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Are there different species of modern day humans?
I've been watching nature shows on Netflix (Wildest series) and different animals of the same "family" are actually different species.
e.g. Asian elephants vs African elephants. Asian elephants are much smaller than their African counterparts.
Also with monkeys, different locations have their own species. Take langurs for example (see link below)
http://en.wikipedia.org/wiki/Gray_langur
http://en.wikipedia.org/wiki/File:LangurMap.svg
Just in the Indian subcontinent, there are many species of the same "gray langur".
In saying all that, how many species are there of modern day humans? It can't be just 1 homo sapiens it's quite obvious there are differences based on location. (Africans have darker skin. East asians have distinctly-shaped eyes and etc). Monkeys have lots of species even of the same "family" (see example above) and we're also primates.
thoughts? thanks

Nope, all modern humans are one species, even one subspecies (https://en.wikipedia.org/wiki/Anatomically_modern_human). I suggest reading on taxonomy to understand the terms species and family (https://en.wikipedia.org/wiki/Taxonomic_rank). Remember that these distinct classifications are concepts developed by us and appliead to biological entities which actually don't form such discrete structure.

By asking a question and then immediately ruling out a possible answer, which in this case is actually the factual answer to your question, you are giving an indication that you may not be open to an answer that would be contrary to your own ideas. Think about editing your question and rewording it in such a way as to remove the impression that you may not be willing to accept the answer if it is contrary to your view. Thanks.

It can't be just 1 homo sapiens. Guess again. A common definition of a species is that members of the same species group can produce viable and fertile offspring. Think about how that works with humans.

Why would skin color be an "obvious" reason anyway? We don't say that about other animals that come with different skin or fur color. Likewise with eye shape.

Also related: Do humans have enough biological differences to be grouped into races or subspecies?

To James: then you have ligers

Not only is there only one species of human, genetically we don't even divide into different races. Pick any male human on the planet, at random, and any woman from anywhere else on the planet, also at random. They are just as likely to be capable of bearing children as any two people from the same village. The whole concept of a species embraces the concept of 'continuous reproductive continuity', so your 'obviously different human species' is profoundly mistaken.

Nice answer, it could be good to add some sources too which would both allow further reading and offer support to your answer :) though I'm not sure I'd bother in this case if I were you - looks like the question is headed for closure and deletion


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Where can I find DNA Sequence data for colon cancer
I am a computer scientist studying pattern recognition, and I am hoping to do some supervised learning on colon cancer.  Unfortunately, I'm having a heck of a time finding DNA data in the following format.
Benign DNA (Adenoma?)     Malignant DNA (Carcinoma?)
A                         A
A                         A
T                         G
G                         G
C                         C

So I just need two columns (don't care if it goes down for 3 billion records/ amino acids): one with the good DNA and one with the bad.
Is there anywhere I can find data in that specific format?

Did you checkout dcc.icgc.org? I think unlikely that someone will have the data formatted precisely the way you described, but you should be able to reformat it to suit your analysis pipeline. What you can download from there is a VCF file which only lists the positions in the tumour where it differs from the Normal so if you really want the entire genome file you would need to start with the human reference sequence, and change the sites to match the annotations in the VCF file. N.B. the will not have a comparison between a benign and a malignant. just tumour vs. normal

You may try the data for "Colon Adenocarcinoma" made by the TCGA project:
http://gdac.broadinstitute.org/runs/analyses__2015_04_02/reports/cancer/COAD/
The file with mutations called by the tumor against a matched normal,
http://gdac.broadinstitute.org/runs/analyses__2015_04_02/reports/cancer/COAD/MutSigNozzleReport2.0/COAD-TP.final_analysis_set.maf
What you need are column 11, 12 and 13. Column 11 is the reference allele (your so-call good DNA). For each row, the alternative allele (bad DNA) is column 12 if column 12 does not equal column 11, otherwise it is column 13. -- It would be a piece of cake to make by coding :)
In case you are interested, column 16 and 17 are the tumor and normal sample IDs.

THANK YOU!!!  This is exactly what I need, and thank you for making the field references easy.  I'm using R to extract the .maf format, so I very much appreciate how much easier your answer makes the data understanding.  Thank you as well for the insight into columns 16 and 17.  Really, very helpful, thank you.

You're most welcome! Here is more information about the .maf file, https://www.biostars.org/p/69222/ , though it might be a bit biology intensive.

One quick question about that data: a couple of the alleles (records for the alleles) have more than one letter.  Do you know what that is about?  Just want to know if I should record it as an A, T, G, or a C.  Thank you so much again.

Those are indels (insertions or deletions) that involve multiple nucleotides. The rest are so-called SNVs, single nucleotide variations. Splitting and merging over indels/SNVs is a common practice in data analysis.

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Why exactly does a scarf help against a neck pain and a sore throat?
I was going out without a scarf and as this day my neck
was more sensitive; after a while my voice was
rasping, I needed to cough and my neck was hurting
slightly.
After coming home I put on my silk scarf and the effect
was almost immediate. The pain cedes and my voiced normalized.
Why exactly is the warmth provided by a scarf so quick and
effective for our neck ? I can see that isolating the neck
is more effective than a warm room (air is a bad heat conductor),
but why does the warmth help us to combat rasping and coughing ?
What causes rasping and coughing by the way ?

It is not like this for everyone by any means; why it is for you is a bit of a different question. Also, there'smore than one question there. The by the way has a long, separate answer.

Placebo Effect.

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Does the assembly of the PLC transcription complex utilize phosphorylation in binding of the GTFs?
in the recruitment of general transcription factors during transcription initiation is phosphorylation utilized?


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Nail polish toxicity studies?
Are there any well-founded studies that authoritatively demonstrate negative effects from the use of nail polish, particularly in children?
I've been brought into the fray of a couple of folks who are having a rather serious debate of whether or not a child of 6 or 7 years of age should be allowed or discouraged from wearing traditional (not the "safe brands") nail polish.  It was my opinion that it is better err on the side of caution and that one should rather be safe than sorry, opting for safer non-toxic alternatives if fingernail paint must be worn by such a young child.
The debate has boiled over into allegations of quack science and over-caution.  Seems absurd to me, but I wanted to do some more research into the biology of the matter.
A recent report appears to urge on the side of caution, but could someone help to point me in the right direction with regards to substantiating valid scientific claims and studies that fingernail polish can, has and/or does contain harmful material that should not warrant careless usage, especially by younger children who may be more hormonally susceptible to adverse effects?
I'm really looking to button up the "quack" or kooky science arguments if possible and to put this debate to proverbial rest.

I seriously doubt you will find any peer-reviewed data on this as no one would be willing to fund the research. You may get a public health department looking into the claims of health issues, but there you will tend to have politics tainting the answers. If you look at the controversy that was generated this year with the NY Times exposé on Nail Salons, there was a response at the state level, so maybe the New York City or State health departments issued reports on the chemicals involved. That may be your best bet to finding a source that is even remotely scientific.

You may want to start by Googling Material Safety Data Sheets for Nail Products. Here is one of the links that came up. http://www.nsinails.com/nail-lab/science-of-beauty/material-safety-data-sheets.html#.Vl6LQ4T41NE . Also OSHA has issued safety guidelines for salon workers https://www.osha.gov/Publications/3542nail-salon-workers-guide.pdf

I wouldn't have thought that the nail polish is a problem. What might be a better reason for caution from a dermatological point of view is the nail polish remover, which is a known allergen. "In addition to blister formation, polish removers may cause irritant and allergic contact dermatitis, onycholysis, paronychia, and brittleness. They represent a fire hazard and may cause systemic toxicity following excessive inhalation."

That website looks like it is about scare-mongering.  I can't read beyond the abstract of the study, but people are exposed to trace amounts of all kinds of chemicals all the time.  You can't avoid them all, and you don't need to, if there is no evidence of harm.  Honestly, the kids are far more likely to suffer harm swimming or bike riding than from wearing nail polish.


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Comparing Embryonic stem cell and hepatic stem cell
So, currently, I want to compare transcriptome data for liver cell development. I found 2 data sets which start from stem cell, hepatoblast, and then adult cell. The first data set use hepatic stem cell and the second data set use embryonic stem cell. I am trying to map the difference in the gene expression during cell development, so it is important to make sure the state of the cell is same. My question is, is this stem cell comparable and can be grouped as 1 category? If hepatic stem cell and embryonic stem cell is different, is there something in common that probably can be used as basis of my analysis?


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Math backbone in biology/genetic
Are there any good books, that shows some advanced models in genetics particularly?
The problem is i don't see any good math model in genetics interactions exept combinatorics. I'd like to know what else math structures and rules are there in genetics.
I'd like create strong math backbone for better understanding genetics, but i can't find any advanced reliable sources for that. Are there any books that could help me?
Thanks a lot.

If population genetics is what interests you (but I don't think it is), then you should have a look at Book recommendation on population/evolutionary genetics? and Mathematical Modelling of Natural Selection.

It would help us to understand exactly what you are looking for if you could link to a specific paper which you would like their work to be reported in the book.

Elements of Evolutionary Genetics; Charlesworth and Charlesworth

I would vote to close as unclear (but I cannot because apparently I already did and then retracted my vote). I do not know exactly what you are looking for. Adding an example of the type of study that you would like to find in your book would help.

Related/ possible duplicate of: A free book/resource for learning genetics? and Which texts are good for beginners to understand evolution on the genetic scope?


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Why can't our eyes smoothly transition from side to side without focusing on a moving object?
Why are we not able to slowly and smoothly look from side to side, or up and down in a single and smooth transition, given that we are able to do this if our eyes are focused on a moving object?

Experimentator here! 1) I am not necessarily focussing on a moving object. 2) even in the complete darkness I failed to transition smoothly from side to side.

@remi.b I don't think it's possible to not focus on anything. We always have a destination in mind, even if we're staring at a blank wall! Consider why you are moving your eyes: you're testing if you can smoothly transition from side to side - that's two points -with nothing in between them. Of course you can't transition smoothly from max left pane to, max right pane. However, if we use our neck to guide our vision (maintaining central vision) we can do so very easily.

"If we use our neck to guide our vision" isn't that the same effect as staring at something moving? I don't know if you meant that as an attempt to transition from side to side without staring at something moving. I could be understanding that wrong though i guess.

@Hooplehead24 I believe that by "maintaining central vision", what R.Doto means is maintaining fixated focus on a point while moving the head. This statement then is certainly true, but irrelevant if I understand accurately that your question pertains to doing so without a focal point.

@R.Doto "I don't think it's possible to not focus on anything." It is actually, but it's not natural under normal circumstances. Try this experiment: Close your eyes and imagine that you feel the sensation of a hair tickling your nose, or hear the sound of a tiny fly buzzing directly in front of you. Then open your eyes and "look" for it. If only for a brief moment, your searching eyes are focusing into a place where there is nothing to see. With patience, calm, and practice, it is possible to even maintain focus on a relatively fixed point where there is nothing. It's a very odd sensation.

Short answer
Smooth pursuit is driven by retinal slip, which is determined by external input registered peripherally in the retina.
Background
The smooth pursuit system is a system designed to minimize retinal slip, i.e., the movement of an image across the retina. Saccades are rapid eye movements meant to fixate quickly on a new target (Purves et al., 2001).
Both movements are readily apparent when sitting in a train and staring outside; the eyes focus on a distant object and pursue that object. Once it exits the field of view, the eyes target a new object via a saccade and smooth pursuit is again initiated (the train window phenomenon).
Saccades can be triggered both involuntary (due to a sudden, unexpected stimulus) and voluntarily (Walker et al., 2000).
The smooth pursuit system cannot be voluntarily controlled, barred in some highly trained observers (Purves et al., 2001). Instead, it is guided by eye movements dependent on the movement (slip) of the fixated target on the fovea (Thier & Uwe, 2005). Hence, this system is controlled by external stimuli, not by internal ones. Retinal slip can of course be voluntarily manipulated by moving the eyes away from the target, for example by moving the head. The smooth pursuit system detects this by registering retinal slip, and keeps the eyes fixated on the target, through smooth pursuit which is involuntary.
References
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates (2001)
- Thier & Uwe, Curr Opinion Neurobiol (2005); 15: 645–52
- Walker et al., Exp Brain Res (2000); 130: 540–4

+1 Excellent answer. Given that this "highly trained observation" is possible (which I can corroborate), I still favor the idea that the involuntary nature of smooth pursuit is probably more from the force of deeply ingrained and continually useful and rewarding habit than actual neurological hard-wiring. (Visual tracking is a skill acquired after birth in our species.) Still because this skill and habit is pretty much universal in acquisition and application (excepting the visually impaired), I think the answer you have given here is functionally accurate. Thanks.

@MarkBailey, thanks! Smooth pursuit is indeed an acquired skill, but most of the visual capabilities are, for that matter. For example, depth perception is acquired afaik, but still hardwired in adults. I have to admit Purves et al. don't provide a reference to the primary literature on voluntary smooth pursuit. However, the book is pretty good.

Your eyes are attempting to see; not merely move. The muscles that move your eyes are voluntary. You control them, but think about how you usually command them. Whether sudden and reactive or careful and deliberate, you think about where you want to be looking and make your eyes look there. There is no functional purpose in looking without seeing, and seeing involves tracking specific features, focusing. It requires quick movement between multiple points of focus to gain information efficiently.
Compare this to the movement of your fingers. That movement can be smooth and fluid even though multiple muscle groups have to work together to make it happen. When you command the movement of your finger, you have a body-map that gives you a detailed idea of where your finger is, and how it is connected to you. You can be aware of its location with reasonable precision even if you can't see it. When it is necessary to move it with smooth, fluid motion, your muscle movement is guided by your internal body-map, and usually your eyes, confirming the motion. In contrast, you have very little concept of the actual position of your eyes within their socket, probably because it's not generally very useful information.
Positioning your eyes precisely, independent of what they are looking at is actually counter-productive. Doing so costs you the ability to see, as you can demonstrate to yourself by crossing your eyes, which, incidentally, is probably your best chance at achieving the sort of smooth movement you are referring to.
Probably the most significant reason you can't move your eyes smoothly is what you have practiced consistently for most of your life. With your motor muscles, countless various activities have required some degree of precise, smooth movement. During those very activities, what are your eyes doing? They are only moving smoothly if they are focused on a single point in motion - either a point on your body, or a point on an object which you are moving. Otherwise, they are bouncing from point to point, gathering information to measure whether your muscles need to adjust to accomplish the smooth movement you are attempting.
When you were born, your motor muscles were not proficient with smooth action either. Think about how a newborn baby jerks their limbs around, sometimes even clobbering themselves with their own hands, and then getting upset about being hit. As a toddler grows toward primary school age, they gradually learn to control muscle movement, but still have trouble when a situation demands very precise movement. Practice, for years, is what ultimately brings graceful movement. But no one ever naturally practices graceful eye motions (not independent of focusing on an object), because such movements are not useful for seeing.
References:
Body Map Concept: This concept is something you can demonstrate to yourself by moving around in the dark or by performing a task that you cannot see directly, like writing or typing, with your hands hidden from view. Here is a fascinating RadioLab discussion on phantom limbs which relates closely to this concept.
Motor and Eye movement: The Wikipedia article on Eye-Hand Coordination provides some context around the way eye and motor movement correlate.
Childhood development: Smooth pursuit is an acquired skill early in life (Van Hofsten & Rosander, 1997), which I can back up with personal observations of my 3 boys growing up.
Smooth Eye Movement: I have verified every statement I've made on this topic via personal experiment. I can move my eyes between more and less cross-eyed quite smoothly, which demonstrates that the muscles in the eye are entirely capable of smooth movement on command. It is clear as I do this, however, that not being able to focus on objects while crossing my eyes is an important part of the process. Otherwise, the instinct to focus on something and see it clearly overcomes my ability to control the movement. I have also learned to move one eye at a time from left to right - again, beginning in a cross-eyed state. This is not nearly as smooth, but the practice contributes to my understanding of the nature of voluntary movement of the eyes. Observation of the blind also contributes to conclusions in this area. A person who has been completely blind for a while will often exhibit the kind of smooth motion you describe (in addition to jerking movements), as does a close friend of mine who sees nothing but complete blackness after his optical nerve was destroyed by a bullet.
Cited paper

Van Hofsten & Rosander, Development of smooth pursuit tracking in young infants. Vision Research vol.37, Iss 13, 1997, Pages 1799–1810

This was a great explanation. Is there a source for this information? Correct me if I'm wrong but, going by what you said, a person should be able to "train" their eyes (eye muscles?) into smoothly transitioning. Is there evidence to support this? I wonder if there would also be an explanation from the perspective of how the brain works with the eyes.

@R.Doto While comments such as yours are not banned here, tearing down others without any support for your allegation is not a productive use of this forum. By what definition of "fact" do you disparage these statements?

@R.Doto Direct experiment, especially when the method is given for others to verify the results is among the most primary sources of all facts. It can be relied on with greater trust than hundreds of internet references if you or someone you know can repeat the experiment. In this case, I can accept that not every person will have the patience to verify these results directly, but put it to a group of people you know (including at least a few adults) and someone will be able to reproduce much of what I've described. (The independent eye movement thing took me months to learn though.)

@MarkBailey personal "direct experiments", unless run with strict relevant controls and peer-reviewed by unaffiliated third parties, are simply anecdotes. Please cite some actual published studies in reputable journals to support your claims.

@MattDMo If enough contributing members see this comment, we can peer-review this right now: Everyone, please upvote this comment if (and only if) you are able to verify at least two of the following: 1) You can move your eyes relatively smoothly without focusing on any moving object by beginning from a cross-eyed position. 2) Very young children are less able to move motor muscles smoothly. 3) Your eyes jerk quickly between different focal points during eye-hand coordination. or 4) You are able to locate and utilize body parts with some precision even if you can't see them.

Saccades are not necessarily under conscious control, which does contradict your first paragraph. I think some references would be useful to support your answer.

@MadScientist All muscles can twitch involuntarily, but that doesn't make them an involuntary muscle. But I agree; I do need better references. I'm actually in the process of generating a reference right now, and your assistance is hereby invited. In the name of science, do a couple of the experiments. Then upvote the comment above. No one can even see it right now.

At this point I'm not sure if your answer is correct or not. The issue seems to be primarily with your sources (as I'm sure you are aware of at this point). This question contains a great example of using references in an answer. http://biology.stackexchange.com/questions/937/how-many-times-did-life-emerge-from-the-ocean

@MarkBailey I'm not sure if you are understanding what we're trying to explain. You cannot do home experiments and use it as proof. Even more so, your results would never be open to opportunity to be published as there is no proof or data collected with high precision equipment by professionals in that field of academia. Period.

I do have to say some referencing would be place; anecdotes are welcome, but only to add to more credible sources. Especially your voluntary smooth pursuit is questionable without a source. I have added a reference to the developmental issue. Hope that helps.

Also: blind folks often have nystagmus as you rightfully say, but drifting gaze is unknownst to me. Citations would be in place.

@Christiaan I read the chat between you and Mark. While it sounds like there is actual damage to the nerve in this case, could there also be conversion disorder at play, given the trauma of the event? If the optic nerve is destroyed, obviously there is nothing that can be done, but might this also relate to the persons ability to be able to perceive ideas and memories by tapping into their visual cortex, so as to "see" their thoughts? That might be helped through therapy.

@AMR Well, he often sees in his dreams. In fact, that frequently makes him lucid, because he knows very well in his dreams that if he can see, it's not real. But yes - extraordinary trauma of the event.

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Transcription of Genes: Are Specific Transcription Factors + Enhancers Necessary?
I learned about transcription in my AP Biology class and we discussed how transcription occurs, but I was wondering whether transcription always requires the enhancers, activators (specific transcription factors), DNA-bending proteins, etc. to be present, or if this is only used for higher-level production of RNA transcripts?
Can transcription occur if only the RNA Polymerase (I, II, or III) and the General Transcription Factors are present?
Thanks!

enhancers, activators, silencers, repressors are necessary in controlling of the transcriptional process. Utilization of enhancers/silencers plays a part in differentiation of developmental processes (i.e. maturation, growth)
https://en.wikipedia.org/wiki/Enhancer_(genetics)


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Relationship between turgor pressure and osmotic pressure?
I would like to know if there is a relationship between osmotic pressure (inside and outside of a cell) and turgor pressure. If so, is there a way to formalize it mathematically?
Thank you in advance,
Eorn

Turgor Pressure(T.P) is defined as the amount of pressure inside a cell solely due to its water content, whereas Osmotic Pressure(Pi) is defined as the pressure required to stop osmotic flow between the cell and a pure solvent when the pressure exerted by water is zero.
Osmotic Pressure is often given as the negative of the Osmotic Potential(or Solute Potential) of the Cell.(Because more the solute, more pressure will be required to stop the osmosis, but against the gradient). (1)
Therefore, it can be easily seen that Osmotic Pressure is solely dependent on the solute concentration of the cell.
The Total Suction Pressure(S.P) of a Cell is the pressure required outside of a cell to stop the water flow in a pure solvent.
The T.P in such a situation would try to reduce the S.P (More the T.P, less would be the pressure on the outside). Whereas, the O.P in such a situation would try to increase the S.P (More the solute inside a cell, more would the water on the outside try to get on the inside)
Hence, Mathematically (considering no other pressures to be responsible for Total Suction Pressure)
S.P = Pi - T.P
This can Also be proved in the following way:
Water Potential(Psi W): Total Pressure inside a Cell.
Solute Potential/Osmotic Potential(Psi S): Reduction in Water Potential Magnitude due to addition of a Solute(solute reduces kinetic energy of water due to bonding)
Pressure Potential(Psi P): Hydrostatic Pressure, i.e, pressure exerted by the water present inside a cell if there were no solute particles.
By definition
Psi W = Psi S + Psi P
(We know, Psi S = -Pi) As written above in (1)
Psi W = -Pi + Psi P
(We know, Turgor Pressure is the same thing as Psi P)
Psi W = -Pi + T.P
Suction Pressure is the negative of Total Pressure inside a Cell
(S.P = -Psi W)
(Water flows from high water potential to low potential, but from low Suction Pressure to an area of High Suction Pressure)
Therefore
-S.P = -Pi + T.P
multiplying by -1
S.P = Pi - T.P


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Bodyweight loss vs calorie shortfall
I have read that 1g of pure fat has 9 Calories.
If I dieted successfully in a way that did not cause me to loose muscle, and I had a cumulative calorie shortfall of 90,000 calories. Would that correspond to a reduction of bodyweight of 10kg? Or would it actually be a bit more, because presumably each kg of fat in the body is tied to a certain amount of water packaged with it?... and if so, how much more than 10kg?

Great question and this is something that is commonly misunderstood – as you lose weight (i.e. Fat mass) your body will compensate metabolically to conserve energy and lower your resting metabolic rate. It's commonly stated that a pound of fat is about 4000-4500 calories which technically is true (with a bomb calorimeter), but you can't just try to burn and extra 4500 cal a day - it doesn't work that way – the body is much more complex metabolically

You hit upon several ideas in your post.  First, you are absolutely correct that body fat is composed both of lipids and water, so a 10kg weight loss does not correspond to 90,000 kcals.  The most commonly accepted figure is 7700 kcals per kg of body fat lost (Hall, 2008), but this is a rule of thumb at best.
The translation from caloric deficit to body fat loss is fairly complex, and is the result of feedbacks between metabolism, weight, and other responses.  The National Institutes of Health researchers built a fairly intricate model estimating the actual responses as a differential equation (simulation and references available here), which would probably be a good place to start.
If you're inquiring not from general curiosity but with an interest in developing your own nutritional plan, keep in mind that nutrition is a lot more than merely calories.  It is critical to get macro and micro nutrients, of course, but other factors such as dietary fiber play an important role in the health outcomes.

that answer doesn't really address the question of how the body adjusts metabolic rate with changes in weight loss and lean/fat mass - that calculator from NIDDK is for calculating a weight loss plan - it doesn't address the physiological adaptations to weight loss - i think that's what Mick was asking about in the question (?)

I don't know whether their public front end actually does account for it, but I believe their model does.

For half a century, dieters have adhered to a simple doctrine: to lose a pound of weight, you must burn 3,500 more calories than you take in. The 3,500-calorie rule has become a universal constant in the complex calculus of weight loss, but the truth may not be so simple: a new mathematical model predicts that the energy deficit required to lose a pound depends on how much fat a person has to start with.
According to the model, 3,500 calories per pound is a reasonable estimate for those who are moderately obese, but not necessarily for others. When dieting, those with a high percentage of body fat will mainly lose fat, whereas leaner people will lose a higher proportion of lean body mass, such as muscle or liver tissue.
Because lean body mass stores less energy per pound than fat, the model predicts that trimmer people require less of a caloric deficit to shed weight. Not that this will always be easy to achieve.
The results do not necessarily mean that it is easier for skinnier people to lose weight, says Kevin Hall, a biophysicist at the National Institutes of Health in Bethesda, Maryland. Lean body mass uses up more of the body's energy than fat does, so losing lean body mass should reduce the body’s overall energy needs. Therefore a person who maintains a steady diet may actually put weight on, as their smaller body needs less fuel to maintain itself.
 Food for thought
Hall first began to wonder about the 3,500-calorie rule when he embarked on a project to model weight regulation. “It took a long time to track it down,” he says. “Dieticians are tested on this idea; textbooks quote it. But no one could tell me where it came from.”
It came from a study published in the 1950s that was heavily skewed towards overweight women. Since then, scientists have learned that not everyone loses weight in the same way. “One of the big assumptions was that when people lose weight, they lose fat tissue,” says Hall. “We now know that’s not true. They lose lean body mass as well.”
Hall decided to calculate the energy stored in lean body mass. He found that the energy density of lean body mass was five-fold smaller than the energy density of fat. His results are published in the March issue of the International Journal of Obesity1.
When lean body mass was incorporated into his weight-loss models, a clear difference emerged. For someone who weighed 100 kilograms and wanted to lose 5 kilograms, the rule of thumb worked well: they would need to burn nearly 39,000 more calories than they use. Assuming no change in energy use and an average daily intake of about 2,000 calories, that means avoiding the equivalent of 2 chocolate bars a day (about 500 calories) for 2.5 months. But to achieve the same weight loss in a 50-kilogram person required a caloric shortfall only two-thirds as large.
Weighty matters
Growing concerns about obesity have fuelled a push to better understand such issues, says Steven Heymsfield of the New Jersey-based pharmaceutical company Merck. Heymsfield notes that several companies, including Merck, have launched large-scale weight-loss studies that include measurements of body composition. “There is a lot of interest in understanding the regulation of long-term changes in body weight,” says Heymsfield. “You’d like to know: are the dynamics for a 60 year old who goes on a diet the same as for a 20 year old? Because they probably aren’t.”
In 2002, Heymsfield and his collaborators showed that the energy deficit required to lose weight varied between men and women, and between young and old2. Their results were in line with what Hall found: women — who have a higher percentage of body fat than men — required a higher caloric deficit to lose weight. Similarly, a person aged about 70 needs a larger calorie deficit to achieve the same weight loss as someone who is 35 years old.
Does all of this mean that the textbooks should be amended? Hall notes that for obese people, the original equation works reasonably well. “For those who are recommended to lose weight, the rule isn’t that bad,” he says. Adding subtleties to this advice might unnecessarily complicate matters.

The number of calories you need to burn per pound is not a constant. Depriving yourself of chocolate will have a different effect on weight from one person to the next.

@user20487 your answer has a lot of great information in it - add some citations and this will be much better. It looks like you cut and paste from another source - you have to manually add the citations using the text editing tools in the toolbar - feel free to edit your post


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Why is there no U3 snRNP in the spliceosome complex of transcription initiation?
snRNP U1,U2,U4,U5,U6 are present in the spliceosome but there is no mention of U3.

U3 RNA with its proteins forming a complex is localized at nucleolar. The box C'/D motif in U3 snRNA is responsible for this localization. Therefore U3 snRNA does not have a chance to go to mRNA transcription active sites. Instead, U3 snRNP play important roles in ribosomal-RNA processing.
Because of necleolar localization, U3 snRNA is called U3 snoRNA alternatively.
https://en.wikipedia.org/wiki/Small_nucleolar_RNA_U3


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What is responsible for soft rot of organic matter?
In soft foods, for example, why is there a limited amount of time before consumption is no longer safe due to soft rotting of material.

Are you asking about why food becomes dangerous to eat or about why food becomes softer? They are related but some food softens without becoming dangerous or becomes dangerous without softening.

Both. Why some foods become dangerous to eat and also what makes the food become soft? Is it the decay of the organic matter inside the apple or is it a breakdown of the structural proteins on the surface?


text:
what benefits does lab procedure Realtime PCR have in gene silencing experiments?
RT-PCR performed in gene silencing but mechanistically what are the benefits of this procedure?

Can you please re-phrase your question? At the moment it is a bit unclear what you want to know exacty.

RT-qPCR amplifies mRNA molecules present in a cell, if you have the right primers for it. The whole point of RNAi (the "gene silencing" that I think you're referring to) is downregulating the expression of a specific gene, so you'd expect the mRNA transcript of said gene to be not present (rather, present at very low concentrations at any given timepoint) if indeed the interference has worked.
Therefore, after RNAi has been performed, you can check by qPCR that there are indeed very low levels of the specific mRNA present in the cell. You might want to also perform a Western Blot against control cells transfected with scramble siRNA (where nothing should be downregulated, think of it as an "empty" siRNA), to check that protein levels are indeed much lower than in "regular" cells.


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Membrane conductance in phase 1 of the cardiac action potential
Correct me if I am wrong, but in phase 1 of the cardiac action potential (for ventricle cells) there is flow of potassium ions due to the opening of transdent potassium channels. To me this would correspond to an (sudden) increase in the conductance of the membrane to the potassium ions, $g_K$, however looking at graphs on the internet  do not seem to indicate such a change in conductance. Please can someone explain why such a change does not occur (sources would be helpful).


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PCR that worked previously is now only showing primer dimers and a smear on gel
PCR amplification of a promoter sequence for gel extraction worked beautifully using Phusion HF enzyme with GC (higher error but less picky) buffer. However, DNA concentration from the gel extraction was too low, so I need to do it again. Now with all the reaction parameters the same it is not working. So far I am using the same Phusion enzyme stock and buffers, the same primers which worked before, the same proportions, and the same thermo-cylcer set up. I have extracted fresh genomic DNA to amplify from thinking maybe the DNA had degraded with no luck. I make a mastermix fresh before each reaction by combining the Phusion enzyme, nuclease free water, dNTPs from a 10mM stock, and the GC buffer mix. Any ideas would be appreciated.

Did you scale up the reaction to get more yield?

Yes, I have gone up to 50ul reactions and load 20ul samples onto the gel each time for the gel extraction.

Don't do that. You change the characteristics of the reaction - bigger volumes heat up and cool down slower. Instead of doubling the reaction volume, rather do two reactions. This usually works better.

When I scaled up I did use thermo fishers tool to recalculate the proportions for the mastermix.  I will keep this in mind when trouble shooting in the future though. Thanks

Have a look at this answer here at bio.se. That's what I have in mind.

You can try performing the reaction again using the purified promoter sequence from the first amplification as template. With the low error rate of polymerases like Phusion, the chance of an error occurring for a ~1kb amplification is low enough to not be a significant issue.


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How much is local blood non-Newtonian in Pathophysiology?
I am studying the Barus effect / Merrington effect / die swell / extrudate swell, which is a characteristic of non-Newtonian viscoelastic liquids (Introduction to the phenomenon in this video) i.e. the medium responds to the stress $\sigma$ of irritator with a strain $\epsilon (= \Delta l/l)$ that increases until the medium ultimately fails in a local pathology

blood has both viscous and elastic components which it can apply in pathophysiological condition
\begin{equation}
\gamma = \gamma_{v} + \gamma_{e}.
\end{equation}

#1 Maxwell material model

total shear stress if blood behaves like Maxwell material in local pathophysiological regions
\begin{equation}
\sigma = \sigma_{v} = \sigma_{E} = \eta \frac{d \gamma_{v}}{d t} = G_{M} \gamma_{E},
\end{equation}
implying $\sigma = \eta \, d\gamma_{v}/dt$ and $\sigma = G_{M} \gamma_{E}$.

I am thinking when blood is not non-Newtonian etc in muscular pathologies and muscular infections. I want to evaluate how much blood is non-Newtonian in particular situations.
I am interested in muscles and their supply with necessities.
How much is local blood non-Newtonian pathophysiologically?

According to this conference proceeding blood is very nearly newtonian at normal shear rates. More accurately blood is very thick and a shear-thinning fluid, but the shear-thinning effects don't scale with a power law like other non-Newtonian fluids.
In terms of blood changing viscosities, I suspect that in living patients blood viscosity is quite constrained, not only by physiological feedback but by the fact that if the blood viscosity changed very much the patient would become nonliving. Blood circulates constantly, and when it stops circulating it coagulates(which complicates efforts to measure its viscosity, I imagine). Any local effects on blood viscosity would be 'washed away' by the fresh blood arriving every heartbeat. If there's no or very limited blood circulating to the muscular pathology you're interested in the blood viscosity is probably not as significant as the ischemic tissue death that's just about to happen.

Thank you for your answer! Your case is general. You cannot assume that all local effects are always washed away after a new heartbeat. Ischemic tissue death happens lastly. I am interested in what happens between the initiator and ischemia i.e. how much local blood is non-Newtonian.

I'm not sure I understand. Between the initiator and ischemia the blood won't move much/at all, so why would it be interesting to study its non-newtonianness? All fluids at rest are perfectly Newtonian. Studies of blood viscosity next to dead or dying tissue would be pretty interesting but under those circumstances blood clots quickly. I'd start with kinematic blood clotting studies like this one but I think most of this research hasn't been done. With the possible exception of people studying angiogenesis and leaky blood vessels in tumors.

Yes, exactly. Blood at rest is perfectly Newtonian. But I am not considering cases at rest. Consider etc low BP and low Chol cases. Why CVD?


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Is there a difference between Luria Broth and Lysogeny Broth?
Is there a difference between Luria Bertani and Luria Broth? Or are they both the same thing? Is it necessary to autoclave LB medium after it has been made?

Although both names are quite common, both are wrong. In the original paper from 1951 Bertani was studying the lysogeny in E.coli, hence he called his media for this purpose "Lysogeny Broth" or LB in short. In the subsequent decades this name was transformed to "Luria Bertani" or "Luria Broth", which is incorrect. See the references 1 and 2 for more details.
For the second question: It is absolutely necessary to autoclave the media after preparation to avoid the contamination and growth of microorganisms which are present in our environment. Only making the media sterile makes sure that we can work with defined microorganisms.
References:

Studies on Lysogenesis I.
The Limitations of LB Medium


text:
Must one autoclave LB medium after it has been made?
Is it necessary to autoclave LB medium after it has been made?


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Gender of BEAS-2B cell culture
I recognize some interesting patterns when analysing DNA methylation of BEAS-2B cells. Does anybody know, if the cell culture is female or male? I already asked the customer support of Sigma Aldrich without success.
Information on the official website just mention "non-cancerous individuals" as source organisms.
http://www.sigmaaldrich.com/catalog/product/sigma/95102433?lang=de&region=DE

The cell line is most likely genetically male. On the English (US) site, the Description box has several sections, of which one is DNA Profile. In there, it lists amelogenin as X, Y. This gene is located on both the X and Y chromosomes (AMELX and AMELY, respectively), which have distinct PCR-detectable sequence differences. It is often used in helping to determine the gender of unknown samples in the realm of forensics - it is not 100% accurate, so other genetic tests (such as for SRY) are also performed.

My DNA methylation data don't show a clear male oder female status. There is definitly an observable "male" effect, but a clear classification is not possible with my dataset. The results indicate a mixture. Anyway, I will remove gonosomal probes from further analyses. Thanks for your answer!


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How is the probability of a sequence occuring with BLAST calculated?
What is the probability that a given nucleotide/amino acid sequence will occur in the whole database program BLAST searches in? How this probability is calculated?

According to BLAST documentation statistics of local sequence alignment, when doing database searches, is done

by treating the database as a single long sequence of length N.

N is therefore a sum of all sequences with varying sizes from a given database.
Underlying assumption is that

query is a priori more likely to be related to a long than to a short sequence, because long sequences are often composed of multiple distinct domains.

To calculate the probability, we need to choose a scoring scheme (for ungapped example: choose a mismatch penalties), which for a query sequence gives us a statistically significance score $S$. Expected number of alignments with score of at least $S$ follows Gumbel extreme value distribution:
$$
E = Kmn\cdot e^{-\lambda S}
$$
where m is query length, $n=N$ and $K$ and $\lambda$ are distribution params.
Again, according to docs and its references, probability of finding at least one such seq would be $P=1-e^{-E_{(N)}}$, where $E_{(N)}$ is E-number for concatenated N-sequence and query sequence.


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What is the difference between the Modern Synthesis and the Extended Synthesis?
The NCBI talks about "Evolution beyond neo-Darwinism: a new conceptual framework." (source).
What is the difference between the Modern Synthesis and the Extended Synthesis?

The term Extended Synthesis has been invented very recently and the concept was defended in these two papers

Laland et al. 2014
Laland et al. 2015

I read each paper when it came out and haven't reread them since. Here is a short summary of what I remember.
Those who want to use term Extended Synthesis
In short, they are arguing new findings have extended our understanding of evolutionary biology so much so that we should rename our theory of evolution. The main findings they are talking about concern the field of evo-devo (merging Evolutionary biology and Developmental biology). The subjects that they consider having radically advanced our understanding of evolutionary biology include niche construction and inheritance of niche, developmental bias, plasticity, cultural evolution and epigenetics.
Those who do not want to use term Extended Synthesis
We have discussed both papers in groups in my department and in short, we pretty much all ended up saying that:
It is true that our understanding of evolutionary processes have advanced a lot since the time of Wright, Fisher, Muller, Kimura, and others. However...

There is no important enough rethinking that deserves a renaming of our Theory of Evolution
Most arguments are based on rephrasing of old concept without bringing anything new. This is especially obvious when reading the 2015 paper.
Do we really care about this debate anyway? It is just a name!

Reading
I recommend reading the 2014 paper as 1) offer both point of views and 2) is pretty short.
Note
I do not know your level of knowledge in evolutionary biology but it might be a pretty bad idea to start with complicated subjects such as evo-devo, niche construction, epigenetics, developmental bias, etc...

As far as I know, Neo-Darwinian mechanisms rely heavily on Darwin's proposed evolutionary mechanisms plus the Mendellian genetics but both were insufficient and even contrary to scientific data. On the other hand, the Extended Synthesis is supported by scientific data. In fact, those who hold onto the Extended Synthesis can explain how organisms evolve (empirically than theoretically) than either Darwin or Neo-Darwinists can.

Yes the basis of what we called neo-darwinism or the Modern synthesis of Evolution is pretty much merging the work of Darwin and Mendel. This work of the early 21th century was heavily supported by evidence (where di you read the opposite?). A lot of work has been done since then and our knowledge have gradually improved. When referring to the Modern synthesis we usually include today's knowledge and not only the knowledge we had in the 1940s.


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Are epigenetic changes involved in evolution?
Evolution leads to phenotypic changes through changes in DNA such as mutations. Mutations are transmitted to offspring. Cumulative mutational changes across many generations may cause evolution and speciation.
As far as I know, epigenetic changes causes an individual to change in how it appears (phenotypic changes). In turn, epigenetic changes may be transmitted to offspring, just as DNA mutations can be.
Is epigenetics a factor in evolution?

Sorry but this is just not answerable. I'm afraid you have completely misunderstood. Epigenetic features have nothing to do with phenotypic changes (they can, but most certainly not always). Please read at least the relevant wikipedia articles and post again with a more specific question.

@terdon - I'm most definitely no expert in evolutionary Biology nor genetics, but I think this question is actually quite cool. I edited the question in the hopes of clarifying it.

@Christiaan that's much better, thanks. Close vote retracted.

The answer is yes. But the question is very broad. Have you read the wiki article on epigenetics or one of these multiple hits you getwhen you google epigenetics evolution?

Note by the way that you are using the term evolution in a slightly wrong way. Evolution is most often defined as any change of allele frequency through time. Therefore you do not need to wait many generations for evolution to occur. Also the phrasing suggest an eventual misunderstanding between evolution and speciation. You might want to have a look at an introductory course to evolutionary biology such as Understanding Evolution for example

My $0.02. Any change that affects an organisms ability to mate and reproduce, changing the frequency of traits in the gene pool has the potential to drive evolution. Take an imprinting disorder like Prader-Willi. I think that we too often think that evolution leads to the winners, but it is equally relevant to all of those that lost the race, with their lineages going extinct, effectively change the make up of the species and altering its direction.

To start I will repost some of an answer I have previously posted, which will explain what evolution is:
Evolution is simply a process of change.  It is a change in trait values of populations over time. It results from four mechanisms: mutation, migration, drift, and selection.

"Evolution means change, change in the form and behaviour of organisms
  between generations. ... When members of a population breed and
  produce the next generation we can imagine a lineage of populations,
  made up of a series of populations through time. Each population is
  ancestral to the descendant population in the next generation: a
  lineage is an ancestor-descendent series of populations. Evolution is
  then change between generations within a population lineage." - Ridley,
  Evolution

Your Answer:
Evolution depends on the inheritance of information from the ancestral population to the descendant population. Much of the time we talk about information in the form of genetic variation, the information contained within the DNA. However, more and more we are realising that other forms of information transmission can occur, including epigenetic effects, and that these can contribute to evolution.

"Epigenetic modifications are a bit like ornaments on a Christmas
  tree; the tree (the DNA sequence) is still the same, but the
  decorations (epigenetic modifications) change how it's perceived." ...
"Over the past few years, several studies have compared the epigenetic
  modifications of our genome with that of other great apes, leading to
  an emerging picture of the importance of epigenetics in our recent
  evolutionary history." ...
"The role of epigenetics in evolution (particularly primate evolution)
  is an active and exciting area of research..." - Nature Scitable

The edited question is also broad in scope, but one can narrow it down by talking about specific conditions. For example, the role of epigenetics markers helping in survival under stress conditions, especially in A. thaliana, has begun to be much appreciated.
Epigenetics could also potentially be an important mechanism facilitating developmental plasticity-formation of two or more phenotypes from the same genotype, a process which helps organisms to adapt to changing environments (Developmental Plasticity and Evolution-Mary Jane West Eberhard, Oxford Univ. Press 2003).
Under both scenarios described above, epigenetic changes could favour a differential success in survival (e.g. under stress) and/or reproduction (e.g. flowering) of individuals in a population as compared to animals without these markers, thus leading to evolution in the next generation.


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How do house plants affect the quality of air in a house?
Do house plants affect the air in the house by taking it from the rooms and it is put in the dirt to make it moist then we have no air.

It is unclear what you are asking.

Plants have pores called stomata, where they generally intake CO2 from the air. There's a transport system in the plant called the phloem which pulls organic compounds down into the roots. When you have pollutants in the air that get sucked into the plant through the stomata, they get sent down to the roots. There are hopefully microbes down in the soil, and the harmful compounds get expelled into the soil, and broken down by the microbes. All the while, the plant is expelling oxygen. This should, in theory, improve the air quality.

I've often wondered, is this enough of a change to say that they "affect" the air quality. As in, "how many plants does it take to get a measurable difference?"

That's something to look into, I don't know the answer myself. In fact, the answer to OP was just an elementary plant structure-function overview.

In my oppinion you corrected and answered the question neatly. I was simply musing. Perhaps it's worth a new question.


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Target cells of adrenaline?
I have been thinking about how adrenaline increases blood sugar levels, but have not been able to find an answer to the target cells. Does it affect the hepatocytes and muscle cells, like glycogen?
Thank you in advance :)

look at the answer for the cAMP question you asked - you already seem to know the answer...  http://biology.stackexchange.com/questions/41084/if-so-many-different-hormones-molecules-work-by-activating-adenyl-cyclase-how-d

epinephrine (adrenaline) has many target cells though - and the effects are many - remember each of the cells that has adrenergic receptors (that adrenaline signals through) can have different effects depending on the cell type

Epinephrine is a hormone that works systemically and will activate any and all cells that express a hormone receptor with specificity for epinephrine.
As stated in the wikipedia article "It plays an important role in the fight-or-flight response by increasing blood flow to muscles, output of the heart, pupil dilation, and blood sugar. Epinephrine does this by its effects on alpha and beta receptors."

Epinephrine (also known as adrenaline) is produced by the adrenal glands and stimulates α- and β-adrenergic receptors. And is responsible for various physiological responses, depending on the type of receptor and the tissue to which this hormone binds.
Epinephrine increase blood glucose level by stimulating glycogenolysis. This hormone binds to  β2 adrenergic receptors present on hepatocytes and skeletal muscle cells and promote the glycogen breakdown.
(Via:  https://www.sciencedirect.com/topics/neuroscience/beta-adrenergic-receptor)

(Image Source:  http://oregonstate.edu/instruct/bb450/fall14/stryer7/21/figure_21_16.jpg)


text:
0.9% Saline or Ringer's Solution for in vivo work
A few of the labs where I currently work routinely use 0.9% saline for in vivo work (washing out debris during surgery, diluting substances for IP/IV/SC injections, etc.)
A few years ago I worked in a lab where the standard was to use Ringer's Solution. Obviously, in both labs the choice was based on an organizatorical/historical reasons. But I was wondering: Does either of these solutions perform any "better" (i.e. causes less physiological disturbances) than the other?
My guess would be Ringer's is better, since it is also suitable for keeping cells alive in vitro - and there is also this paper that calls 0.9% Saline into question altogether. But I could not really find any good comparison tests.

saline versus lactated Ringer's is still a matter of preference - but I agree with you that Ringer's is better - pH and electrolyte composition are more closer to physiologic values, while saline is pH of 5.5 and slightly hyperosmolar compared to plasma.


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Why guard cells need to turn malate into postassium malate to become turgid?
According to the Active Potassium Transport Ion concept given by Levitt et.al, stomata open due to turgidity in guard cells. It seems that guard cells turn the starch produced by photosynthesis into malate (which is a stable solute and should increase the osmotic pressure of the cell) but then go on to invest energy to exchange the hydrogen ions of malate with potassium ions.
Thus guard cells basically invest energy to turn malate into lots of potassium malate (so that water will enter due to increase in osmotic pressure), but why should such a process evolve if they can become turgid by just producing lots of malate?


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Why do you die if you cannot breathe?
I was wondering what the actual reason for death by suffocation is. Obviously it is related to oxygen deprivation. But what is the underlying cause of death?

Is it due to insufficient oxygen for aerobic respiration, and the resulting lack of ATP (as anaerobic respiration forms less ATP)?
Or is it because of the build-up of lactic acid, causing enzymes to denature?
Or is it the lowering of the pH of the blood because of a build-up of carbon dioxide which forms carbonic acid and subsequent denaturation of enzymes?

Your brain, being the most oxygen-hungry part of your body, goes to sleep-mode and eventually dies due to insufficient ATP levels. Glycolysis (carried our by glial cells, not the neurons themselves) doesn't produce enough energy. You may want to read this.

@Chris I'm afraid I lack enough expertise in the field (and enough free time to overcome this) to expand my short comment into something worth a full-blown answer. Moreover, Christiaan has it covered pretty well. If you want to elaborate on my comment, I would really appreciate the effort and the information.

Short answer
This is a difficult question to answer. As far as I am aware, asphyxiation results in excitotoxicity, which causes unconsciousness, brain damage and eventually, death.
Background
Asphyxia is a condition of the body that occurs from severely inadequate oxygen supply, or because of excessive carbon dioxide in the body (First Aid and CPR courses). The brain is the organ most sensitive to hypoxia (Medscape). Nerve cells in the brain can survive only up to four minutes without oxygen (First Aid and CPR courses). Consciousness is lost after approximately three minutes (Forensic Pathology). Permanent brain damage begins after approximately 4 minutes without oxygen, and death can occur as soon as 4 to 6 minutes later (Medline). Asphyxial deaths typically involve respiratory arrest with bradycardia / asystole (low heart rate / cardiac arrest) because of the hypoxia-induced dysfunction of the respiratory centers in the brainstem (Forensic Pathology).
Despite the small size of the brain (2% of body weight), it is, however, the largest consumer of total body oxygen (20%) and glucose (25%), which are delivered by 15% of the total cardiac output (Schur & Rigor, 1998).
A lack of oxygen may result in so called hypoxic-ischemic encephalopathy (HIE), i.e., neuronal cell death due to hypoxia. Its pathophysiology is related to the lack of energy because cellular respiration diminishes. This initially causes neurons to stop firing, and eventually in an arrest of cellular functions and cell death. Even sublethal HIE can set in motion a series of toxic reactions that kills injured neurons and even neurons that have not been damaged during the initial insult. Thus, following global brain ischemia, neurons do not die suddenly or all at once. In some of them, damage develops hours or days after the insult. Most neurons undergo necrosis. In some neurons, HIE triggers apoptosis (Neuropathology).
Specifically, energy depletion is believed to result in a failure of the Na+,K+ ATPase, leading to depolarization of the neuronal membrane (Fig. 1). Synaptic function and conductivity cease at this point. Depolarization causes neurons to release glutamate (Glu) into the synaptic cleft. Glu is the most common excitatory neurotransmitter. In small amounts, it is indispensable for neuronal function. In excessive amounts, however, it is neurotoxic. Some Glu receptors, such as the NMDA and AMPA receptors, are non-selective cation-permeable ion channels. Initially, over-activation of these channels causes a passive influx of  Cl- (and Na+) into cells causing osmotic (cytotoxic) edema and rapid death (Neuropathology).
Additional structural damage develops hours or even days later as a result of Ca2+ influx into neurons through NMDA and AMPA receptors (Fig. 1). This delayed cell death is caused by an over-activation of NMDA and AMPA receptors by the excessive release of glutamate, which causes massive influx of Ca2+ into neurons. Ca2+ activates catabolic enzymes (proteases, phospholipases, endonucleases), and also NO synthase. NO is a free radical and other free radicals are generated due to the impairment of oxidative phosphorylation. Free radicals and activated catabolic enzymes destroy structural proteins, membrane lipids, nucleic acids, and other cellular contents, causing neuronal necrosis. DNA damage from endonucleases and mitochondrial injury from free radicals trigger apoptosis (Neuropathology). Collectively, these effects are referred to as excitotoxicity (Choi, 1992). When enough brain cells die, the person perishes with them.

Fig. 1. Schematic showing the excititoxic effects of excess glutamate in the brain. Source: Neuropathology.
References
- Choi, J Neurobiol (1992); 23(9): 1261-76
- Schur & Rigor, Dev Neurosci (1998); 20: 348-357

Really nice answer +1. One thing that isn't really addressed is that the depletion of oxygen does bring oxidative phosphorylation to a grinding halt. Oxygen is the final electron acceptor and without it ATP Synthase can no longer generate ATP. Without ATP most cellular signaling and a lot of enzymatic function stop systemically. DNA repair fails and cells die. I also think that mitochondria begin to release calcium and cytochrome c into the cytoplasm, which is pretty bad.

@AMR - Thanks for the appreciation. I did quite some research into this one, and the tricky part is whether your proposed mechanism is what causes neuronal death. Your mechanism is definitely true in general, but in the brain it is shown that anaerobic respiration can keep stuff going quite well (see the cited Schur & Rigor paper). Instead, the lethal consequences to the brain, afaik, is more directly related to excitotoxicity.

True. The question itself is a bit more general than just neuronal death. The reason I didn't attempt an answer was I really am not sure what will kill you. Obviously damage to the brain stem will short-circuit everything, but I didn't know the rates of damage, whether other vital organs could survive the lack of oxygen longer. I guess if we keep the brain alive these days, we can artificially get most of the other systems to function. Changes the calculus. I was also wondering how cryotherapy helps to protect the brain, as it seems to extend time to damage, but that is a different question.


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Chitin, homo or heteropolysaccharide?
My teacher told me that Chitin is a heteropolysaccharide but my book regards it as a homopolysaccharide.I am so confused

Even teachers are sometimes wrong. ;)
Chitin is a homopolysaccharide. This just means that it is made up of repeating units of the same monosaccharide - in this case that monosaccharide is N-acetylglucosamine. Other examples of homopolysaccharides are glycogen and cellulose.
The basic structure of chitin is shown below as a polymer of two N-acetylglucosamine units:

Homopolysaccharides can be linear chains or branched, as long as they are made up of just one type of sugar unit. A heteropolysaccharide is made up of multiple different monosaccharide units. Glycosaminoglycans would be an example of a heterpolysaccharide as they contain two different sugar units.


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Biological term for close species rivalry
Is there any phenomenon/force in biology when two very close species fiercely fight each other (as a sign of a strong tendency to deepen the difference between species)? If there is, what's the name of the phenomenon or any similar phenomenon? (Question from a layman in biology, thanks for an answer.)

What do you mean by tendency to deepen the difference between species? Are you talking about evolutionary process that yield the two species to differ due to competition?

Oh you are talking about speciation? Not talking about relationships between the two lineages of interest, I answered your question below but I am not sure this is exactly what you were looking for.

Citing wikipedia

Character displacement refers to the phenomenon where differences among similar species whose distributions overlap geographically are accentuated in regions where the species co-occur, but are minimized or lost where the species’ distributions do not overlap. This pattern results from evolutionary change driven by competition among species for a limited resource (e.g. food). The rationale for character displacement stems from the competitive exclusion principle, also called Gause's Law, which contends that to coexist in a stable environment two competing species must differ in their respective ecological niche; without differentiation, one species will eliminate or exclude the other through competition.

In ecology, the competitive exclusion principle, sometimes referred to as Gause's law of competitive exclusion or just Gause's law,[2] is a proposition that states that two species competing for the same resource cannot coexist at constant population values, if other ecological factors remain constant. When one species has even the slightest advantage or edge over another then the one with the advantage will dominate in the long term. One of the two competitors will always overcome the other, leading to either the extinction of this competitor or an evolutionary or behavioral shift toward a different ecological niche. The principle has been paraphrased into the maxim "complete competitors cannot coexist"

Character displacement is very close to what i'm looking for. When small differences suddenly start to play a big role and result in split. Cheers

Can you try to explain what is the difference? Maybe you are specifically including a (allopatric/sympatric) speciation event into the story...

I'll accept your answer, i'm new member, it says to wait for 5 mins. The crucial point you made right - when small differences are accentuated. I was looking for this thing

Sure take your time. I just wanted to invite you to explain why the answer does not answer if it does not. Make sure to wait to see if others agree with my answer or if they downvote or comment on it.

For my non-biological purpose it fits well. I was looking at the term that denotes the situation when differences between two very close species get accentuated in their proximity.


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How to build a trimeric protein structure from monomeric PDB file?
Problem: I have a PDB file, with a monomer, but I would like to show the entire structure - which is trimeric - but I don't understand how to merge/build or combine the monomeric units to its full structure in COOT, SWISS-PDBviewer or pymol?
Here is a link to the protein complex I am looking at
I would appreciate: Guidelines on how to do this (preferably in coot, pymol or Swiss-PDBviewer), or referral to a tutorial that actually goes through this would be great!
For reference: I found some descriptions on how to "build/merge" with Swiss PDB viewer here. And in threads from this discussion I found descriptions of how to do it with other molecular graphic tools as well (although I don't completely understand it)
What I have tried: In the tutorial for the SWISS-PDBviewer ( link ), I am able to follow some of the instructions, but I can't follow them for long:

I upload three of the same PDB file in SWISS PDBviwerer (they are layered on top of each other)
I can access/see the layers in the "layers info"
I am told to open the "text icon" to see the PDB text file, and look for "mtrix" rows - which should come right before the "atom" rows. As cited from the instructions:

" Scroll down the pdb file until you find MTRIX lines (they are just
  before the ATOM lines). You can see 9 lines MTRIX. They represent
  three transformation matrices, and allow you to build the
  non-crystallographic symmetries of the protein"

I cannot find the "mtrix" rows in the PDB-text file, and am very unsure of how to follow the next instructions (link) after this as well. I am not able to click anywhere in the text file, then I get the error: "sorry can't recognize any clickable information under this pointer..
This is what I see above the "atom" row:

I also found that the trimeric state can be downloaded as "biological assembly", however, I would still like to know how to do this on my own.

The PDB-file only contains the asymmetric unit, and no information on a potential biological relevant multimer. So you will need to get information about the state in solution experimentally.
That being said, one can often deduce from the size of the contact surface whether you have a potential quarternary structure. You can do this by hand, but the PISA-server is quite helpful there, and it will also output the multimer PDB-file:
http://www.ebi.ac.uk/pdbe/pisa/
If you just want to apply symmetry operators to your asymmetric unit in order to create symmetry mates, you can do so in
Pymol:
- click Action/generate/symmetry mates/within X Å
- from the command line:
        symexp prefix, selection, cutoff
        , e.g. symexp sym,1GVF,(1GVF),5
   see also http://pymolwiki.org/index.php/Symexp

Coot:
- if you just want to look at the symmetry mates, activate View/Cell&Symmetry with an appropriate radius and/or select "Symmetry by molecule"
- if you would like to actually create the symmetry mates, try Extensions/Modelling/New Molecule from Symmetry Op  - however you will have to specify the SymOp manually.

You will need to have the CRYST1-record in your PDB-file with the correct space group.

Remark 350 can be used to describe the biological unit.

There are no MTRIX cards for that molecule. This seems like the easiest path:
http://www.rcsb.org/pdb/explore.do?structureId=4G3Y
Download Files -> Biological Assembly 1
i.e.:
http://www.rcsb.org/pdb/files/4G3Y.pdb1.gz
And read that file into Coot (should you wish)

Thanks for the link, but as i commented on my own post - I do understand that I can get the biological assembly (whole structure). But what is an mtrix card? and why is it not possible to combine the monomers (due to lack of mtrix) ?  I am more interested in how I would do this on my own, regardless of that the whole PDB structure exists. Are you saying it is not possible with this file?


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Why are truncations in Receptor Tyrosine Kinases so sommon in transformations?
Receptor Tyrosine Kinases (RTKs) present themselves on the surface of a cell as monomers until a ligand (such as a mitogen) binds and causes the formation of the active dimer. However I do not understand why truncations are so commonly seen in retrovirally delivered oncogenes or in oncogenic mutations. My confusion here is that if mitogen binding of RTKs facilitates the close proximity of two monomers, then simple overexpression should allow for increased transphosphorylation of monomers, and therefore be mitogenic (which it does). But then what advantage would a truncation that removes the extracellular portion of an RTK have in increasing transphosphorylation of monomer units?

I've edited this a little (defined the abbreviation as a start) but the question is so badly expressed I think it should be let die in the absence of a revision of the answer provided by @Mr-Bauer providing references.

As you said the simple overexpression can lead to transphosphorylation and activation of mitogenic signalling. This helps the cancerous cells to survive.
By truncation of the molecule the cell also gains a benefit, because it could prevent inhibition of the receptor from outside the cell.
The truncation furthermore could be induced by treating cancer with inhibitory antibodies against the receptor. For example a treatment with anti-EGFR antibodies could induce resistance by mutation and selection. One of this mutations could be the truncation of the receptor.

Welcome to Bio. References are appreciated here, most notably when making strong statements like anti-EGFR antibodies like Cetuximab could induce an evolution of the cancer cells whereby the truncation of the receptor benefits the cancerous cells.

http://www.nature.com/nrclinonc/journal/v7/n9/full/nrclinonc.2010.97.html maybe

Though I have to agree, it basically says "Hey, nothing wrong, nothing to regulate here" to the outside of the cell, much like truncated NKG2D ligands make it harder for immunosurveillance to do it's job.

Thanks for the comment, I changed my answere a little bit.

The reference from Kendall is very good. Also I would reference this paper link to show annother treatment induced mutation of cancer.

It technically isn't a treatment induced mutation ; K-Ras simply is a subclonal event in those patients that leads cells with it to acquire a selective advantage in the presence of an EGFR inhibitor, but are selectively unfit when the EGFRi is removed.
http://www.ncbi.nlm.nih.gov/pubmed/26030179


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Why do asparagine and glutamine have two different abbreviations?
I'm looking at amino acid abbreviations and on every site I visit, asparagine and glutamine have two different abbreviations. Is there a reason for this? Do they represent different forms of the amino acid that may have different properties?
I'm looking at the abbreviations on this site as an example:
http://www.hgmd.cf.ac.uk/docs/cd_amino.html
On the page, asparagine has an abbreviation of 'N' and an abbreviation of 'B'. The abbreviation 'B' doesn't correspond to a codon so why is it there?
Glutamine also has two abbreviations ('Q' and 'Z'). The abbreviation 'Z' doesn't correspond to a codon either.

Welcome to Bio. Are you askinh whether Arg and Gln are different amono acids??

Great edit - @Roland has given the right answer - see the official IUPAC website

The abbreviation Asx (B) is used if it is uncertain whether the amino acid at a given position in a peptide sequence is Asparagine or Aspartate. Similarly, Glx (Z) is used when there is uncertainty between Glutamine / Glutamate.
These two pairs of amino acids can be ambiguous in peptide sequences because Asp/Asn and Glu/Gln differs only by a terminal amide (-NH2) group in the side chain, and this amide group can be spontaneously lost from proteins by a deamidation reaction. When this occurs, asparagine is converted to aspartate/isoaspartate, and glutamine to glutamate/glutamate. These cannot be distinguished from "real" aspartate or glutamate by classic peptide sequencing, nor by mass spectrometry, since their mass is identical. Hence, protein sequences obtained directly from protein frequently contains Asx/Glx entries.

Asparagine (Asn) and glutamine (Gln) are derived forms of the amino acids aspartic acid (Asp) and glutamic acid (Glu).
Both amino acid pairs (Asn/Asp, Gln/Glu) consist of the same carbon backbone,
their side chains only differ in their functional group.
Aspartic and glutamic acid include a carboxylic acid (-COOH), whereas asparagine and glutamine are carboxamides (-CO-NH2).
Here you can see asparagine and aspartic acid as example:

Asparagine (Asn)

Aspartic acid (Asp)

The reason is simple: These are two different amino acids with different side chains. They look very similar, but they are not:

This is L-Glutamine, its chemical formula is C5H10N2O3.

This is L-Asparagine, its chemical formula is: C4H5N2O3. This shows that L-Asparagine has one CH2 less than L-Glutamine.

From the reference in the question, the query seems to be asking "Why does an amino acid have two abbreviations, such as Asn and N for asparagine, and Gln and Q for glutamine?"
This is because both abbreviations are commonly used in the scientific literature.  The longer, 3-letter, abbreviation is useful because it is a recognizable shortening of the amino acid's name.  The 1-letter abbreviation tends to be very arbitrary (e.g. Q for glutamine), so it is not very mnemonic. However, the single letter form is much easier to make use of for long sequences of amino acids, as in giving the sequence of a particular protein.


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I know how to solve these equations, but I'm not sure what t' represents?
I am investigating the Wilson Cowan neuron population model, and I can follow most of it, but I'm not sure what is meant by t' in the equation for proportion of neurons in the refractory period. The equation of interest is below.

As a side note. The mathematical expression you drew is not an equation (there is no equal sign).

I figured it out, t' is just a dummy variable used to represent time over the refractory period since the integral is from t-r to t.


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What are two butterflies doing when they fly together, 'hitting' each other?
I've Googled this subject extensively but couldn't get an answer:
My country is full of butterflies and moths, I've seen a lot of butterflies performing what looks like some kind of fight or mating ritual: Two butterflies of the same species flying together and 'hitting' each other, and when they do that a noise can be heard, I don't know if it's from the actual 'impact' or a noise they produce, but sometimes it's very loud and resembles an electrical arc.
I'm extremely curious on what that is all about. I thought they were actually mating but I've seen so many species doing that, including some that I know don't mate like that.
I live in Brazil - in the humid southeast region.
Any help or clue is really appreciated. I'm putting a link to a YouTube video below which shows more or less what I'm talking about, but strangely the butterflies in the video aren't of the same species:
https://www.youtube.com/watch?v=FpRQLtyIRog
Thank you for your time.

They both appear to be eastern swallowtails (the females can be black or yellow); the yellow one definitely is an ES. I can't speak to your Brazillian butterflies, but butterflies can be aggressively territorial with mid-air fighting. Like birds.


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Any nerves/fibers in foot similar to ulnar nerve in elbow?
I just noticed that when I gently run my fingers along the top of my right foot, I get the same exact "funnybone" sensation in my toes that I get when I hit the ulnar nerve in my elbow.
So I ask: are there similar nerves/fibrous structures running along the top of your foot as whatever is going on in your elbow with the ulnar nerve?
Not medical advice; just curious about the anatomy here.

Why would peripheral anatomy determine subjective sensation? In the end, the cerebral cortex determines the sensation associated with peripheral input. Rewired hamsters can have visual sensations in their auditory cortex (Frost et al., 2000) and visual sensations through tactile stimulation have been reported in man (Ortiz et al., 2011).
The sensations you describe are related to tactile stimulation of peripheral nerves. Peripheral nerves are pretty homogenous, and typically carry a bunch of afferent nerve fibers up to the somatosensory cortex.
References
- Frost et al., PNAS (2000); 97(20): 11068–73
- Ortiz et al., PLOSone (2011)

Thanks @Christiaan (I'd upvote you if I had the rep to do so) - however, as someone who is totally green in this field (biology), I find your answer a bit cryptic and vague! It sounds like you're saying that, no, there aren't any similar structures in my foot that would be causing this sensation, and instead, the sensation is coming from the way my "somatosensory cortex" is processing the tactile input. If that's the case, why would this happen all the sudden? Thanks again!

In the 2nd paragraph I try to explain that peripheral nerves are pretty similar all over. And linking peripheral anatomy to subjective percept may be tricky. That's all I'm saying. 5 more rep and you can upvote :)


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Why do humans masturbate?
Why does masturbating seem to be like an addiction?
What controls or initiates the urge to masturbate?
Is it good or bad or both and why is it so? I have heard guys who say that the do it regularly. Also there is a relaxing feeling; what generates that?

You probably mean masturbate instead of masterbate. I edited it. I also remove the triple interrogation mark, remove the spaces around interrogation marks and points and not use both interrogation mark and point.

The question is more on-topic on Health.SE. But before you ask your question over there, note that if you google your questions you will find millions of hits because you are very clearly not the first one to ask this kind of question.

I searched on google but most of time i get only one answer that it is good...

Maybe you should using the word masturbate instead of masterbate and try with a more accurate question. There is definitely loads of information. Way more than what you could read. For example, in your question you do not specify whether you are interested in physical or mental health. In its current form, I am voting to close the question as too broad.

I think it's on topic, there are Evolutionary hypotheses for masturbation and studies of how it affects sperm and ejaculate quality, and how that in turn can affect fitness

One word. DOPAMINE
See this article on Reward System and this one on Dopamine Those basically answer your question as to addiction, urge, and feelings of relaxation.
There is absolutely nothing wrong with masturbation, so long as you realize that it is a healthy expression of one's sexuality, that is observed, quite frequently, in our nearest relative, the Bonobo. There is no shortage of the study of primate masturbatory practices in the literature, and one could make a career out of its scientific study and analysis, so if you are interested in learning more, conducting a Google Scholar search on Primate Masturbation should give you literally years worth of reading material.
As for an actual addiction, it would only develop into a pathology if it became disruptive to one's life and was pursued at the exclusion of other basic activities.

Masturbating can yield to a strong addiction that can be bad for health just because it prevents one to have a normal social life. Also some are masturbating so much that they can injure themselves. So it is not as easy as to just say There is absolutely nothing wrong with masturbation.

@Remi.b I agree that that statement should be qualified, but I think AMR was speaking to religious/cultural conservatism that frowns upon masturbation as some sort of "sin" or social ill.

@Remi.b If you notice I had qualified my statement as to when it can become pathological. However, as with alcohol, or shopping, or food, or sex, or gambling, most can maintain a healthy balance and control without developing an addiction to the stimulus.

@Remi.b Scientific literature would contradict your impression. http://www.tandfonline.com/doi/abs/10.1300/J056v14n02_02 and http://link.springer.com/article/10.1007/s10508-010-9722-0 as examples.

Oh... I guess I missed your last sentence. Sorry about that. +1

@MattDMo More cultural than religious. Just as antivaccine ignores the scientific data to support an agenda, so to do those spreading superstition when it comes to sexual development. The scientific reality is far different from Remi.b. Yes, there will be a few that can become addicted, as it is linked into the neurological reward system, but for most it is a healthy part of development and coming to terms with their sexuality. Also physical injury is a fallacy, perpetuated with the same agenda looking to suppress the behavior.

@AMR I agree. I was raised in a fairly conservative religious environment, which is why I read religion into your statement.

@MattDMo, Don't need to be conservatively religious to have been sold an unhealthy view of normal sexual development. Just think of Seinfeld's Master of My Domain episode.


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Why is water flavorless?
I read recently that humans have an innate preference for sweet-tasting foods. That seems feasible since carbohydrates are necessary for cells to undergo cellular respiration, but why then is water not similarly good-tasting? The thirst mechanism is a very long, multi-step process that ensures that humans intake a sufficient amount of water, and it can be really satisfying to drink water when you're really thirsty, but why is it flavorless if it's so vital to life?

because water is ubiquitous. Every living object is made up of water. So it would not make sense to have a sensory perception for water. Imagine you always feeling the taste of your own saliva.

Is it flavorless or is it just something we consume so often that we just learn it to be the neutral flavor?

Try tasting distilled water : ) It stings.

Water is a compound and like many other compounds it has its own properties. Some compounds have smell while others do not, some have characteristic taste while others don't and the same happen with colour.

Because there are no taste buds or olfactory nerves that associate a taste with water (distilled). With that said, regular non-distilled water will have slight taste in it due to minerals, treatment chemicals (example: weak chlorination), and microbes.

Nice question. Water is tasteless and smell-less that leads us to think water is inert. But it is rather opposite. Water actively take part in many biochemical reactions.

@Agent_L Distilled water stings? However I never tasted distilled water.

Consumer water is not flavorless. Sources of flavor include (1) the chemical and microbial content, which is most influenced by geology and ecology; (2) chemicals added or removed during water treatment, and (3) inputs and reactions that occur during distribution and storage (Dietrich, 2006).
Two examples of ecology-related flavors are geosmin and 2-methylisoborneol, which are respectively responsible for earthy and musty odors, produced by cyanobacteria and actinomycetes (Izaguirre et al, 1982). Humans detect these earthy and musty odors at concentrations of only a few ng/l. The ability to smell geosmin and 2-methylisoborneol is affected by other factors, such as the presence of chlorine, which masks odors (Dietrich, 2006).
The capability of organisms to detect microorganisms like cyanobacteria is not trivial, as cyanobacteria produce toxic microcystins with hepatotoxic and neurotoxic properties that can cause illness and even death (Blaha et al, 2009).
In my opinion, from an evolutionary perspective, it would be more important for survival to taste pollutants in the water than to mask these components by generating a taste to water that could potentially make the detection of toxins less effective.
References
- Blaha et al., Interdiscip Toxicol (2009); 2(2): 36–41
- Dietrich, J Water and Health (2006); 4(Suppl 1): 11-6
- Izaguirre et al., Appl Environ Microbiol (1982); 43(3): 708–14

To add to the water is not flavorless point - generally speaking water you drink in cities and water you drink in rural areas tastes notably different.

Food & drink that are very cold are characteristically less flavorful than anything at room temperature or hot, it's definitely something to consider. You can also control the solutes in the water to obtain a desired taste. Reverse osmosis plants remove all solutes in water, and they'll add calcium, magnesium, etc. after the process. In my hometown, the water from the fountain in the reverse osmosis plant lobby was the best-tasting I've personally had, as it hadn't traveled through the city water lines, yet (this adds some flavor).

@DavidGrinberg you do not taste the water when you say water from two sources taste different. You are actually tasting the dissolved solutes.

Then why are all other foods (fruit, meat, vegetables) full of flavor? Wouldn't it better than to have, say, apples flavorless so that we could taste any rotting? Or I could ask the reverse question - wouldn't it better for the human body to assign a good taste to water so as to make it a nutritional "award", like most other natural good foods?

Because thirst is quenched by a liquid and in nature there are almost no liquids that are not mostly water, and none of them taste even mildly pleasant. Water doesn't need to taste good becasue water is all you have. But there are lots and lots of solids out there so certain ones have to taste good. You also can detect water more easily by its ability to wet then trying to design a chemical sensor that works to detect water in water laden mucus.


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Pepper plant leaf curl and "sweating"
The "sweating" and leaf curl have been going on for about a week. I've done some extensive googling and have found mixed diagnoses. For context, the ambient temperature is 74°, I'm using 6,500 K lamps and there are some flies around, but they are small and seemingly harmless. The plants are about 67 days old. Pls help.


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Is ATP Synthase a channel or an enzymatic protein?
Today in a biology lecture about plasma membranes and functions of proteins, we learned about channel and enzymatic proteins along other kinds of proteins. ATP synthase is considered an enzyme that synthesizes ATP, but it also creates a channel for H+ ions to pass through into a lower concentration area.

My question is could ATP synthase be considered a channel protein as well as enzymatic protein? Or no since the ion channeling is part of the enzymatic reaction? Also are there more examples were some proteins could have more than one kind of protein to them?

ATP synthase is an enzyme, a molecular motor, and an ion channel all wrapped together in one structure (Fig. 1). It is an enzyme, because it generates ATP. It is a molecular motor, because the central rotor part turns about 150 times every second during ATP synthesis (Source: MRC mitochondrial Biology Unit). It is an ion channel, because it funnels protons into the mitochondrion during ATP generation (Source: Davidson College).

ATP synthase. Source: Ace Biochemistry
ATP synthase is composed of two subunits, F0 and F1. The 0 subunit is embedded in the inner membrane, and the other, containing the catalytic parts, protrudes into the matrix.
F0 contains the proton channel and is connected to F1 with a stalk.
F1 consists of five polypeptide chains, alpha (a), beta (b), gamma (g), delta (d), and epsilon (e). The alpha and beta chains make up the bulk of F1 and are arranged in a hexameric ring. Both chains bind nucleotides, but only beta participates in catalysis (Source: ACE Biochemistry).
Another example of complex proteins are G-protein coupled receptors, for example those linked to ion channels (Fig. 2).

G protein coupled receptors. Image source: Wikipedia
Here, a receptor is bound to a G-protein, that becomes activated after receptor binding. The G protein then leaves the receptor and travels to an ion channel and activates it (or inhibits it).

You explained how ATP Synthase works, but could it be considered both an enzymatic protein as well as a channel protein?

@JovanyMerham - First sentences of the answer! Because it is ultimately ATP that is the final product of the protein, ATP synthase is what it is called, as a functional reference.

So the idea is a protein is considered to be one type or another is by the major function of the protein, am I on the right track?

@JovanyMerham - nomenclature is often murky and there are no strict rules. If the H+ gradient reverses it may even become a H+ pump that hydrolyses ATP, making it a a H+-ATPase instead of a synthase. The important thing is that everyone calls it ATP synthase, which is its physiological function.


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Are there human-ingestible liquids that do not contain water?
My son asked me a question that stumped me: Is there anything a human can drink that does not contain water?
It stemmed from a conversation in beverages in general where I was pointing out that they all are based on water...coffee, soda, milk, etc.
That's when he asked if there are any beverages that don't contain water. Given that nearly all of the water and even solid food I could think of contains water, I couldn't come up with anything, but now I'm curious about it to so came here to ask the experts!

Ethanol, glycerol, plant and animal oils/fats (triglycerides), etc. This link might help: https://www.reddit.com/r/askscience/comments/2nbs8p/can_humans_safely_drink_any_liquid_besides_water/ Great question by the way.

Forgot to add deuterium to that list. Just a disclaimer, obviously none of those could be a substitute for water, but you could definitely drink them ;)

@CDB - Deuterium is a hydrogen isotope. Hydrogen is not a fluid under normal earthly conditions. Further, EtOH always contains traces of water. The glycerine alternative and other oils, however, are a very nice example I guess. Worthy of an answer?

@Christiaan - Apologies, my bad. I meant deuterium oxide, which is actually, however much I hesitate to call it, a form of water. Still not really water though, seeing as it is 2H2O, so I thought it would fit in nicely on that list. Thank you for catching that and I apologize for the confusion.

@CDB - no need for apologies! However, water containing deuterium (D) is still water, just heavier. Water is water from a chemical point of view, so I disagree with your notion that DHO or D2O isn't water.

@Christiaan - From a chemical point of view, I completely agree with you. However, from a biological point of view, seeing as it cannot be used quite like water, I see it as more of a water variant, therefore I thought the OP might be interested.

@CDB - and why can't it be used as water? Chemically and hence biologically it's one and the same thing. The extra neutron goes unnoticed. In fact, D is naturally occurring in (tap) water afaik.

Yeah. Tritium is the only relatively stable hydrogen isotope(half life of 12 years) that would be noticed when it changes from T2O to He2O or from THO to HeHO. This would give us helium dioxide and helium hydroxide both of which are unstable.

@Christiaan - Not quite. Since deuterium is among the heaviest of stable hydrogen isotopes, its bond to oxygen is much stronger. In small amounts, this is fine, but if you replace 50% or more of a higher organism's water with deuterium oxide, it results in cell lysis and ultimately the death of the organism because it cannot perform its regular biochemical reactions with such powerful hydrogen-oxygen bonds in place.

@CDB I don't think anyone has ever tried drinking 100% ethanol, glycerol or heavy water. I have heard (but not seen) that traditional wrestlers from Indian subcontinent drink a substantial amount clarified butter (ghee) which is 100% fat. Normal people can consume a few teaspoons without much problem.

Is there anything a human can drink that does not contain water?

Yes, there are a lot of liquids that do not contain water, but mostly they are not safe for human consumption.
Mercury is a liquid at room temperature. Can a person swallow it? Most assuredly. Motor oil has no water in it. It's not a satisfying beverage. Canola oil, olive oil, and many other food derived oils can be imbibed in even reasonably large amounts, but it won't do your digestive tract a big favor.
I've treated goats with propylene glycol (a liquid), parents treat their kids with mineral oil for constipation, etc. etc.
It depends on what you mean by "drink".

The previous poster is close to true but olive oil, canola oil, and any vegetable oil does indeed have water in it. It's small traces but the vegetables themselves feed off water and makes it way into the oil. https://www.oliveoilsource.com/page/what-olive-oil Motor oil indeed has no water. Mercury as well has no water.

@Sean, you could heat up some edible oil to remove water traces, and it would still be edible.

Add in 100% pure Ethanol, it will hurt like hell, is really hard to obtain but yeah. you can drink it allright.

Also add pure acetone. There have been cases where humans ingested significant volumes of it and lived.

I actually like this question.