything beyond the pleasure button. Eventually succumbing to exhaustion. If allowed they will continue pushing the button and die as a result. This is an extreme case because with electronic stimulation the regular negative feedback that results from overstimulation of the pleasure centers appears to be absent. chemical stimulation of the pleasure centers causes tolerance and the feeling becomes harder to obtain the more one uses. Although many addicts chase the high until it kills them as well.

can you add some references to your answer? we always appreciate external references to questions and answers on BiologySE - thanks!


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Why do you retch when you see something disgusting?
Why do you retch when you see something disgusting?
I imagine it is some sort of evolutionary response, although I can't see the connection between receiving a signal that unhealthy conditions are in the current environment and wanting to empty the contents of one's stomach, which likely were eaten elsewhere. The response I would have expected to have developed would have been one of fleeing, rather than vomiting.
As a subquestion, why does the same reaction sometimes occur when imagining something disgusting, even if it is not real?
(I know "disgusting" is subjective; I'm referring to things humans may want to not be around for health reasons, e.g. rotting flesh, infestations of traditionally disease-carrying insects, etc.)

I wonder if this question isn't more appropriate on CogSci SE, as not all people are effected in this way, and there may be more of a psychosocial aspect to it than one that is strictly biological.

@AMR That's a good point. I'm going to give it a bit more time to marinate here to see what comes of it before moving it.

I am not very familiar with neurology, but I know that people can have sensitivities to things like blood draws etc. because of vasovagal response. Some may be more highly sensitive than others.

Seems to me your body telling you to stay away from something rather than it just being unpleasant to to look at is, is a stronger more reinforced manner of personal protection/preservation. Interesting ? Though curious to see what else era posted. I think it's fine here on bio SE By the way

Physiologically speaking, your body is reacting to something you have known associations learning. An extreme form of this phenomenon is seen in drug addiction.  After chronic use of a substance there are certain cues a person associates with the drug effects. Whether that be a certain group of people, a sound, a place, or an object the stimulant is eventually associated with the drug effect. After a certain amount of time a physiological reaction occurs with just the introduction to the stimulant without the drug. Often, if an addict receives a stimulation without a drug they are, at first, excited, calm, or feeling whatever the drug effects caused. But then, if no drug is received, the withdrawal effects come into play and makes the addict feel worse and crave the drug more intensely.
Anyway, so when you see something you associate with being gross or awful, your bodies physical reaction is essentially prepping you for the event.The biological and cellular effects of associative learning are regulated in the central nervous system (brain). The main theory is that the initial effect of the stimulus is regulated by dopaminergic channels, and the learning and associations are regulated by serotonergic channels. However, it is more like a complex network of synaptic channels at work in various parts of the brain. The regions known to be apart of associative learning are the emotional cortex of the brain are the amygdala, prefrontal cortex, and hippocampus.
For gastrointestinal upset the stimulus is most likely associated with an event that caused GI upset previously. For example, let's say you went out to a party and had too much to drink. You throw up everything you've eaten that day and you just generally feel awful and 'sick to your stomach.' Now, every time you see, smell, or taste that brand or flavor of alcohol you consumed, you immediately gag because your body is remembering the previous event and associates that stimulus with the vomiting and sick feeling. Does that make sense? Let me know if you would like more clarification.
Sources:

Drug Addiction Drug Habituation - Profiles in Science
Control of cocaine-seeking behavior by drug-associated stimuli in rats: Effects on recovery of extinguished operant-responding and extracellular dopamine levels in amygdala and nucleus accumbens
Neural and psychological mechanisms underlying appetitive learning: links to drug addiction
Physcopharmacology by: Meyer and Quenzer (ISBN 978-0-87893-510-9) (best source)

That sort of makes sense, except why vomiting / gagging? Not only are there other conceivable reactions to disgust (for example why not experience a sudden urge to wash one's self rather than purge stomach contents), but there are other conceivable reactions in general (for example, fear instead of disgust, that is an urge to flee rather than purge). Or, in other words, when you say "prepping you for the event", what event is being prepared for and why is vomiting preparation for it?

The association is usually something gastrointestinal based if you are gagging. Aka. usually the event associated with the stimulus is related to gastrointestinal upset, like eating bad food one time, or throwing up after drinking too much. I'll try to add that to my answer :)

So, the claim is, it's not an evolutionary response, but rather the remains of a learned response, specifically related to eating and now sometimes applied inappropriately, to stimuli encountered previously?

Essentially. It could be evolutionary, but it would be extremely difficult to prove and the less logical of the concepts. You would have to have a gag reflexes to stimuli you have never seen or have associations with, which most people don't. It is also pretty much impossible to research because babies are getting sensory overload and making learning associating from the second they are born, and we can't look at the animal lineage because there is no way to detect a gag in an animal.

I wonder if there is any studied and documented correlation between people who are more prone to having this response (such as those who gag at the site of blood) and some sort of specific eating-related events during childhood. I'm going to pursue that and see if I can find anything. I am also becoming more convinced that this may be a CogSci topic.

Hahaha, that depends upon the part of the question you are interested in pursuing. If you're interested in understanding the neurology of learning associations and blood-response cues, then it could stay on bio. But, if you are simply interested in the psychology of the event, then yes it is more a cogsci question.


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How to measure GnRH in menstrual cycle?
I am interested in pulse frequencies of GnRH (gonadotropin-releasing hormone) in the menstrual cycle (MC) i.e. 28 +/- 7 days.
I would like to study its pulsatile nature i.e. within one MC, not same as cyclic nature within many MCs; but possible cyclic dynamics could be found in one MC too but not focus there.
GnRH releases human chorionic gonadotropin (hCG) which can be monitored by beta hCG but also by (source DynaMed Plus on Chorionic gonadotropin)

serum progesterone, Luteinizing hormone (LH)
estradiol levels
ovarian US 7-14 MCD i.e. in late follicular phase
onset of ovulation at 14 MCD
pelvic exam
cryptorchidism: signs of precocious puberty

Two articles on GnRH monitoring:

Monitoring gonadotropin-releasing hormone administration by measurement of urinary steroid conjugates in the morning urine samples.
some gene studies: Episodic gonadotropin-releasing hormone gene expression revealed by dynamic monitoring of luciferase reporter activity in single, living neurons

Possible cases to study

Amenorrhea: Kallmann syndrome where congenitally deficiency of GnRH but how low?

However, I did not find any publication describing direct/indirect continuous measurement of GnRH.

How can GnRH be measured continuously during the menstrual cycle?

English-speaking doctors and scientists would never use the word "pulsative." Maybe pulsatile, but not "pulsative."

GnRH is found in very low concentrations (2-10 pg/mL)
Options:

A highly sensitive analytical method (e.g. radioimmunoassay)
To sample directly from the hypophyseal-portal system
A surrogate measure

This abstract: http://www.ncbi.nlm.nih.gov/pubmed/9749566 describes direct measurement.
Direct sampling could only be done under general anaesthesia and in a short window, so I'd avoid that altogether unless you're talking about using an animal model and can surgically impact a cannula.
This abstract: http://www.ncbi.nlm.nih.gov/pubmed/21646369 describes use of the $\alpha$-subunit as a surrogate of GnRH (the $\alpha$-subunit is the same for FSH, LH, and TSH and is released under the control of GnRH).

By the way, GnRH does not promote secretion of hCG so much as it does LH and FSH (LH is fairly homologous to hCG).  For the most part hCG is secreted by trophoblasts (in the placenta) and is quite low except in pregnancy or the presence of certain germ cell tumors, so wouldn't be worth measuring in non-pregnant women or males anyway.
The bigger point is why do you want to measure GnRH pulsatility?  This has been done and the you know that it is pulsatile is because it has been done.

I want to get a 1D signal of this event's potential and study it by FFT. I want to study the fertility by studying GnRH's properties.