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Why is there no way to remove an immune response?
We've known for a long time now how to "add a new entry to the database," as it were, of immune responses.  It's called vaccination, and it's been one of the greatest success stories in the history of medicine.
And yet, allergies and autoimmune disorders, both caused by an immune system gone rogue, are still serious problems today.  If it's so easy to add a new immune response, why don't we have any way of deleting one?

I estimate about 25 years of hard work until we know enough to do that. It is not as easy as you think to create a vaccine or modulate immune responses.

It is an interesting question. The reason for why new immune responses can be launched but the memory of old ones are not deleted is based on the concept of irreversibility of certain chemical reactions.
Launching an immune response involves clonal expansion of cells expressing the epitope sensors such as the immunoglobins and T-cell receptors, accompanied by maturation of these receptors. Some of the reactions involved in this process are irreversible, which include VDJ recombinations, class switching and affinity maturation.
In an overall sense, immune response is analogous to natural selection- in the presence of the antigen the best binders are selected and expanded. Now to make a species extinct you would have to find each individual and kill it. Or you may have to develop a technology that will identify and kill a certain species in an automated manner. This is difficult to implement; how to engineer a mechanism that will precisely seek and destroy all the epitope sensors for a particular antigen. In contrast selection happens spontaneously because it does not proceed with a reason. It just selects the best from available stock.

"how to engineer a mechanism that will precisely seek and destroy all the epitope sensors for a particular antigen" it's called a virus. Sounds like the solution would be synthetic virus particles that specifically latch on to those epitope sensors and sabotage the rogue immune cells. Another alternative would be a synthetic programmable organ that produces antibodies specific to the epitope sensors.

Too long for a comment: Because we don't know how to do this.
The immune system is an extremely complex and highly regulated function of the human body and it is not easy to shut down single pieces of it without affecting the whole rest. We can completely block immune responses (more or less), which is beneficial for people who got a transplant. These people couldn't survive without this intervention, since their immune system would otherwise turn against their transplant.
The downside for them is, that they are more likely to get severe infections. A friend of mine, which got a kidney transplanted has to be very careful to not get pneumonia, since his immune system can barely fight this.
The other problem with fighting of these immune responses is that they are widely distributed. Lets take allergies as an example: Here you make antibodies which are highly specific for the antigen. This means that you make relative short living plasma cells which actively make large amounts of this antibody and long living memory cells which keep this memory alive. The later are then homing into the bone marrow and wait for another exposure to make them proliferating into more plasma cells and a few memory cells again. This process works for every antigen for which we acquire immunity, including vaccinations.
How should we selectively delete one subgroup of memory cells from the bone marrow without affecting all others? How do we find all versions (one protein, which causes an immune reaction has a lot more than one antigenic peptides) of it? And what else do we mess up, when we try to do so?


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Why is it difficult to bend the waist while keeping the knees straight?
It's easy to keep your legs straight when you're standing up or laying flat on your back, but as soon as you try to sit up or bend down, you need to bend your knees as well as your waist.  (Try it.  Lay down flat on the floor, then try to sit up straight while keeping the backs of your knees pressed against the ground.  You'll have trouble long before you reach 90 degrees.)
Why is this?

First off, I would be careful generalizing people's experiences with this exercise (..."Try it...You'll have trouble long before you reach 90 degrees"...):

Source: Yoga Tune Up
The muscles you are feeling at 90o, and the lady pictured above perhaps not even at 180o are the hamstrings. They run along the back of your thigh, attaching at both the hip and the knee. They flex the knee and extend (straighten) the hips.

Source: Precision Nutrition
When you do the exercise you are describing, the pelvis starts pulling on the hamstrings from the top because your knees are staying in place. Bending the knees releases the stretch.

source: Stack Exchange

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

sort: votes


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Regarding the difference between cDNA library and RNA sequencing (Biochem. technique)
I was wondering why establishment of cDNA library required the step of reverse transcription (i.e. turning the sequence into DNA) why not directly using the extracted RNA for sequencing and converting the U to T base? Why bother to have one more step? super super confusing

because you are stabilising a cDNA library of different expressed products, which you might want to sequence and amplify which is perhaps easier if the product is a DNA?

The construction of a cDNA library involves making a DNA 'copy' of the mRNA because the aim is to synthesise a large set of recombinant plasmid molecules, each containing a different cDNA and each propagated in E. coli.
The heyday of cDNA library construction predates the invention of PCR.
The key difference between the two approaches that you are comparing is that one (cDNA library) involves creation of a physical representation of the expressed genome whereas the other is an informational representation.

oh I see I see thank you so much, but then i have come up with another question...mmm..so sorry i have quite a poor background about this aspect....i was wondering why PCR is only applied to DNA why not RNA?

Oh n also I was wondering what the physical representation means?

I mean that a cDNA library exists as something tangible, not just in a computer.

PCR is carried out with a DNA polymerase, which can only deal with DNA as a template. The exception to this is of course reverse transcriptase, but that can't be used in a PCR because it isn't thermostable and it can't copy the DNA copies that it makes from an RNA template, so exponential amplification cannot take place.

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What is the difference between a DPY-10, DPY-11, and DPY-13?
My TA mentioned these three mutations of C. elegans since we started working with the worms but seems to skip over what the differences are...

Dpy is a class of genes. Usually they're written in lowercase when referring to a mutant allele. The name Dpy itself stands for dumpy and comes from the morphological change that occurs when one or more of the genes are mutated: the worms appear short and fat, or dumpy.
Another big class is Unc. Mutations in those genes cause uncoordinated movement.
For a description of the genes, see http://www.wormbase.org


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Is there any way the food industry can benefit from biofilms?
I realize all of the disadvantages, but I am wondering if the food industry can actually benefit from the formation of biofilms.

"In the production of some fermented foods, biofilms are an essential element for optimum production. During the production of vinegar, acetic acid bacteria are allowed to grow on wood chips. The biofilm that is formed helps make the conversion of substrate to acid more efficient." - http://www.foodsafetymagazine.com/magazine-archive1/februarymarch-2005/beating-back-biofilms-in-food-processing/

inf3rno's comment provides a great example, in the production of vinegar (Food Safety Magazine):

In the production of some fermented foods, biofilms are an essential element for optimum production. During the production of vinegar, acetic acid bacteria are allowed to grow on wood chips. The biofilm that is formed helps make the conversion of substrate to acid more efficient.

This paper, Biofilms in the Food Environment (Czaczyk & Myszka, 2014) also provides examples of biofilm use in industrial food production (on page 75, 14th page in the linked PDF):

Bioreactors
  with biofilms (biofilms represent a natural form of cell immobilization) are used to obtain acetic acid, citric acid, ethanol, and polysaccharides.

You can also check out Chapter 7 of this book of the same name, Biofilms in the Food Environment, for more information, if you're interested. It's not available for free online but you may be able to find it in a library.


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Which C. elegans would be appropriate for general study?
Would wild type N2 be best or Dyp-11? I know they're different, but I just want to observe the worms to see life stages, movement, etc. Dyp-11 seems like it would be easy to see but N2 is the wild type so I need help making an appropriate decision.

What do you want to see? Just the worms?

What question do you want to answer? The "appropriate" decision will depend on what exactly you want to investigate. What conclusions will you want to draw from your research?

Yes, all I want to see is the worms themselves.

I suspect that that dpy-11-mutants (that's what you likely meant) are not very representative neither from the morphological nor from the behavioral points of view, because they have anomalies in body shape (dumpy appearance) and male tail morphology (see in WormBase and in Ko and Chow).
For a general purpose the wild-type should be best.


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Does "squinting" make you concentrate better on a logic test?
We have all had those moments of intense concentration on some tough exam, perhaps a college test or whatever...
Why is it that when we squint, it feels like we can focus and concentrate better on the test, and get answers more easily?
Do we actually get a better mental performance when we are squinting?  If so, why?

Isn't it a social tool to show others you're thinking. Could you cite something that actually says it helps focus?

@GoodGravy the use in the situation you mention is correct. But and additional usage, at least for me, is when attending a lecture and if very sleepy, closing my eyes or even keeping them half closed reduces drowsiness and increases focus on the talk. My guess is it has something to do with reducing resource consumption. Or maybe an effect similar to what happens with blind people that get other senses enhanced. But these are just wild guesses, can't back them up.

@ddiez Sorry to be awkward, but when I'm squinting due to tiredness I'm straining to keep my eyes open, not enhance my focus! It's semantics sure, until you assume it enhances normal focus. If you don't think Ilan's answer is correct I think you're mixing up "enhanced focus" with something else.

@GoodGravy, OK. Are we talking about sight focus or mental focus? In my case I am talking about mental focus (i.e. the ability to enhance concentration). It seems to me that the OP refers to this meaning whereas Ilan's answer is dealing with sight focus (and in that regard it seems like a fine answer to me).

@GoodGravy To add a bit more detail, when tired, of course I also have to force my eyes open because they tend to close themselves. However, if I give up and close my eyes or put them half opened, then I somehow get a bit of relief and can concentrate better. Also, when thinking about some difficult problem, like mathematics, sometimes I close my eyes and that allows me to concentrate better in the problem. I have seen others doing the same... but maybe it is us! Again, all this refers to mental focus rather than sight focus.

The phenomenon in question is probably related to people with uncorrected/undercorrected myopia.
This "ancient" phenomenon is called stenopeic slit effect (a case of pinhole effect): when the person squints the visual acuity becomes better because of smaller blur circles: the "slit" between the eyelids is the key point improving blurring.
One can check if it works by creating slit in paper or plastic:

Some "charlatans/witch-doctors/quacksalver/etc" can "treat" refractive error with pinhole/stenopeic glasses:

It is known that children with refractive errors have attention issues because they cannot see the objects sharply (this is why they can be mistakenly diagnosed with ADHD), thus your concentration improvement related mostly to your vision improve and not a better "understanding".
If you mean by squint using mimic muscles and corrugator muscle the answer should point out that not a "squint" improves your concentration, but your attempt to improve your concentration causes this type of "squint".

Doesn't squint mean strabismus?

@WYSIWYG "squint" means strabismus (eyes misalignment), but also it means "stare" gaze: (google translater):verb
look at someone or something with one or both eyes partly closed in an attempt to see more clearly or as a reaction to strong light.


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What is the best time to exercise
So, after starting to gain weight on sitting in front of my computer too long, I have decided to take the plunge and maybe stick to an exercise regimen. As has been reported by some studies, exercising in the morning can be more beneficial than doing so in the evening. Now, personally, waking up in the morning is a huge chore for me. Furthermore, I have people advising me to hit the loo (toilet) before exercising as it may not be good for my health and leads to waste accumulation in the body. Now, search as I may, I cant find any basis that supports this theory. I understand that hygiene might be a factor but does exercising in the morning before going to the loo have any effects on health in general? Thanks.

WHO's definition about Health

Health is a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity.

In other words, Good health means active life where you can express yourself freely, you can succeed and can make mistakes, can reach your goals, can understand your body and others, and can say no when you see your limit to yourself and others - and can set new targets to yourself, feel accepted in your society and accept yourself as you are.
Best time to Exercise for successful results in competitions - dependent on Age

Endurance atletes during ages 25-30 years in this answer about Why does max heart rate decrease with age?

Short-term and long-term effects of exercise on Vitality
There are many stages in your question in Physiology, Pathophysiology and Microbiology, for instance.
I can cover here only the surface:

very short effect of short exercise (20 min) on brain
long term effect of regular short exercise (20 min) on brain, hypothalamus and biologic clock - wakefulness (limbic system)
long-term effect of regular weekly exercise (3.5 h) on brain
long-term effect of regular weekly exercise (3.5 h) on body muscles
long-term effect of careful regular stretching and appropriate resting on congestion of body
long-term effect of regular weekly exercise (3.5 h) on metabolism
effect of regular exercise on circulation system (blood and lymph) - known to increase i.e. include temperature distribution and defence bodies distribution
short-term effect of short exercise on PTH secretion (calcium); autoregulation of renal blood flow with two major theories: myogenic mechanism and tubuloglomerular effect

where I only briefly cover one term in Pathology.
There are two unanswered questions about the renal function [Costanzo, 2013]

(1) What component of tubular fluid is sensed at the macula densa? The
  major candidates are luminal Na+ and Cl−. (2) What vasoactive
  substance is secreted by the juxtaglomerular apparatus to act locally
  on afferent arterioles? Here, the candidates are adenosine, ATP, and
  thromboxane.

so to understand the effect of short-term morning training on PTH secretion, we should understand the two questions first.
Evidences to some things

Short-term exercise can work sometimes as prophylactics for allergic symptoms.
I think the most important thing is the irritation of your skin which is the most important endocrine organ in our body.
Skin's temperature change secretes many hormones than help us to stand irritations from the environment.
What are the effects of short-term exercise in the morning depends on the patient at hand.
I cannot say much general.
For instance, if your heart is not strained; that it has too high T peak, too heavy exercise can cause you harm.
My personal experience

Short-term exercise suited to a person with no deficits in sleeping can help to alleviate symptoms of allergies and decrease stress in a normally physiological balances without viral infections,

but the real world is not that nice.
The problem comes if the patient has any disease that uses our immune system against us such as some viral infection.
The immune response is also the source of pathogenesis for many viral diseases.
Unlike for a bacterial infection, the ultimate goal of the immune response in a viral infection is to eliminate both the virus and the host cells harbouring or replicating the virus, [Murray, Medical Microbiology, 6th ed].
Actually, some drugs are immunosuppressant like cortisone, and some procedures like radiation therapy.
However, with some medication plans, you should avoid drugs, living styles and habits that immunosuppresses your body.
For instance, HIV patients with HAART medication plan (medication combination is antiretroviral but possible immunosuppressive pathways may exist in different conditions) that involves a strategy depending on the condition, since HAART medications are life-long and cannot be stop, so other conditions etc TBC must be treated first, to avoid too much burden on the body at the same time.
In a similar way, avoiding living style or habits that puts immunosystem down can help with HIV.
Doing sport when you have slept badly many days and feel exhausted, puts your body under immunosuppression.
So the state of the disease or your physical wellbeing determines when sport is useful and when not.
Other part of your question
To hit toiled before exercise is good because then

you decrease the risk of gastrointestinal bleeding and venous congestion.
effect of exercise on constipation is one topic here; depends on you, since there are many types

The more stuff you have in your colon and gastrointestinal system, the harder it is to use fully your muscles of your body.
Try pull-ups with more empty colon vs full one.
Pull-ups require many muscles from upper trunk and lower trunk.
You cannot use all your stomach muscles if something is blocking your middle body muscles.
Good Hygiene is the easiest way to decrease the risk of any infections caused by many factors.
I estimate that 2-5 % of people visiting public toilets wash hands correctly; one video here about how one should do it.
Many people leave their hands wet.
If you have infection in your body, you should not exercise because failure to resolve the infection may lead to persistent or chronic infection or death.
It takes much energy from our body to handle with infections.
To recover from training, it requires good balance of many factors.
Summary
The best time to do sport when you are healthy

you do not have any infections (viral particularly) because a failure to resolve the infection can lead to persistent or chronic infection or death
when you have prepared early enough for the exercise with enough sleep

where pathologies and/or teratologies are not limiting your process.
You compete only against yourself and then grow from that to see you how good person you are really.
The morning exercise in a body which has rested well before the exercise and prepared accordingly to the exercise can be useful because

short-term effects on the brain (process things during exercise) (See Figure 1)
possible short-term effects during day after the exercise

and if the exercise becomes a habit in a healthy person, then

long-term effects: increased metabolism and many other positive effects described above
and many other possible reasons from social to better self-esteem

when the the person listens to his body and stops when it hurts or something goes over; can rest accordingly.
Good motivation is useful in gaining good health.
Motivation is the strength and direction of the effort.
If you are interested in morning exercise, then you can set target and make a realistic plan.
Listen your own body and be able to refit your plan accordingly.
Actually, here is an important step that the consultation of many doctors can be useful; one doctor cannot always see the main problem for instance of prolonged and deepened allergic symptoms.
Consultation and discussions of other people can also be useful - like discussing where to help for this and this; who has enough capabilities to understand it.
The person cannot always know himself what is a main disease underneath.
Anything can come that postpone some training sessions.
Sources

Infectious disease courses 2015-2016
Gleeson. The effect on immunity of long-term intensive training in elite swimmers.
Anderson. Effects of Exercise and Physical Activity on Anxiety. 2013.
Laires. Exercise, magnesium and immune function.
Gunzer. Exercise-Induced Immunodepression in Endurance Athletes and Nutritional Intervention with Carbohydrate, Protein and Fat—What Is Possible, What Is Not?
HAART and HIV in DynaMed Plus. Visited 7.8.2016.
WHO. Health Education. Visited 7.8.2016.
...

Can you please add references to your answer? Especially the first part about exercising and and allegies needs this.

@Chris To investigate such a thing is very difficult in a general subject. I need more specific patient data to give references: sleeping rhythm, age, gender, training history, allergies, blood picture etc to give exact references. Otherwise, the scope of this answer cannot be reached in a lifetime. Please, say exactly to which statement you want a reference so it is easier for me to find it. There are very many sources which I have used in my text. Please, specify what is your exact interest here.

This is not hard - you claim that exercising improves the symptoms of allergies. To do so, there should be some studies proving it. If these do not exist, than you can simply not claim this. If this is your experience than this is anecdotal and also no proof.

Your post could still do with references for it's points, particularly: "Short-term exercise can work sometimes as prophylactics for allergic symptoms".  HIV treatment is also not by immunosuppresant drugs (this is what you are trying to avoid).  There has been some very limited research into trialling immune suppression but clinically it's treated with HAART - antivirals not immune suppressors.


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Motifs in undirected networks
I have an undirected network and I am currently analyzing both three and 4 node motifs in the network. However, I can't find any articles which describe the biological significance of 3 of 4 node motifs in my network. Comparing with randomly generated networks, I am able to deduce that the number of three node motifs and 4 node motifs are significantly higher. However, I am unable to infer any biological significance for this finding.

Can you clarify what is your network? Is it a network of genes, protein-protein interactions or something else?
Also do I understand right that you randomly generate networks without considering the fact that most biological networks are actually scale-free networks?

@MaximKuleshov Its a transcriptional regulatory network https://price.systemsbiology.org/research/honeybee-transcriptional-regulatory-network/

@MaximKuleshov  I understand that TRNs are directed and bipartite comprising of transcription factors and the genes they regulate. I was just curious about motifs in co-expression networks.

@MaximKuleshov Also, I understand that Biological networks are scale free networks, I actually split my network into 8 clusters and the whole comparison to random networks is to prove that the clusters in themselves are real.

What is the structure of the 3 of 4 node motifs of your network for which there is no description of biological significance? - Which type of random network did you compare to?

I am not 100% sure that I understand the question, but I am going to try to answer, based on the following assumptions:

The "number of 3 and 4 node motifs" is not very clear. If I understand correctly, it should be a quantity determined in large part by the degree distribution. You could rewire your network to lose all information about the TRN other than degree distribution and this number is probably very similar (or it is a quite weird network, which would make me suspicious of the data).
Therefore, the number of such motifs of size $k$ is not particularly interesting biologically, specifically due to technical issues such as incomplete ascertainment of edges, etc. The true network may have many more edges, and this will change this number, so the degree distribution is not itself interesting- it is in fact the thing you want to control for.
Therefore, when you compare with randomly generated networks and find different numbers of motifs of $k$ nodes, I suspect the random networks were generated with a different degree distribution. (It is pretty easy to generate networks of the same degree distribution, using e.g. the rewire() function in igraph)
Therefore, I interpret the question to be more specifically: "Among all 3 and 4 node motifs, a subset are overrepresented in my TRN compared to randomized graphs of the same degree distribution. What are some ways to interpret these motifs?" This is the kind of question that is traditionally asked with TRNs in my experience.

As an example of how other groups have analyzed TRN motifs, I suggest looking at Figures 5 and 6 of this paper. For instance, the "feed-forward" motif is overrepresented for links involving some TFs. I believe that it is standard to compare motif distributions to other biological networks, such as the C. elegans neural network. There are references in the Cell paper that could probably help you out further. The wikipedia article on network motifs also looks to have some information, and there are other resources on the internet if you google.
While there is not necessarily a strict biological interpretation of such motifs, they nonetheless can be informative in identifying specific patterns peculiar to different TFs or master regulators.
Caveat
It is possible that I have misunderstood the question or made bad assumptions- my graph theory is superficial. But if I am wrong and you are actually interested in the simple number of motifs of size $k$, that observation is of interest as a "I have a weird graph" theoretical problem, not as a "this is biologically interesting" problem. As a biologist I would care much more about which specific motifs of size $k$ you have, rather than the summed count of all motifs of size $k$.
On the other hand, forgetting about motifs for a moment, a "weird" network could be quite topologically interesting biologically. For instance, do your different clustered components associate with different pieces of biology, like sugar metabolism vs. morphogenesis? That would be expected, but it has very little to do with motifs- they may just be a side effect of that functional topology. In that case, it would be not only degree distribution but also that topology that you would have to control for to make interesting statements about motifs.
good luck!


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Gene networks in insects
I am working on gene networks and I currently have the honey bee gene network to work with. What I am missing is a gene network that I could compare it with. Could you please guide me to a database/website that I could use to download a gene network and use for my study. I am looking for gene networks from closely related species (hopefully another honey bee gene species (other than Apis mellifera or a hymenopteron. I am open to all flying insect species really. Kindly advice.

I am not sure what a gene network is (in so far as it is hypothetical concept) but the kind of data you have for honeybee must exist for the insect to end all genetic insects. Have you looked?

Not closely related but Drosophila is well-annotated: http://www.droidb.org/DBdescription.jsp. Unfortunately interaction networks are most likely to be found in model species, of which there are not many. Some work on wasps seems to have been done by Amy Toth (https://scholar.google.com/citations?user=kzt2orQAAAAJ&hl=en) and by others (https://bmcbiol.biomedcentral.com/articles/10.1186/s12915-016-0285-y) but they are not clear well annotated networks. I got that just by googling I am sure you could find something.


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Haplodiploid species that are not eusocial
Haplodiploid species need not necessarily be eusocial and eusocial species need not be haplodiploid (reference). Everywhere I look its been mentioned in general terms that some species of bees, termites and wasps are haplodiploid but not eusocial. What are some specific examples of haplodiploid species not being eusocial? I was specifically interested in bees but examples from other species are also welcomed. Thank you in advance.

https://en.wikipedia.org/wiki/Bee#Solitary_and_communal_bees

@mgkrebbs That wikipedia page doesn't mention ploidy but the wikipedia pages for the species of bees do mention their ploidy. If you can write an answer, I can accept it and close the question. Maybe you could also mention a haplodiploid non-eusocial termite and wasp too in the answer.

feel free to post your own answer with that in it; that's allowed under site rules.

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How do neurons send electric pulses even though they are surrounded by liquid which is mostly water?
I just thought about the fact that people move through electrical pulses traveling through neurons in the brain and muscles through the body. Here is what i know: the body is full of 97 or more, percent of water. the thoughts we have and the moves we make are a result of electrical impulses within the neurons and cells.
  My question is why the water does not disperse the impulse and or make it completely ineffective. My personal guess would be that each neuron is made of or has an outer layer of electric resistance material that( is it conducts) electricity.

You might want to begin to look at ion pumps and channels (plenty of good wiki articles).  Remember pure water is not a good conductor but with ions it becomes so.  In biology, signals are propagated by the control of ions across membranes and other gradients.  Have a look at action potentials as well.  I'd answer this but I know there are some really good nuro people on here and I'm not one of them.

Ooh, even more interestingly, how do we control ions, hormones and catalysts?

read about synapses

We are not made of 97% water https://en.wikipedia.org/wiki/Body_water

Neurons have sodium, potassium, as well as some calcium channels all over the surface of the cell (I'm giving a very generalized explanation here). The "electric pulses" that you are mentioning is more of electrostatic potentials generated from the interactions of cations and anions flowing in and out of the channels. Water at the specific pH surrounding the cations is a good conductor of these electrostatic interactions.
You have to remember that there are large negatively charged anion proteins inside the neurons which attract the cations (sodium ions for example) to rush into the cell. Once threshold is reached all gates open and an action potential is produced.


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What could cause a forest of bent trees?
While hiking on the northern Idaho-Montana border, I encountered a large area where virtually every tree is bent at the base in the downhill direction.  Only the very largest and very smallest trees are straight.  What could cause this?

Avalanche?  Or just a heavy accumulation of snow bending them towards the ground one year.  I could find you some hereabouts that are bent into U-shapes, or even S-curves.

Forgot to remove the fisheye lens?

This case is much different, but you might find it relevant: Crooked Forrest.

A forest near my grandparents farm has a bunch of bent trees due to a tornado 40 years ago. That being said, if they are all bent at such a similar angle geotropism seems more likely.

Prevailing winds, you see a lot on the coast.

Also see,the Dancing Forest https://en.wikipedia.org/wiki/Dancing_Forest they think it might have been caterpillars.

The phenomenon in question is probably related to geotropism.
If the hill soil is "on the move" it will cause the bend on the trees -

If the soil in a slope is moving downward, the trees on this slope
  will tip downward.  As the tree continues to try to grow upward, the
  trunk will show a curve. The degree of bending could indicate the rate
  or amount of movement of the soil.

source

This was a surprisingly interesting question and answer.

@canadianer :) thanks, nice to help to community %)


text:
How did the first sexual animal come to exist?
I am more or less familiar with the evolution theory based on mutations.
Now, starting with a nonsexual being, how did the first organism that reproduces sexually come to exist.

Your question is too broad. It won't be possible to provide a precise answer to such a question. Please add details to your question to make it more precise.

I think this is answerable - you need to look at fungi though.  animals did not invent sex. will try to put up an answer tomorrow if someone else doesn't.

related: Evolution from Mating types to different sexes

Big topic yes, but lets hit some high points.
First, sexual reproduction is a no brainer in evolution.   In its basis, sex only requires a segment of the chromosome to be heterogamous - that it will not be recombined.  In male humans this is both X and Y chromosomes, in other animals it is the female which has heterogamy.  Its not the entire chromosome either - the pseudo-autosomal regions of X and Y in humans do recombine.
Sexual reproduction allows some individuals to combine their genomes by donating some but not all chromosomes to offspring. The heterogamous regions are always donated by one parent and the same sex is not allowed to combine with others.
Sexual reproduction is found in plants, single celled eukaryotes as well as animals.  The forces that drive the emergence of sex show up frequently enough and are persistent enough for sexual chromosomes to have evolved hundreds of times in plants.
Even in animals, where asexual reproduction is very rare there are multiple configurations of sex determining chromosomes.
Sex goes back to a very ancient trait in eukaryotes related to the haploid / diploid life cycle.  In fungi, who are related to the original metazoans, sex shows up when its needed.  There the combination of haploid phases may be limited by more than one combination of specific elements.  Fungi can have many genders (mating types) - each of may only allow mating to specific types.  Others like Saccharomyces allow recombination between any two different mating types.
The earliest single celled eukaryotes related to animals show mating types.  The various sexual characteristics related to sexual reproduction, such as placentas, eggs, sperm form
and function are all embellishments from sexual selection which vary tremendously from one form of animal to another.  The chromosomal functions which became sexual traits are ancient and predate metazoans.  They are not necessarily conserved though - they are simple enough to reproduce that they change their characteristics often in evolutionary history.
I should say that all this doesn't apply to bacteria and eubacteria.  Why?  Because bacteria are much older and have their own systems of gene transfer and recombination with their own rules.  They usually have a single copy of their genome (I'd like to hear about exceptions - I think I know of maybe one) which makes quite gender different.  The do have something called 'sex' where a pili gene can be found on a plasmid which allows the bacteria to transfer DNA directly, which is like a sex determining locus.  But a bacteria may catch gender like a cold - it can not have it, it can get it, it can lose it.
Bacteria are also capable of transferring a single gene or a segment of DNA by various means, including pili, plasmids, phage, and simply taking in the naked DNA that they find laying around.

I’m not sure I would agree with “no brainer”. As far as I know, sexuality has only evolved once. Also, could you expand a bit on the heterogamy argument? In particular, wouldn’t the same apply to plasmids? Yet we don’t see anything particularly resembling sexual selection emerge from that. /EDIT: Your answer might actually contradict my first assertion (I should have read the full post first) – I’m still interested in an answer to the second.

you can argue the terminology, but i do have references saying that sex has evolved independently several times in plants etc, so i'll leave that to you and the authors or to post to your answer. I've added a section on bacteria. sex in bacteria is more of an analogy than a correspondence from what i know.  The question focused on animals originally.

Actually your text already convinced me, concerning the number of times sex evolved (hence the edit).

This is a very broad field, with many complementing, overlapping, and contrasting theories. I suggest that you read this part of the Wikipedia article on this topic:
http://en.wikipedia.org/wiki/Evolution_of_sexual_reproduction#Origin_of_sexual_reproduction
Here is what I got from the Wikipedia article (this is just one hypothesis, read the article for all the others):
There are many advantages to sexual reproduction, two main ones are greater genetic variation and recombinational DNA repair (occurs during meiosis).
There are certain species that can reproduce both sexually and asexually. They choose to reproduce sexually during times when the environment is uncertain (changing). This provides evidence that greater variation is one reason for sexual reproduction.
Asexual organisms only have one copy of each gene, therefore if this copy is mutated in a bad way, they are out of luck. Organisms that sexually reproduce have two copies of each gene, when one goes bad, they can use the other copy to repair the original copy, during meiosis.
As you may know, stress has many harmful effects, one being that it leads to DNA damage. There are certain species of bacteria who, in response to stress, uptake/integrate nearby bacteria cell's DNA into their own. They can then use this new copy to repair their own copy in case they experience DNA damage.
This "trait" of up taking/integrating other's DNA may have been evolutionary selected for (because these organisms repaired their DNA, they survived and passed on their genes), therefore eventually leading to organisms that sexually reproduce.

I’ve had to edit your answer, “just one theory” sounds a bit too similar to the “just a theory” creationist canard for comfort. I’m wary that it might feed the common misconceptions about what makes a scientific theory.

I fully support your edit, that was a nice catch :) Thanks Konrad.


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Ray wu DNA sequencing methodology understanding
I'm trying to understand the method which Ray Wu, developed to sequence the DNA 5' cohesive ends of a lamda phage. I'm reading these two papers written by him, but i stuck at the point where he uses the 32P nucleotides.
Structure and base sequence in the cohesive ends of bacteriophage lambda DNA
Nucleotide sequence analysis of DNA: II. Complete nucleotide sequence of the cohesive ends of bacteriophage λ DNA
It's not clear to me, by reading the papers, the step in which he runs the polymerization of the DNA. Did he use all the 32P nucleotides at once or each one at a time. As i understood he made the DNA pol to use the tritiated nucleotides to fill in the gaps of the 5' cohesive ends and then he cleaves with a DNAase in many  oligonucleotides which later fractionize with electrophoresis. If he added all tritiated nucleotides at once how did he recognize which one is at a specific place ?
Can someone describe the process in more detail using step by step aproach?
Thank you,

Those two articles are located behind a paywall

Do you want me, to upload them somewhere else or is it illegal?

I'm not a lawyer (I'm a biochemist). Don't worry, I think I have a new account for access. So you're still seeking an explanation? How did you come across these classics?

I just wanted to see how people used to think back then with their only tool the analytical chemistry and some little knowledge of enzymes. 2 days i read it again and again and tried to put an order of the process/method he was used. His work is about 28 pages and he finally read about 20 nucleotides. Maxam's and Sanger's  papers are around 8 pages and they cloud sequence 100 - 1000 nucleotides at once. Times are changing and it seems fascinating to me knowing a little bit of history. If you want the papers, let me know.

That's very cool (IMHO). As my martial arts sensei used to say "You gots to know the basic fundamentals" (he was not a native english speaker). I think the second paper has the full story(?) because based on the abstract in the first paper he only found out which bases were present, not the order or sequence. Can you upload PDFs here to Stackexchange as attachments? I don't remember how that works.

What stage are you at in your education/training?

After reading your original post again, I am going to speculate that the combination of isotope labelling and DNAse digestion means he used a combination of something called nearest neighbour analysis, probably coupled with wandering spot thin layer chromatography (TLC)

Nope, according to this review article I was wrong "It was around this time that various researchers began to adapt their methods in order to sequence DNA, aided by the recent purification of bacteriophages with DNA genomes, providing an ideal source for testing new protocols. Making use of the observation that Enterobacteria phage λ possessed 5′ overhanging ‘cohesive' ends, Ray Wu and Dale Kaiser used DNA polymerase to fill the ends in with radioactive nucleotides, supplying each nucleotide one at a time and measuring incorporation to deduce sequence [17,18]"

Check out this site: http://www.whatisbiotechnology.org/exhibitions/sanger/dna

I couldn't create attachments in comments so here are the links for the files
http://s000.tinyupload.com/index.php?file_id=73908298645007027481
http://s000.tinyupload.com/index.php?file_id=30732501249180823829
I just started my Msc. at protein biotechnology.
I've already read that page. All i wanted was to understand the chemical perspective they used.

Also,  by reading these papers, a new question came in the air posted here. https://biology.stackexchange.com/questions/52809/doesnt-the-radioactive-labeled-molecules-of-dntps-or-dna-harm-themselves-or-the
If you have an idea for that too... let us know :-)

I am not going to post this as an answer, but I have skimmed the paper, and it is an absolute beast.  Some facts worth noting. They do not use electrophoresis, they use ionophoresis.  They also use a scintillation counter to calculate the number of molecules of radio labelled dNTP incorporated.  After ionophoresis they purify the radioactive peaks and analyse those by nuclease digestion, and nearest neighbour analysis.  Essentially they use the labels to purify the new oligos, and then fragment them to figure out the sequence of every dinucleotide. Then they build a map.


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Plant's phylogeny tree to identify which of them are closer (genetically) with another plant
I'am trying to create a phylogeny tree from some plants, as the post's title says, to help me conclude which of those plants are closer genetically with another one plant.
So let's say that this is the plant list:
Nicotiana tabacum , Zea mays, Oryza sativa, Solanum lycopersicum,    Solanum tuberosum, Erythranthe guttata, Hordeum vulgare, Vitis vinifera, Prunus persica, Glycine max, Populus trichocarpa, Medicago truncatula, Phaseolus vulgaris, Morus notabilis, Citrus clementina, Setaria italica, Theobroma cacao, Acacia mangium, Cicer arietinum, Triticum urartu, Brachypodium distachyon, Aegilops tauschii, Panax ginseng
and i want to see which of those species is closer with Sorghum bicolor.
Is there any easy way to conclude something like that or it needs to get results out of bioinformatics using a specific gene , align it , and then see the tree ?

If you want to compare the relationship, you need to use a gene which is present in all plants you list here and then do a comparision. This will allow you to build such a tree.

Ok. i have took one gene and translated into protein for all these plants. Aligned them and now which algorithm should i use to produce the phylogeny tree ?

Single gene trees are unreliable. You should concatenate and align at least 50 genes, e.g. ribosomal proteins, and then build a tree with e.g. RAxML and PhyloBayes. Be sure to pick an out group wisely too..

In general for plants, before you start trying to make your own phylogeny, you should try to find an existing phylogeny. Phylogenetics is complex, and a lot of people have already done the hard work. You can start by looking at the Angiosperm Phylogeny to figure out which species are most closely related. To make use of the tree you will usually have to look up each species to figure out what order or family it is in.

In this particular case, Sorghum bicolor is a grass, so of course it's going to be closed to Zea, Oryza, Setaria and Brachypodium (all grasses) than any of the others. You can see where it places relative to the other grasses by looking at a grass-specific phylogeny. Because all three are model species, their phylogenetic placement relative to one another is well established. A simple Google image search for [grass model species phylogeny] gives you your answer (from the Setaria genome paper):

This shows you that Sorghum is closest to Zea out of the species you listed.


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Applying saliva to mosquito bites
Is it true that; when you apply your own saliva to a mosquito bite it would stop itching ?

There have been many personal experiences documented where people have experienced relief from itching of mosquito bites on the application of their own saliva to the itchy spot (reference 1, reference 2) It helps to reduce the itching because saliva has been proven to speed up tissue repair and has antibacterial properties. It also provides a moisturising effect on the itchy spot (reference). Salt is also known to provide relief to itching (reference) and the slight salt content of saliva helps in that respect too.

If the skin is broken from scratching, though, it would also be inoculating an open wound with oral bacteria - which can lead to infection.

@DoctorWhom Most of what I found on the advantages of applying saliva to reduce itching is based on personal experiences and I couldn't find any reliable source or research for the same. I wouldn't depend on it as a sure fire cure for itching as such. Of course, in the case of open wounds there definitely is a risk of infection. Might work as a first stage to reduce itching before scratching your skin off.

Agreed - I hadn't heard of it before actually, so it's an interesting concept.  I just wanted to mention infection to go along with the saliva, because a lot of people suck on skin-breaking injuries (and to put a plug in for that, the best thing (even more than antibacterial ointment, which has limited utility and isn't often recommended) is washing it IMMEDIATELY with soap and lots of water).   Our mouths are quite full of life - microorganism life ;)


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What's inside the perinuclear space?
The cell proper contains the cytoplasm in general and the cytosol in particular when referring to the fluid/gel without notable organelle.
Once we move inside the nucleus there is the nucleoplasm and the nucleosol.
My question is in the intervening void of the perinuclear space (between the inner and outer membrane of the nuclear envelope) what if any is the terminology used to refer to the internal chemistry in that space - and what is known about it's makeup?

The outer nuclear membrane is connected to the endoplasmatic reticulum (ER), so the perinuclear space will share some characteristics with the ER as well. However, there are bound to be specific differences as well, which I don't know about.

Interesting so the perinucllear space could almost be thought of as the innermost sack of the endoplasmic reticulum.

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


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If gene differs between chromosome pair does individual get a mixture of protein shapes?
Do diploids such as humans end up with a mixture of two different shaped proteins where the appropriate gene is expressed differently in the two halves of a chromosome pair or is there some governing factor that dictates that only one of the alleles is ever used to direct protein synthesis?

Yes, that mixture of shapes can happen.  Differences in the nucleotide base sequences between the two alleles of a gene can lead to differences in amino acid sequence, which in some cases large differences in protein shape.  One example would be if one allele changed a cystine codon to any other codon, leading to loss of a disulfide bond needed to stabilize the tertiary structure of a protein.  For an extreme example, consider a mutation causing sickle-cell anemia; in this case, the disease-causing allele leads to altered shape of the entire red blood cell.
If a heterozygote carries a healthy allele and a disease-causing recessive allele, the protein produced by the healthy allele provides enough activity to mask the lack of activity of the "broken" protein provided by the recessive allele.  If, instead of being a true recessive, the disease-causing allele is partially penetrant, then the heterozygote would suffer from the reduced level of the active protein (only one allele is providing the good stuff).


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What's the technical terminology for call-and-respond type behaviour?
The groups of some species such as water birds display a behavior that once out of line-of-sight a member will periodically initiate an interaction by make some type of sound, which will be followed up by responses from all the other members - presumably to confirm they haven't been silently snatched by a predator. I have observed this in person at a local botanical garden where the water birds sound off like this every 10 minutes or so all day long.
What is the technical term for this behavior and some examples of species that demonstrate it?

if you are referring to call and response in rapid succession, ethologist use the terminology "turn-taking" or "antiphonal calling".
Many species do it with different degrees of precision.
A rapid research on google scholar will give you several results.
I do not know whether it would apply specifically to your case, which might be more general and it could be simply "contact calling".
Regarding the hypothesis you formulated ("(...)presumably to confirm they haven't been silently snatched by a predator"),   it would be nice to know if actually everyone respond, who is calling first (always the same individual?) and if they would behave different if someone does not reply.
Hope it helps and have fun with your observations.


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Does antidromic conduction occur in the brain under normal conditions?
So I am reading a book on neuroscience and they mentioned in passing that the action potential is capable of travelling in either direction along the axon (orthodromic vs antidromic), The wikipedia antidromic article states that the effect is often used to confirm connections in laboratory experiments.
What I'm now wondering is if the phenomenon has been observed with normally behaving neurons in situ (as normal as a neuron under experimental observation can be anyway) and therefore possibly needs to be factored in when modelling neurons in software or is it safe/justified to treat the information as only flowing in one direction (orthodromic)?

Under physiological conditions, action potentials are generally assumed to travel one-way. Action potentials are generated in the dendritic region, and travel from the soma to the axon terminal. Because voltage-gated sodium channels are inactivated after having been active during action potential generation, the action potential cannot travel backwards because the tail-end of the action potential is basically temporarily shut down (Fig. 1). The duration of inactivation of sodium channels determines how fast a neuron can fire, i.e., it determines the refractory period of neurons (Purves et al., 2001).

Fig. 1. Action potential conduction and refractoriness. Source: Zoology.
When neural tissue is artificially electrically stimulated, however, action potentials can be generated anywhere along the neuron. When an axon is activated somehwere in the middle with an electrical stimulus, an action potential will travel both ways, i.e. normally to the axon terminal, but also antiodromically to the cell body.
However, it has been noted in vivo that some neurons do show antidromic action potentials under physiological conditions (Jansen et al., 1996). For modeling purposes I would not bother too much about this, though, because antidromic action potentials are generally only observed under artificial conditions.
References
- Jansen et al., J Neurophysiol; 76(6): 4206-9
- Purves et al., ed. Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates; 2001

Any chance you could expand on/summarize the Jansen et al. article (It's behind a $20 pay wall)

@norlesh - what do you wish to know? The authors found antidromic responses in some neurons in an animal model, but they don't expand on how and where they were generated. If you can say what you are after I'm happy to elaborate.

Guess I'm wondering in the article what effect/outcome the antidromic signal had in the animal model? did it just fizzle out once it reached the hillock or was there some observable function/benefit?

@norlesh - It was merely observed. They just monitored this type of neuron and saw that some spikes were out of sync. By doing the math they figured they must have been antidromic. It's a short observatory report (4 pages only). Happy to email the pdf, grab me on chat


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Can life forms exist from simple structures not made of the four bases?
I understand that all life forms on the planet are made from adenine, gauatine, cytosine and thymine, which chemically joined together to form RNA or DNA (correct me if I'm wrong). This goes on to form all complex life as we know it.
I was wondering if it was possible- even studied theoretically- that other life forms could exist made of different elements and compounds, perhaps let's say iron, cobalt or tungsten? Or are the 4 bases the only possible way of life as we currently know it?

If we think of a cell as the unit of life, these constructs are made up of lipids, carbohydrates, proteins and nucleic acids. Of course, viruses are considered non-living, and are composed typically of just nucleic acid and protein. At that, we have to make a cutoff between what is living, what's non-living, and what constitutes one or the other. For reference, nucleic acid is DNA/RNA. The take-home point though, is that you need more than nucleic acid to get a living organism as far as knowledge contends; ergo we'd need more than an element/polymer.

You seem to have a severe misunderstanding of biochemistry. The 4 nucleotides you mention A, G, T, and C are used to make DNA, but in RNA, the T is replaced with uridine, U. Additionally, RNA can contain many modified nucleotides. Of course, there are many many more compounds in living organisms than just the nucleotides. I recommend reading some wikipedia articles to get a better understanding, such as on DNA, RNA, how they're related.

possible duplicate of http://biology.stackexchange.com/questions/90/life-without-dna ?

Nobody knows for sure, but search Google News for "Life on Titan".

@user137 I was aware of the U base. When I said all life forms are made of the four bases, I just meant a large amount

So this question is difficult to answer because it has some errors in it, in that lifeforms being dependent on rarely used elements is a different question than lifeforms using different DNA bases, but I will answer both.
So for the question about whether or not organisms could exist that use DNA bases not found in organisms on earth, the answer is certainly yes.[1,2]
The above reference shows a very elegant example of completely synthetic DNA bases being incorporated into E Coli and propagated in culture without providing any noticeable negative effects. This provides strong support that life on Earth developed around the same 5 bases (CTGAU) by chance.
As for whether or not organisms could rely heavily on elements other than H,C,N,O, and P, this is certainly possible and evident already here on Earth. Extremophiles are a general class of organisms that have some pretty interesting properties to them. Some metabolize sulfur or metals, others live in really extreme temperatures or in areas of high radiation.
So really yes in both cases, life can really take numerous shapes and forms even when it seems completely impossible for them to do so.


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What is the focus distance of a 3D screen?
I've thought long and hard about wheter this is the appropriate section for this question, because I guess it's kind of an interdisciplinary subject.
My understanding of stereopsis (please, correct me if I'm wrong), basically depends of the way we cross our eyes when we attempt to see objects at different distances.
The more "our eyes are crossed", the greater the difference between the images we receive in each eye, which it's more effective to look at closer objects. In order for an object to be in focus, it needs to be at the point where the vision of the eyes intersect (including "at infinity" for very far away objects).
Now, with this mindset, how would such a gadget as Oculus VR work?
It consists of two separate screens (one for each eye) attached directly on an helmet-like device strapped to the user's head. It is capable of convincing 3D representations and has similar features which make it of close interest for gaming and similar applications.
So, my question is: in order to deliver such an illusion of depth, do the users' eyes need to be focused at the screen's distance, or at the represented objects' distance?
Sorry for the long question :P
Thanks in advance!

my anwer is that 3D is usaly in movie theaters with spestil glasses that are black lenes

There are a number of aspects to the perception of a 3D world. While looking into how cinema and TV 3D systems work recently, I found the following Wikipedia articles useful on how the illusion of a 3D world is generated:

Stereoscopy
Depth perception

The articles on 3D Television, 3D film and Head-mounted displays have some coverage of the issues with 3D display systems, since they do not work the same for all individuals.
Generally 3D display systems ignore convergence and accommodation as a mechanism for generating depth and instead depend on parallax and the brain being able to assemble an approximation of the 3D scene without the information from those cues.
In head-mounted display systems such as the Oculus Rift the image focus is usually at infinity.


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Would using positive numbered glasses while using a computer help prevent myopia?
There are multiple web pages linking screen-time and myopia. While this is not necessarily proven, for example as shown on the NIH page here https://pubmed.ncbi.nlm.nih.gov/31943280/ , it seems logical that exerting our eyes to look closer than "infinity" for long hours might cause that (myopia).
So I was thinking, what if we use reading glasses, glasses with positive prescriptions, while using computers, effectively changing the screen distance to be our "infinity" distance. Would that help alleviate the strain on our eyes and therefore myopia, or its worsening?


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Is it possible to focus only one axis of astigmatism?
When we look at something close, we focus our eyes as a circle. But what if someone has astigmatism and focuses on something close, is it possible for the eyes to "focus" only the axis that needs focusing, thereby getting clear vision without astigmatism? (Provided, of course, that the object is at such a distance that it's possible for the eye muscles to "focus" on it so that that that axis would be focused but the other not.)

What do you mean by "possible"? If it were something humans are generally capable of I don't think there'd be glasses for astigmatism.

@BryanKrause Glasses are for general use. Even if a person can play around looking at something for some time until they succeed, that doesn't mean they can walk around doing it at will throughout the day. I'm asking if it's theoretically possible by spending some time looking at something. Not if people can do away with glasses for astigmatism.


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What is the extent of the CSF system out of the brain?
Does it spread sideways from the spinal cord at all?
How far down does it go?
I've found a lot of information about the spinal cord itself but not about the central canal, and more specifically if it's all there is to CSF out of the brain, or if there are small canals exiting it.


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Where do the 31 spinal nerves start/meet?
Which part of the brain is the first place (from top to bottom) where all 31 pairs of spinal nerves (on each side) meet? Or if they all start at one place - where is that?
Nominally, the beginning of the spinal cord is the medulla oblongata, but perhaps the spinal nerves or some sort of "root" of every nerve start at the Thalamus?

They don’t meet.
Some framework:

Spinal nerves contain motor, sensory, and autonomic fibers. Each of these have different pathways.
Spinal nerves don’t go to the brain. Rather, they synapse in the spinal cord with other neurons which in turn go to the brain (sometimes requiring one more synapse).
In the case of motor neurons, we talk about upper and lower motor neurons. In the sensory system, we talk about first order and second order neurons. Explanation below.

Regarding sensory (afferent) neurons:

Touch and limb position sense are mediated by the dorsal column-medial lemniscus system. The first order (primary sensory) neurons from the spinal nerves, synapse on a second order neuron in the dorsal column in the medulla. There it decussates (i.e. courses to the contralateral side) and ascends via the medial lemniscus to the thalamus. There it synapses with a third neuron that courses via the internal capsule to the primary somatic sensory cortex.
Pain, itch, and temperature sense are mediated by the anterolateral system. These first order (primary sensory) neurons synapse at the spinal level they enter. The second order neuron decussates at that level and courses rostrally via the anterolateral column, ending up in the thalamus. There it synapses with a third neuron that courses via the internal capsule to the primary somatic sensory cortex.

Conclusion: It takes three neurons (inclusive) to get from the spinal nerve to the primary sensory cortex in the postcentral gyrus of the parietal lobe.
Regarding motor (efferent) neurons:

Limb muscles are innervated by circuits beginning in the primary motor cortex. These upper motor neurons descend to the medulla, decussate here, and continue caudally via the lateral corticospinal tract. At the level of the spinal nerve, they synapse with neurons in the lateral ventral horn. These are the lower motor neurons that become the spinal nerve.
Axial/girdle muscles are innervated by circuits that also begin in the primary motor cortex. These upper motor neurons synapse in the midbrain, descend, and decussate at the appropriate spinal level. They synapse there with the lower motor neurons that exit the spinal cord and end up in the muscles.

Conclusion: It takes two neurons (inclusive) to get from the primary motor cortex in the pre-central gyrus of the frontal lobe to a spinal nerve.
In the cortex, these circuits also don’t all come together. They are actually quite diffusely organized across the sensory and motor cortices. Here is a representation of the sensory cortex.* It is a schematic of the post-central gyrus with pictures to indicate where the signals from various body parts end up. The motor cortex is similar. (Google homunculus if interested.)

In addition the pathways described for cognitive perception and control, there are others that help with sub-conscious control of movement (e.g. those involving the cerebellum and basal ganglia), sub-cortical perception of pain signals (e.g. amygdala), and even spinal reflex arcs that never reach the brain. Not all circuits that begin or end in the spinal nerves are destined for or originate from the cortex
This is already considerably over-simplified, and the autonomic system is more complex yet and is not confined to spinal nerves, so I won’t detail it. These signals originate in and feed back to an entirely different area of the brain (mostly hypothalamus). Similar to the motor and sensory systems, at least one synapse is required to connect the brain to the peripheral nerve.
Conclusion: they don’t meet.

Reference:

Martin, John. Neuroanatomy: Text and Atlas. McGraw-Hill Medical; 3 edition (March 27, 2003)

*The source of this image is: http://www.mindtrippingshow.com/mind-trip-of-the-week-17-how-do-we-feel-the-world

Thank you very much. This is exactly the type of answer I was looking for. And though technically they don't meet - what I meant was that (according to your answer) they meet at the somatic sensory cortex / primary motor cortex. Do I understand correctly that the muscles aren't affected by the Thalamus, and the limb muscles - not even by the midbrain? And that sensory perception is not affected by the midbrain?

If I understand correctly - Though the cerebellum doesn't act as a relay for these messages (both afferent and efferent) -  doesn't it communicate with the rest of the body through the spinal cord (again, both afferent and efferent)?

@user133943 I have edited the answer to address your second comment. Regarding the first, the nerves don't really meet, but the circuits (partially) head to the same area, so I'm glad I was able to provide some useful info. As for the thalamus, the midbrain....everything is affected by everything, and the sub-circuits are really too complex to describe here (or for me to remember - I'd be copying from my neuroanatomy text; I suggest you just buy a copy for yourself if interested!).

I am not sure whether I grasped the gist of your question appropriately, but let me provide some clarifications.
$\text{Nerve}$ is simply a collection of axons. Therefore, all the spinal nerves are just bundles of assorted nerve axons.
Now, the origin of nerve is slightly ambiguous as far as its meaning is considered. It can mean the physical origin, the place where the particular branch of nerve starts off from a main trunk or some other nervous organ. It can also mean the location of the cell bodies the axons of which comprise the nerve, the functional origin.
Now coming back to the question, the physical origin of the spinal nerves is not common. Each pair of spinal nerves originates from a specific segment of the spinal cord via two roots, the dorsal and the ventral. Therefore, each nerve originates separately and different spinal nerves cannot be traced back to a common physical origin. (The cauda equina, is actually a collection of several spinal nerves which move dorsally and periodically gives of the nerves out of the vertebral column. Although the nerves comprising the Cauda Equina, second lumbar nerve onwards, appear to have a common origin, they actually originate from their own specific segment and then move caudally as a bundle to overcome the developmental constraint of spinal cord being shorter than the vertebral column, necessitating the caudal movement of nerves within the column to emerge at appropriate points)
The functional origin is a bit more complicated. This is because each spinal nerve has a variety of nerve fibres. There are some sensory fibres with cell bodies in the dorsal root ganglion, there are motor fibres with their cell bodies in spinal cord, there are sympathetic fibres with cell bodies in the series of collateral or the sympathetic ganglia, connected to the spinal nerve via gray and white ramus communicans. There can also be cell bodies located directly in medulla which passes nerve fibres in cranial nerves as well as through its branches into the sympathetic ganglia and ultimately into the spinal nerves. Sacral nerves also contain parasympathetic nerve fibres functionally originating in the CNS. Thus, considering the functional origin, though each spinal nerve has a lot of origins, there is a slight convergence of origins for different nerves. The sympathetic ganglia and the spinal cord are two places where the origins of different spinal nerves may coincide or be structurally and functionally integrated.  But it must be kept in mind that this is a very limited convergence. There is an appreciable uniqueness to the functional origin of each spinal nerve and hence we cannot say that they "meet".
IMAGE

Thank you for your answer. However, it seems that you understood the question differently than how I meant it. For example, you wrote: "Each pair of spinal nerves originates from a specific segment of the spinal cord via two roots" (yes, I have read your whole answer. This is just an example). I'm asking "Which part of the brain...". and "Nominally, the beginning of the spinal cord is the medulla oblongata..." - I want to know which part of the brain "decides" to send a "message" through the spinal cord. (or receives, of course...). But thanks again.


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Ion Channel gating
I have been studying ion channels and there is one thing i am confused about, gating between open and closed states in channels.
Am i right in thinking gating is so fast that it is effectively always open for ion flow? So that if ten ions flow through a channel, then one can imagine that the channel opens and closes so quickly it is basically always open for the flow of the ten ions, or does a channel open allow one ion through, close and then open again for the next ion?

There are several types of channels, but probably the type you are referring to is voltage gated ion channels.
The state in which these channels are, open or closed, depends on the action potential across the cell membrane.
If the potential is at the correct energy for the channel to be open it will remain open allowing a steady flow of ions through. Once enough ions have passed so that the potential across the membrane changes to meet the deactivation energy, the channel will close. It then enters a refractory period which requires repolarisation across the cell membrane so that the ion is reset ready to open and let ions through again.
Different ion channels have different activation potentials, deactivation potentials and different refractory periods. This results in different rates of opening and closing.
So based on the above, in answer to your question, no gating is not so fast that it is always open. There are significant periods of time where channels are closed allowing no flow of ions and significant periods of time where they are open allowing continuous flow of ions.


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Is it possible for neurons themselves to manifest cancerous behavior?
From what I understand, one form of cancer is a faulty gene responsible for the programmed death of a cell.
Not long ago, popular wisdom used to say neurons don't regenerate. However that is no longer believed to be true, if I am to believe what the internet says. For me, this begs the question: can neurogenesis result in faulty death genes which in turn result in overgrowth of the number of neurons? Would those neurons be functional? And if so, if theoretically such a brain could be artificially sustained without a body, would its growth be beneficial (in terms of intelligence)?

Yes, but rarely.
Other types of brain cells are much more likely to form tumors. Oligodendrocytes, astrocytes, and more generally glial cells all form tumors with some regularity.
Nerve sheaths can also form benign growths.
Nerves themselves can even manifest cancerous behavior, even though they are nearly always benign and very slow growing. Unfortunately, they tend to cause seizures, increased intercranial pressure, and decreased neurological function in affected areas.


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Hiding identical sequences in NCBI web interface
Sometimes there are identical sequences in Genbank/Genpept, most often coming from the same species but different strains. Ie if I look up "bacteria chitin synthase", the 624-aa protein from Dickeya dadantii shows up three times. There even is an "identical proteins" link.
Is there any filter that I can use to get only one sequence from every group of identical ones? I mean, other than parse downloaded file on my own computer.

Use the NR database and restrict to the species of interest

@WYSIWYG you mean the "partially" non-redundant database? :P

What's your end objective? It is trivial to download the sequences and only keep one but would that be OK for you or do you need this to happen on the web site itself? Using RefSeq will bring the duplicates down to 2 for your example but since multiple sequences exist for different strains, it will be hard to avoid them altogether from the NCBI databases. What is your end objective here? There may be better ways.

@terdon.. LOL.. yeah partially non redundant..

I'm not sure if there's a way on GenBank, but UniProt offers UniRef where you can cluster redundant sequences or specify a lower cutoff (like 90% identity).

I don't need clusters, I need non-redundant set of sequences, preferably with a proper access (ie reading entire nr to find what I need is too much). But thanks for answer anyway.

well, just take one sequence from each cluster! if you download the UniRef databases, you actually get the non-redundant set.

I've written a little script to remove identical sequences from fasta to get what I need. To print the list of removed sequences, uncomment line 22
#! /usr/bin/python3
# Removes identical sequences from fasta file

import sys
from Bio import SeqIO
sequences={}
#This is where sequences will be stored
#likely calling str(seq.seq) on every test will be slower
with open(sys.argv[1], 'r') as fasta:
    parser=SeqIO.parse(fasta,'fasta')
    for seq in parser:
        sequences[seq.id]=str(seq.seq)
l=list(sequences.keys())
for j in range(0,len(l)-1,1):
    try:
        s=sequences[l[j]]
        for k in range(j+1,len(l)-1,1):
            if sequences[l[k]]==sequences[l[j]]:
                del sequences[l[k]]
    except KeyError:
        pass
        #print(l[j],file=sys.stderr)
for j in sequences.keys():
    print('>',j,'\n',sequences[j])

This is for offline execution for which many other tools can also be used- EMBOSS or even awk. Wasn't your question about the online search.


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FRET only works for interactions between 1nm to 20nm.
FRET only works for interactions between 1nm to 20nm.
How can you be sure that the interaction that you want to study isn't less than 1 nm/greater than 20nm apart?

The answer is to perform a FRET experiment.
FRET is most commonly used to find out whether something is nearby something else in this range.  Its chosen as a technique when two points of attachment for FRET probes might be within 20 nm, but are not known to be, or might be only in certain conditions.
There are some rules of thumb though. 1 nm, or 10 Angstroms, is about the length of 6 chemical bonds.  To be that close the two FRET probes (which are fluorescent molecules) would typically be attached to the same molecule.   3-4 amino acids apart in a peptide, at the opposite ends of a steroid.  These are schemes for a FRET experiment you would typically avoid out of hand.
FRET is often used for proteins, which are often wider than 20 nm.  For instance FRET probes might be attached to specific positions in two proteins which are known to bind to one another.  A FRET signal would indicate whether the two attachment points of the FRET probes are physically in proximity, allowing one to narrow down the orientation of the two proteins which are binding.
So its more or less an educated guess as to whether to do a FRET experiment, but using simple spatial reasoning you make a safe bet.

good point.  FRET is pretty hard to do.. its not my favorite sort of evidence.  its used in so many contexts - we're not necessarily talking about proteins here for instance - that its hard to go too deep...

To get an elaborate answer on this one, I guess you should ask at physics. Very basically, FRET works by that an excited chromophore transfers energy to a nearby chromophore, through dipole-dipole coupling, which in turn emits energy (light) which can be detected. This is a quantum mechanic effect, i.e. these are very small energies. The emission energy between from the donor to the acceptor chromophore is inversely proportional to the distance between to the power of six according to the equation:

Where r is the distance and R0 the Förster distance between the donor/acceptor-pair (distance which the energy transfer efficiency is 50 %).This means that the energy to be detected very rapidly decreases. The Förster distance is in the range 2-10 nm for different chromophore pairs, which leads to the upper limit of FRET use.
The lower limit I don't know if it's due to steric effects or some quantum mechanical effect I do not know about. But since proteins are in the size range of the lower limit they must be in really close vicinity in order for their interaction to be detected using FRET.


text:
What causes humans to be physically weak compared to animals like gorillas?
Animals like gorillas seem to have a physical fitness and muscle mass that don't depend as strongly on how much exercise they get, compared to humans. E.g. gorillas living in the wild sleep and rest a lot. While they do get quite a bit of exercise (a lot more than the average human), they are not going to exert themselves much more than is necessary. So, they push themselves a lot less than people who exercise very hard. Yet the average gorilla would easily outperform even a well trained human being in bodyweight exercises.
So, there seems to be something fundamentally different about maintaining physical fitness in humans compared to gorillas.

Humans would outperform gorillas on endurance. We evolved with different needs.

@Remi.b: But wolves and most dogs (especially sled dogs) far outdo humans in endurance, at least in colder climates.

And whales far outdo humans in apnea.

Yes, as someone who is into running (an hour per day), I do appreciate that we are have quite good aerobic fitness in the sense that it is relatively easy to acquire and maintain extremely high levels of aerobic fitness. But my experience with strength training is that it is extremely hard to make progress. Perhaps the point @DavidBlomstrom makes about animals walking on all fours is also important for core muscles. A very strong core is needed to do exercises like this that I've tried but failed to do for quite a while now :( .

Finding references for this is difficult (I've tried before), but there are probably three major reasons: (1) Lever attachment of muscles to bones optimizing for strength vs. fine control; (2) Relative muscle mass - Chimps have proportionately more upper body than humans, and human leg strength is probably as good as chimps; (3) Genetic changes - humans lost a muscle-related gene that makes their muscles weaker, although this may be only a factor in masticatory muscles.

Evolutionary tools that are not needed for increased survival rate of offspring of a certain lineage deteriorate with time. The deterioration might have a form of gene expression changes or mutation accumulation. For example, gene MYH16 encodes a protein that facilitates strong jaw muscles in primates, but humans carry a mutated gene that had lost its function (Stedman et al. 2004. Nature). We cannot bite hard, but we can articulate.
With respect to muscle strength, the common ancestor of apes and humans was likely stronger than we are now. Their descendants that formed a lineage diverging towards humans increased their survival by being smarter rather than stronger than their contemporaries.


text:
Why do we have nerves in our teeth?
Toothache is a useful signal to us as we can visit the dentist who can try to fix any problems with our teeth. But what is the natural biological role of toothache? Does toothache make animals take action that helps them to deal with their dental problem?

Why do you think this is different from pain anywhere else? (that is, could your question be simply "why is pain useful?")

@BryanKrause teeth really due have a unique problem with pain, because for the most part they do not heal.

Because your teeth evolved as a sensory organ.
The material teeth are made of evolved first in placoderms, it existed to sense the electrical current in the water around it, so it has to form around a nerve. in modern animals the nerve mostly functions in sensing stress and thermal stress on the tooth.
And because mammals are weird.
Teeth did not evolve to be permanent, they evolved to be lost and replaced, that is what everything that is not a mammal does. So having a nerve was not a big disadvantage (in say, reptiles) since that nerve would eventually wither and die as the tooth was lost. toothaches were not permanent they were a temporary irritation, and served do dissuade any behavior that caused them, like trying to eat food that was too hard, it was little different than the pain of thorn telling you not to grab sharp things.
Mammals are unique in retaining their teeth throughout their life so now a system shaped by evolution to be temporarily has been dragooned into something permanent. So now what would be a temporary irritation becomes a permanent thing when the tooth is damaged in mammals. Worse permanent teeth means things like stress on the teeth is even more important since you are stuck with damaged teeth so mammals actually make the nerves bigger. The addition risk of a toothache is not an issue because mammals are stuck with that risk anyway because they retain the tooth. The earliest mammals did not have long lifespan so the risk of a debilitating toothache was minimal, however we their descendants live for decades, so a structure evolved to last a year or two now has to survive for decades and it just fails sometimes. Evolution can only change what it has it cannot throw out a problematic system and start over from scratch, so it often gets stuck with such haphard thrown together solutions (kluges) And we unfortunately have to pay the price in this case

Abscesses happen easily in teeth and they are close to the sinuses and the brain. It's important for animals to be wary of permanent tooth damage and abscesses that can lead to death.
Good teeth are crucial for survival and reproduction, to avoid starvation. Nerves prevent animals from being careless with their teeth.
Teeth get chipped from cracking nuts, seashells, marrow, hunting, fighting, kocking a slack jaw, gritty food.
The nerves are pretty well tuned to guide the mammal for safe and proper use of his teeth.

I would guess that humans and "smarter" animals (animals with strong cognition, culture learning etc.) figured out that some kind of oral hygiene and diet helps against toothache. However, it turns out that apparently animals don't get tooth decay and don't need special oral hygiene.
In any case, nerves in teeth cause pain when a tooth breaks. This allows animals to develop an avoidance response in the future: "This kind of nut/bone/bark/root/seed/whatever may seem tasty, but chewing it last time hurt for a long time. Avoid it." It might even prevent any broken teeth in the first place if chewing starts to hurt. As @BryanKrause wrote in the comments, it serves the same purpose as pain anywhere else.


text:
Is sweat salty because we eat too much salt?
The Yanomamo Indians eat about 100 times less salt than we do. It has been argued that their salt intake is the natural salt intake for all humans. Obviously, if the salt intake is this low, then there is no room for there to be much salt in the sweat. However, most guidelines will say that if you sweat a lot, you should replenish the salt lost via sweating. But if the natural salt intake is much lower, then we're only losing excess salt via sweat.
So, is our sweat salty only because we eat way too much salt, or are we really losing essential salt via our sweat that we must replenish?

I feel like the sentence "Obviously, if the salt intake is this low, then there is no room for there to be much salt in the sweat." isn't necessarily true. Is there data on Yanomamo sweat saltiness?

@kmm Yanomamo sweat saltiness cannot possibly be high, given their extremely low salt intake and the fact that in the tropic rainforest where they do very strenuous work, they are bound to sweat a lot.

I think the question is Yanomamo sweat saltiness relative to western diet sweat saltiness. Your certainty that Yanomamo differ from western diet needs some justification, I think.

The article you reference is only referring to supplemental use of salt; many foods are naturally salty, and I don't see any evidence there that Yanomamo are actually low on salt, merely that they have adapted to a lower sodium diet. The authors are simply making a case that the contemporary diet is very high in salt.
When animals move water around their bodies, such as by excreting water to sweat, they do it by creating an osmotic gradient by pumping some ions: this is why sweat is salty.

Consolazio, C. F., Matoush, L. O., Nelson, R. A., Harding, R. S., & Canham, J. E. (1963). Excretion of sodium, potassium, magnesium and iron in human sweat and the relation of each to balance and requirements. The Journal of nutrition, 79(4), 407-415.
Schwartz, I. L., & Thaysen, J. H. (1956). Excretion of sodium and potassium in human sweat. The Journal of clinical investigation, 35(1), 114-120.

Human sweat is hypotonic and body fluid sodium content and osmolarity are regulated by the kidney, not the skin. I think these are two key misunderstandings in the OP (and the marketing of sports drinks ).


text:
How do I prepare a solution? (Calculation)
I have to make 100mL of 400mM NaOH. How do I go about calculating what I need to prepare this?

This is relatively easy. First: Look up the molecular weight of sodium hydroxide: Wikipedia gives a molar weight of 39.997 grams/mole (lets round this to 40 g/mole thats easier to calculate and the error in this is marginal).
So when you dissolve 40 g of it in 1 l of water, you have a 1000 mM (or 1 M) solution. Since you only want to have a 400 mM solution, you need to multiply the final concentration with the molar weight to get the amount of NaOH for one litre:
40 g/mole * 0.4 mole/l = 16 g of NaOH per litre. Since you only need 100 ml, you only need 1/10th of the NaOH (1.6 g).
So to prepare 100 ml of a 400 mM NaOH solution you dissolve 1.6 g of NaOH in 80ml of water and fill up to 100ml in a appropriate messuring cylinder.

Thank you. I have struggled with these types of problems since we were first introduced to them. For future reference, I would do a similar technique if say I needed a different amount of solute?

This is usually the easiest way. Calculate the amount for 1l (since this is usually the basis) and the take the fraction for the actually needed amount. With the calculation above you could easily calculate this for 250ml or also 600ml.


text:
What is the most critical step of plasmid purification?
During the process of plasmid purification and quantification, which step is the most critical to the success of the process?

What scale are we talking about? Because Giga preps are different from mini preps.

It's for a mini prep.

Dear friend, there are many ways to extract plasmid. Which ones are you talking about?

There are a few critical steps (which sounds horrible if written together, but the method per se is robust and usually without problems):

Resuspension of the pellet: Make sure it is really resuspended and not floating around as a big blob. If it is not resuspended properly your yields will go down dramatically.
NaOH/SDS-Lysis: Don't lyse for too long as you may end up with low quality DNA. This denatures the plasmid and makes it often useless for subsequent enzymatic reactions.
Mixing: Don't mix too harsh once you lyse the cells, otherwise you may break up genomic DNA of the bacteria which subsequently stays in solution and is not precipitated during neutralization.
Neutralization: Make sure you mix good here (by inverting the tubes 4-6 times) but not too harsh. It is critical to neutralize the whole lysate, otherwise proteins may stay in solution.
Drying: Overdrying of pellets can cause problems when you try to dissolve them again.

Just to add some details, don't lyse for more than 5 minutes, have the neutralization buffer ready to go so after you get your last sample lysed and mixed immediately add neutralization buffer to the first samples. When mixing, it's only ok to vortex the cell pellet prior to lysis, after adding lysis buffer, ONLY MIX BY INVERTING THE TUBE. Vortexing after this point can shear DNA. If you overdry the pellets, you can resuspend them by leaving them in the TE buffer for several minutes at 37C. And don't do too many samples to handle them all, with practice you can do 24 samples without trouble.

Thanks for this additions. More than 24 is usually not possible, since this is the limit for most benchtop centrifuges. Some even take up only 18 tubes.

So, in summary, all of the steps are critical.

@AlanBoyd You can loose yield in all of them. I wouldn't say one is much more complicated than others.

@Chris I agree, I was trying to stress to the OP that the whole process should be carried out carefully, which is what you said.  Remembering to add antibiotic to the cultures is also critical!


text:
If hermaphrodite C. elegans can reproduce with females?
C. elegans can self fertilize, or they can mate with males. But are they able to mate with females? Or is there some kind of morphological barrier that prevents that?

By "females" you probably mean hermaphrodites: C. elegans have no females.

There are female mutants, actually.

Since only the male tail is equipped with various specialized sensory and copulatory structures that enable him to locate the vulva and successfully inseminate the hermaphrodite.  Hermaphrodites can self-fertilize, but only males can cross-fertilize a hermaphrodite.
sources: Wormbook: Male development
C. elegans II (2nd edition): Sexual Dimorphism

The C elegans hermaphrodite is basically a female, except that she makes some sperm of her own. (Judith Kimble likes to say that a hermaphrodite is a female who's learned to be independent.) C elegans is derived from male/female species by a small change in sex determination in the female germ line. As you'd expect for a female, she can mate with males, but not other females.


text:
How exactly can dsRNA be introduced to a cell?
Is it just by viruses or are there other means by which it gets into cells, such as plasmid uptake?

Artificially or naturally?

Besides viral infections there are different pathways for cells to take up dsRNA. Inside the cells these dsRNA are processed by Dicer which processes these RNAs into small interfering RNA, which play an important role in the regulation of gene activity.
These pathways have mostly been researched in Drosophila and C. elegans, I am indicating where evidence for them in humans is available. The different possibilities for the uptake are:

Uptake via transmembrane proteins: In C. elegans two different transmembrane proteins have been discovered which passively transport
dsRNA into the cells. They are called SID-1 and SID-2 (systemic RNA-interference defective protein), at least for
SID-1 a homologue exists in humans as well. These receptors are important for the uptake of systemic (produced by the own organism) dsRNA. See references 1-3 for
details.
Uptake via Endocytosis: In drosophila cells active transport happens through the scavenger receptors SR-CI and Eater. They bind
the dsRNA and are then internalized. Knockdown of these genes
inhibited the import of dsRNA and inhibited the endocytosis mediated
knockdown of genes. This process seems to be evolutionary conserved,
as knockdown of the orthologous genes in C. elegans led to similar
results. This mechanism seems to be more important for the uptake of environmental dsRNA. See references 4 and 5 for more details.
Uptake via Phagocytosis: At least for drosophila, there is evidence for a phagocytosis mediated uptake mechanism, which is
independent of endocytosis. See reference 6 for details.

References

SID-1 is a dsRNA-selective dsRNA-gated channel.
Uptake of extracellular double-stranded RNA by SID-2
RNA interference: a mammalian SID-1 homologue enhances siRNA uptake
and gene silencing efficacy in human cells.
The endocytic pathway mediates cell entry of dsRNA to induce RNAi
silencing.
Double-stranded RNA Is Internalized by Scavenger Receptor-mediated
Endocytosis in Drosophila S2 Cells
A phagocytic route for uptake of double-stranded RNA in RNAi

SID-1 looks interesting. Do you think there's a size limit or would it take up long dsRNA molecules?

@user137 This paper suggests that very different length (they tested from siRNA length to 500bp) are taken up. The longer the dsRNA gets, the more effective (meaning smaller concentrations of the dsRNA outside the cells lead to a downregulation) the process seems to be.


text:
The suspended cat clavicle
I know the clavicle of the cat floats freely as opposed to be attached as in humans. This is supposed to allow them to be able to squeeze through spaces, according to a quick google search. But how does that allow them to move through tight spaces in comparison with humans?

Based on what I learned from my comp vert anatomy class, the clavicle does not articulate with other skeletal elements, thus allowing the scapulae to retract further along with the forelimbs

Can you add a reference to your answer?


text:
What is the importance of hydrogen bonds in water? and other questions:
These are extremely simple questions — basic biology — but I would like to make sure that the way I have answered is at the very least correct.

Hydrogen bonds are very weak, so how is it possible that they are so important in the properties of water? Hydrogen bonds in water provide many characteristic benefits to water: cohesion (holding water molecules together), high specific heat (absorbing heat when breaking, releasing heat when forming; minimizing temperature change), high heat of vaporization (several hydrogen bonds must be broken in order to evaporate water), lower density of ice (molecules in ice are spaced farther apart), and solubility (polar molecules are attracted to ions and polar compounds, making them soluble in water).
Why do we feel cooler immediately after we go swimming than we do after we have fully dried off? We feel cooler immediately after we go swimming than we do after we have dried off because it takes a lot of heat to evaporate water; however, once we dry off we remove much of the water from our skin, and the water is evaporated much more quickly.
If water were non-polar, would our temperature heat up less quickly or more quickly if we went outside on a hot day? Why? More quickly. Because hydrogen bonds within water slow down the movement of molecules and allow for water to have a very high specific heat.

General chemistry questions are off-topic on Biology.SE, but instead should be asked at [chemistry.se].

You are saying what hydrogen bonds are doing, not why are they able of such achievements, despite being so weak. Their strength is in numbers. At room temperature, fully one fifth of the water molecules are engaged in four bonds with other water molecules, while the remainder forms two such bonds. (More detail at http://www1.lsbu.ac.uk/water/hbond.html ). In contrast, hydrogen sulfide forms essentially no hydrogen bonds with other hydrogen sulfide molecules, despite significant similarity between oxygen and sulfide. The difference in size between oxygen and sulfur makes the former much more electronegative. I could go on with other hydrogen compounds, but the fact that answers your first question is: each water molecule is involved in a series of bonds with other water molecules, on an unequaled scale.

Also, hydrogen bonds are stronger, pickier about distance and angle than the alternatives available to other molecules (dipole-dipole, van der Waals etc.) So even if they seem feeble, and even if the alternatives were as plentiful as hydrogen bonds, the latter would still be more capable of tying up molecules.

The effect of water drying (which comes after swimming, but also after sweating, bathing, or cleaning oneself with a hot oshibori) is caused by water evaporation. Each state transition, including that from liquid water to air-borne vapors, is a heat-consuming phenomenon. When skin dries, the heat to turn water into vapors has to come from somewhere. In perspiration's case, it is one's body.

Note that cooling down while water evaporates is not only something we feel, but a physical reality, occurring even in innate systems. For example, Amazon forests and Sahara are similarly close to the Equator, but the former is cooler than the latter, in part because heat it receives is in part used up to evaporate water.
Your answer was good.

Again, you are right. Were water non-polar, it would have lower latent heat, or, in lay terms, it would evaporate without much heat consumption. Were sweat made of a non-polar liquid, it will fail to consume heat when evaporating, leaving one to warm up sooner / faster.