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Why do we urinate more when we are nervous?
This question is a result of my personal experience... But I guess that is common for many of us.
My school timing is 8:00 am to 1:30 pm (usually). During normal school days I typically urinate one time - at most. Last month when we were having our practical exams. There was a fair amount pressure to score high marks and on top of that we did not have any experience with such exams.
On the day of the exam; I was a little nervous about it. The duration of the exam was 3 hours (from 9:00 am to noon) on this day I urinated 4 times.
Several of my friends also experienced the same thing.
I was nervous also because for two days before the exam I was afraid that I hadn't even touched any book. I was thinking that there was no way I could cover the whole book and so I didn't even touch them.
Now that I have final exams in about two weeks, I was revising my syllabus but for the last 4 days I'm not touching the books. Whenever I start solving problems from any chapter then I have to look back for the formulas. Questions in which reasoning is asked, I love to do that. I'm not very good at memorizing things and so when I compare myself to my classmates then I feel like I don't know anything and so I give up. I have never tried to memorize anything, but I understand the reasoning and the concepts.
Kindly give me the answer of the question.

Check this out http://www.ncbi.nlm.nih.gov/m/pubmed/11116129/

It's all about chemical reactions in your body triggered by your brain.
Lot's of researches and documents confirmed this is what happens when you face a stressful situation.
Stress -> hypothalamus -> sympathetic nerves -> Epinephrine (Adrenaline) -> more urine flow
Domino neural connectivity (Thinking) => Domino Chemistry (Body reaction = stress and anxiety)
Situations like thinking about exam and how hard it would be or how it could change opportunities and feelings in your life you are triggering a chain of neural and chemical responses.
If your thoughts (Activated neurons) end with unsolved vital problem, it activates parts of your brain that is related to anxiety and stress and these neurons activate hypothalamus.
Hypothalamus turns sympathetic nerves on.
The sympathetic nerves release adrenaline (epinephrine).
And adrenaline cause more urine flow.
This example shows two more kinds of polyuria
If you are interested in how increasing level of adrenaline results in more urine flow read this and this and this.

Your last two links both state that an increase in adrenaline causes renal flow rate to decrease. So how does an increasing level of adrenaline result in more urine flow?

Copy and paste exact part to approve your claim. You are wrong about decreasing of the urine flow by the higher blood pressure. It's almost 50 years that scientists confirmed adrenaline has direct effect on urine flow as I explained from sources. For more info read these two like below.
http://ajplegacy.physiology.org/content/192/1/131
AND
http://forums.studentdoctor.net/threads/blood-pressure-and-urine-production.920866/
The higher your blood pressure gets, the more urine flow

I can see easily that increased blood pressure increases renal flow. But is there not a second effect that decreases renal flow? Your newest link in your answer mentions "by acting directly on the kidney to decrease the output” and your first link mentions "Postganglionic neurotransmitter of the sympathetic nervous system norepinephrine causes particularly in the afferent arteriole vasoconstriction, thereby reducing the renal blood flow (and thus the GFR).” Also, my textbook (Campbell Biology) states that the sympathetic nervous system inhibits urination.

I found an interesting article that dealt with anxiety and micturition. There are no proven or accepted view on this. There are a few theories as to how this happens.
I am quoting it:

There are several beliefs for what causes frequent urination from anxiety, and the likelihood is that all of these factors play a role:
Muscle Tension – This is one of the most likely causes of frequent urination. When you have anxiety, your muscles get very tense. This tension puts pressure on your bladder, which in turn makes you feel like you need to urinate more than you would otherwise.
Evolutionary Adaptation – Another theory is that there is an evolutionary reason that frequent urination would be advantageous. Remember, anxiety is the misfiring of your healthy fight/flight system. In times of fear, urination may keep the body lighter by losing extra weight, making it easier to flee.
Light Overload – It's also possible that, because anxiety is a misfiring of the fight/flight system, your body may simply be lightly overloaded. The fear is not intense enough to cause immediate urination, but it may make it harder for you to feel like you can hold it back.
  Also, those with anxiety are more prone to focusing on different sensations unintentionally. There are often times when you may feel the need to urinate slightly but your body has no problem ignoring the feeling and holding it back. With anxiety, it's possible that your brain is focused on the sensation, potentially causing you to feel like you need to urinate more than you do.
Finally, anxiety can also change your body chemistry, altering your digestion and changing the way you process nutrients. That may cause more water to pass through your body.

Source:http://www.calmclinic.com/anxiety/signs/urination-problems


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What's Incomplete atrioventricular heart block (AV)?
This is unclear for me and I can not understand differences between complete and incomplete atrioventricular heart block.also I want an electrocardiograph of incomplete atrioventricular heart block.

Welcome to Biology S.E.! If you need additional assistance, please visit The Help Center. This question is not necessarily off-topic unless you are asking a personal health question. If this question is a health question; there are plenty of excellent health forums online that are staffed by trained doctors who will be happy to help you.

@Mad Scientist I didn't know about it at all, when i read about it.I edited my answer as it is acceptable.

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Why did the Brain develop in the front in most organisms?
I was wondering: why most, well, pretty much all organism with a brain have it right in front of their bodies or at the top.

I believe the general argument goes like this: it's expected that the sense organs appear toward the anterior end of the organism (you want to see, smell, hear what's in front of you). For the ease and efficiency of processing inputs, it makes sense that nerve bundles appear close the sense organs. These nerve bundles eventually became brains.

I agree with @p.s.w.g.

@p.s.w.g - while your explanation makes sense, it doesn't hold true, especially in insects (butterflies 'taste' with their feet, etc.). It does hold true for eyes, though. Optic lobes are a large part of insect brains. Interesting to contemplate.

@anongoodnurse - humans feel touch, heat and pain in their limbs. Fact stands that neuronal cell bodies congregate in the anterior parts in humans and insects alike. I think that's the PO's question - why is the brain (i.e., ganglions in insects) situated in the head region?

The wiki article on cephalization may help.

everyone is talking about eyes and ignoring the mouth :0

TL;DR Visual and auditory systems are crucial for survival, especially in higher animals. Also, visual/auditory systems have great number of cells. For processing to be effective, it should be performed closer to data acquisition (eyes).
First of all, for example, in mouse or human, central nervous system includes brain and spinal cord. Since spinal cord is extremely important at regulating different physiological processes as well as in performing complicated motor tasks, it would be unjust to not think about CNS as a whole.
If you talk only about brain part of CNS, it makes sense to locate important processing pathways near sensitive organs for two reasons. First, it saves material on running long axons from many sensory cells. Secondly, longer axons deliver information slower. If there is a sense that is important for survival, than information in that modality must be delivered and processes as quick as possible.
In comments to the question @anongoodnurse mentioned that "butterflies 'taste' with their feet". I would argue that a) taste in butterflies is not vital for immediate survival and b) number of taste buds is very limited, whereas retinal cells are count up to more than thousand per eye.
But what about humans? We also able to "taste with our feet", e.g. feel temperature. For survival it is crucial to be able to escape hot surface as fast as we can. And we do, thanks to a direct reflex arc going from sensory cells to spinal cord and motor neurons. Which brings back point about CNS as a whole system. Crucial information and immediate decisions are made closer to sensitive organs.

I was wondering: why most, well, pretty much all organism with a brain have it right in front of their bodies or at the top.

I believe you're confounding origins. Complex brains -- like those in us and other mammals -- are situated in the position that has been the best-protected over millions of years of evolution.
Evolution did not decide where the front of the animal should be and then put the brain there. Rather, evolutionary pressures resulted in the brain being an excellent survival tool, and the species that could protect it best kept its benefits. It just so happened that, since complex brains require an enormous amount of resources and are quite fragile, wherever the organism could best protect the brain became its "front".
In mammals that became a skull. In some insects it's in the thorax or abdomen. In sea slugs... well, there really isn't a complex brain in sea-slugs... so the difference between their front-end and back-end is pretty minimal. Same with worms and other very simple creatures.
So think of it like this:
Brain = Good for Survival, but Fragile --> Brain Needs Protection --> Wherever Protection is Best = Where the "head"/"front" has evolved

I thought about it too, but isn't such an argument mixes cause and effect? Fly shouldn't care where to have its brain, abdomen works as well for protection. I would expect to skull evolve around brain, rather than brain evolve around skull. Otherwise brain should be located throughout insides of thick bones, as protection is best there.

@aandreev -- They co-evolved. As brains became more complex and bigger, there needed to be a better place to store them. Thick bones aren't very spacious. Hollow bones aren't very protective. The compromise for organisms evolving a larger brain was the skull: A hollow, encapsulating bone that can also be very dense (especially among goats, bovines, etc.). It's also a design that means there's only one area to protect instead of every single thick bone in your body.

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Enzymatic error rate
I am aware that each enzyme generate a certain amount of misproducts.
This is well documented, for example, for the DNA polymerase.
I am interested in enzyme involved in biochemical processes, so for example methytransferase, oxidoreductase, carboxylase and so on.
I have been looking for any reference that could report the error rate or the amount of misproduct for any of these enzymes, but I was not successful.
Does anyone know a reference reporting the error rate, or any other information about the misproduct generate by these enzymes?
EDIT
I will try to clarify a bit better my question.
Let's assume that we are considering an enzyme that add a methyl group to a molecule, we can choose propionic acid for example.
In theory the correct product would derive from the addition of a methyl to the C3.
For the biochemistry study we know that the activation energy is decreased by an enzyme for example by orienting the molecules in the right way to react with the second molecule.
Therefore, if the enzyme in question will not be able to orient the molecule in the right way there is a certain probability that there will be a mis-product.
For example the methyl group could be added to the C2 and not the C3. Now. the probability for this process is quite low, but it cannot be excluded from happening.
My question is, if there is anything known about this type of error rates in the different type of enzymes.
I hope this make things a bit more clear
EDIT 2
Lets consider the imagine below that was taken from here

In B you can see the interaction of the active site of the enzyme with a substrate (for the example it does not matter if it is the real substrate or an inhibitor). I would say that among al possible interaction that this active site can make with substrates there are some much more likely than others. An hypothetical chart could be created considering the free energy of the complex enzyme-substrate, higher the free energy lower the stability.
Therefore among all possible enzyme-substrate combination we will have just few possibilities that have a low free energy. In the first place we will find the "correct" substrate, then we will find eventual competitors and other molecules that have similar chemical features as the substrate. Even though with low probability these interaction, enzyme-competitors, will happen.
This might led to the formation of "unwanted product" that I refereed to in my question as "misproduct".
I am interested in reading some paper that are considering thie phenomenon and also quantify its rate. I am also curious if this phenomenon can happen with different rates in different enzymes.

I think these enzymes are different. There is one chemical reaction that they catalyze and thus this will take place or not. This is different for the DNA polymerase where 4 different nucleotides can be incorporated (which raises the possibility for some errors).

There can certainly be enzymes other than polymerases that catalyze errant reactions. Aminoacyl tRNA synthetases immediately come to mind as an example. Some even have proofreading mechanisms to correct errors.

DNA pol only appear different because enzyme is influenced by template strand, in a sense. Chemical reaction catalyzed is still a chemical reaction

please let us know if you find answers sufficient. I think that question is important

If you ask references for all the enzyme then I am afraid that this question would be closed as broad. I am giving you one example and the basic idea behind the problem. You can search for the other cases.

I think you should clarify what you mean about error: a.) the enzyme uses a different substrate and the result is a different end product b.) the enzyme uses the same substrate and the result is a different end product. I think b.) is unlike, but I may not know everything about enzymes.

@WYSIWYG I ask for some reference that consider the issue I indicate as example. It would be really helpful to have a suggestion as hint

@efrem I don't know an example from from the back of my head. Have to look for it. In general what you are asking is unlikely because it is rare that a same molecule will have many similar groups where the reaction is supposed to occur.

First it is important to define what actually an error is. What you call misproduct is actually a right product for a different substrate. The enzyme has a low specificity; but you won't say hexokinase is error prone because it has wide substrate specificity. The question is — is specificity critical?
Coming to the example of DNA polymerase, you should note that DNA polymerase only adds a nucleotide to the DNA strand. Here the template DNA strand acts like a co-enzyme and it is the template DNA that provides specificity to the reaction. In this case the specificity is really critical and there are mechanisms that help in ensuring that.
Other enzymes also make errors and the probability of making errors depends on different parameters. Take the example of restriction enzymes that are supposed to cut at a specific site. When this specificity is lost we say that the enzyme is showing a "star activity" i.e. non-specific cleavage. This depends on different parameters such as buffer composition, enzyme concentration etc.
In general specificity is provided because of high affinity of binding towards one molecule compared to the other. These binding reactions are second order — a high affinity substrate will bind to the enzyme even at a low concentration, however if you increase the concentration of the low affinity substrate or the enzyme, then at some point the rate of binding may be significant enough to create a "wrong" product.
Sometimes there are cases where the enzyme can bind to a wrong substrate but cannot create a product. This is the typical case of a competitive inhibitor. It is also possible that a certain molecule is good at binding but the conversion rate is slower.
To conclude, these kinds of "errors" happen with many enzymes but it is very critical in case of DNA polymerization. You can get information on star activity of restriction enzymes (just google it).

Rubisco is an enzyme that is involved in the biochemical process of carbon fixation in photosynthesis, but also has an economically important error (photorespiration) which incorporates the wrong molecule (oxygen) into RuBP, therefore wasting the energy captured by the plant and producing toxic downstream products.
Rubisco's error rate in carbon fixation ranges from approximately 1:10 to 1:80.

Thank you very much for your answer. However, the paper you refer to neither contains the information about the error rate nor the table. Did I miss something or you took these data somewhere else?

@efrem Rubisco makes an error when it incorporates oxygen instead of carbon, and therefore the error rate is Vc/Vo.

Chris is right here, polymerases are generating sequences,  the enzymes your asking about do a single type of reaction, so you would be assessing its activity not its fidelity. A good resource I've found for looking at qc data for enzymes like these are just the product inserts from the manufacturer. NEB for example generally seems to provide sufficient qc data in my opinion. For example:
https://www.neb.com/~/media/Catalog/All-Products/B2D1E3A4F480489EAD7A1CD43E164DA0/Datacards%20or%20Manuals/M0233Datasheet-Lot0031209-1.pdf

DNA polymerase does single type of reaction too, namely, creates covalent bond between dNTP and DNA, releasing diphospate group $PP_i$

Since chemical reactions are governed by quantum physics, there is a whole lot of products that can come out of mixing together several multi-atom molecules. And all of those will have non-zero probability of occurrence. But this probability is extremely low at normal temperatures, so you don't see those products.
Enzymes lower activation energy and so increase chance of reaction, but only for certain substances and products (spatial position of reagents can influence outcome). In case of DNA replication, when wrong nucleotide is inserted, it happens because enzyme/template nucleotide complex has not enough specificity. All 4 nucleotides have rather high chance of participating in the reaction (but errors are still on order of $10^{-6}$ and lower).


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How does it make thermodynamic sense for photosynthesizers to turn CO₂ into O₂?
My understanding is that animal metabolism consists of exothermic reactions like
$$\ce{C6H12O6 + 6 O2  ->6 CO2 + 6 H2O + energy}$$
This makes thermodynamic sense to me. Animals need an exothermic reaction to produce the energy we need to move around, etc. However, the other half of the picture, plants and other photosynthesizers producing oxygen, has never made complete sense to me. Are plants consuming $\ce{CO2}$, a "low energy" (I think) substance, and producing higher energy $\ce{O2}$ as a waste product? Is there so much energy available for photosynthesis that plants can afford to waste some of it producing $\ce{O2}$ simply to have enough carbon atoms to store energy via sugars?

The purpose of photosynthesis is to convert a non storable source of energy into a usable and storable form of energy.  If looked at from this perspective, it makes thermodynamic sense to produce higher potential energy substances in photosynthesis.

I've posted a related question to get a few clarifications so I can understand the answers below.

@kuzzooroo What do you not understand in the answers? If you need clarification you should request for it using comments. Also, please accept the answers if they have provided the right answer to your posted question.

OK, thanks for the guidance, @WYSIWYG. I think maybe the clarification I should have asked for is, is it even reasonable to via photosynthesis (in its totality) as $$\ce{6 CO_2 + 6H_2O + light -> C_6 H_{12} O_6 (sugar) + 6 O_2}$$ and is it reasonable to consider the resulting oxygen as a waste product?

@kuzzooroo That reaction is not correct representation of photosynthesis. Oxygen is a byproduct but as mentioned in the answers the light reactions and production of oxygen is not directly coupled to sugar synthesis from $\ce{CO_2}$.

Oxygen in photosynthesis does not come from carbon dioxide. It comes from water and this is the step that actually requires light: Photolysis of water.
The proton produced in this process is used to synthesize ATP and NADPH by a chemiosmotic process similar to what happens in mitochondria.
These biochemical pathways are also referred to as Light reactions.
Carbon fixation (or Calvin-Benson Cycle) requires energy (in the from of NADPH) and is therefore dependent on light reactions. The light has no direct role in carbon fixation. Oxygen production also, is not directly coupled to carbon dioxide consumption.

This idea about photosynthesis is not correct.This reaction consists several reactions in between. O2 is produced by oxidation of H2O to get electrons which are used to revive PQ(plastoquinone) to transport electrons. Chlorophyll can easily get an electron from a Revitalizing(H2O) to transport the electron to cyt-bf and photosystem 1.

This reaction shows the conversion of H2O to O2:
$$\ce{2H2O ->O2 + 4H+ + 2e-}$$
As you see in this reaction. Producing O2 is useful and the plant can receive  4 H+ for ATP synthase to produce ATP and e- for producing hydrocarbons.
CO2 is fixed in this reaction of Calvin cycle:
$$\ce{6Ribulose-1,5 bisphosphate + 6CO2 + 6 H2O ->12 phosphoglycyrate}$$

@WYSIWYG I agree.so I changed it.

you can say that but the primary objective of calvin cycle is to fix CO₂. By saying that it is used in a certain reaction you are actually understating that fact.


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In insects, does the Alanine repeat occur on the homeodomain sequence of the abdomen or does it occur on a different sequence?
By "Alanine repeat", I am referring to the suppression of the formation of extra insect legs due to Ubx gene suppression through Distal-less repression.

Some background:

The new work involved misexpression of the Drosophila Ubx protein in the presumptive thorax of transgenic fruitfly embryos. Limb development was suppressed because of repression of Dll. By contrast, the misexpression of onychophoran and crustacean Ubx proteins did not interfere with Dll expression and the formation of thoracic limbs. These results raised the possibility that the Drosophila Ubx protein is functionally distinct from Ubx in onychophorans and crustaceans. One study suggests that Drosophila Ubx has acquired an alanine-rich peptide that mediates the repression of gene transcription; this peptide is lacking in onychophorans. The other study provides evidence that the crustacean Ubx contains an additional peptide that modulates the activity of the alanine-rich peptide, and possibly other repression domains, in crustacean Ubx.

Insect-restricted sequences include four regions N-terminal to the
  homeodomain (I1–I4), a peptide motif (QAQAQK), and an extended run of
  alanine residues C-terminal to the homeodomain
The onychophoran Ubx protein might function as an activator of appendage development. When the onychophorans and arthropods diverged,
  Ubx acquired an alanine-rich repression domain near its carboxy
  terminus. This domain mediates constitutive repression in insects.
  But in crustaceans the addition of the regulatory peptide causes it to
  function in a conditional fashion. As a result, Ubx does not suppress
  limb development in crustaceans. But it eliminates abdominal limbs in
  insects, greatly reducing the overall number of appendages compared
  with crustaceans.

You can read about it here:
Levine, Mike. "Evolutionary biology: how insects lose their limbs." Nature 415.6874 (2002): 848-849.
Galant, Ron, and Sean B. Carroll. "Evolution of a transcriptional repression domain in an insect Hox protein." Nature 415.6874 (2002): 910-913.


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Redheads and pain receptors
I remember reading this in a biology textbook, and decided to do a little digging. Redheads have a lower sensitivity to some pain and a higher sensitivity to other compared to people of other colored hair.
Sciencenordic.com and webmd.com note that redheads have a higher sensitivity of pain when it comes to dentistry, yet can tolerate more pain subcutaneously. According to the Journal of the American Dental Association, redheads require more anesthesia due to some mutation in the MC1R gene. What mutation could account for this difference, could this be a point mutation or nonsense mutation?
Source: http://www.webmd.com/pain-management/features/whats-your-pain-tolerance?page=2
http://sciencenordic.com/redheads-feel-different-kind-pain

I think it's best to break this question up in to two parts:

What mutations account for red hair and fair skin in humans
How might these same mutations affect pain sensation

MC1R variants & red hair
The MC1R gene encodes a transmembrane receptor protein (belonging to a very common family of receptors), called melanocortin 1 receptor. It also has another name describing its best known role in the body: 'alpha melanocyte stimulating hormone receptor'.
This receptor binds ligands - both agonists and an antagonist - outside the cell, and passes signals to the pigment-producing pathways in melanocytes; activation favours eumelanin (brown) production over pheomelanin (red).
Common MC1R variants are all single point mutations which cause an amino acid substitution and reduce/impair the normal function of the receptor - i.e. loss-of-function mutations. E.g. Arg151Cys, Arg160Trp, Asp294His, the most common variants in european red-heads probably arose ~80,000ya in a eurasian population, and have a reduced ability to activate adenylate cyclase inside the cell.
How & why could the same mutations affect pain sensation?
Genetic linkage, or dual role of MC1R?
Firstly, it is possible that MC1R variants are linked to a mutation at a separate nearby gene; the two making a haplotype.

In this diagram, mutation A might be a red-hair MC1R mutant, and mutation B might be some other pain-sensitivity mutant. Through random effects on small populations, group Hg B might have 'seeded' the european population, say; meaning that the two mutations are inherited together in that population. If the two loci are very near, their linkage is less likely to be disturbed by recombination.
This is an obvious possibility whenever two seemingly unrelated traits co-occur.
However, there's good reason to believe that this case is due to a dual-role of MC1R...
Arguments against linkage; for dual role of MC1R: The existence of many different haplotypes in redheads argues against linkage, if this pain sensitivity effect is found across all/many redhead haplotypes, and not in wildtype MC1R europeans.

Indeed, this study shows that europeans with 2 MC1R mutant variants (homozygote or compound-heterozygote) have increased pain tolerance to electric shocks compared to people with 1 or more functional copies of MC1R. The second panel shows that a mu-opiod analgesic (morphine) has greater effect on those with no functional MC1R. The effect coincides with presence of functional MC1R, not a particular haplogroup.
MC1R is also expressed in a region of the midbrain responsible for pain modulation. This region produces endogenous opioids to control pain. As far as I can gather, researchers are trying to work out what exactly it does there.
The study by Mogil et al suggests MC1R in the brain somehow counteracts pain inhibition by the opioid receptors, and so MC1R mutant redheads have more effective ex/endogenous opioid pain inhibition, which reduces noxious pain.
This study found that redheads are slightly less susceptible to pain-sensitisation by capsaicin.
Whereas this study found a contradictory result, that redheads are more sensitive to thermal pain and that lidocaine is less effective for them. (This study didn't genotype the subjects, and red-hair may be caused by mutations in other genes.)
Overall, the number of subjects in these studies (both humans and mice) is fairly small; and the science of MCR pain modulation seems early-days.
But at least we can answer your question: the mutations apparently responsible for red hair and altered pain sensitivity are amino acid substitutions in MC1R causing loss-of-function variants.
The fact that MC1R probably has totally different roles in the brain and in the skin is an interesting general point of biology.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1288200/ < about the evolution of MC1R mutant variants.
http://www.ncbi.nlm.nih.gov/pubmed/10403794/ < about the mechanism of loss-of-function
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1736101/pdf/v042p00583.pdf < evidence of increased pain tolerance & greater morphine effectiveness
http://www.scandinavianjournalpain.com/article/S1877-8860%2810%2900111-4/abstract < evidence of resistance to hyperalgesia
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1692342/ < evidence of decreased pain tolerance & lesser lidocaine effectiveness


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How much of what we eat ends up in the toilet?
An awkward question. Bear with me...
In terms of mass, what percentage of the food that we eat do we end up excreting? Of course, it depends on a whole host of factors so lets assume a healthy average build/height male with a balanced diet in his 30s who doesn't drink or smoke.
I ask this because I am quite intrigued by my own bowel movements (typically 2 or 3 days apart and average in size - I have no problem passing them btw they've just never been that regular). I know my bowels are not excercised like most other adult males but what's more intriguing is that when I do finally "go", it looks like and feels like I've hardly eaten over the past few days! Take this weekend for example, it's fair to say I've been overdulging and overeaten but by the end of this week I will probably "see" only 10% of that in the toilet.

It depends on what you eat. Not everything can be absorbed. Cellulose for example is not digestible by humans cause of missing enzymes and its a big part of every plant. Nevertheless your digestive system needs something to work on. Pure starch or glucose if its not too much would be totally absorbed.
If you eat a lot of white bread and meat but almost no vegetables this could be a reason.

Very little of what you excrete actually come from food.

By conservation of mass, almost all solids that you excrete come from food.

It very much depends on what specific kind of food you are taking.
Say, if we eat more green vegetables then we are supposed to excrete more compared to a highly meat-rich diet.
Also, it depends on the food-intervals, more the interval more the absorption by body so less amount going out(but giving extreme interval is not good either).
All depends on the need of body, if body needs more than what you are giving to your body it gonna obviously excrete more.
And always keep in mind to take sufficient water, because without it all things go malfunctioning in our body.

Can you provide a citation that a longer meal interval allows a greater amount of absorption?

link this may be of some use @MarchHo

Can you give an example based on an average american diet? Guesstimate


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Proteins: Post translational modification
I am a physicist and trying to understand some protein chemistry for a small project. Basically, amino acids combine to form proteins and after forming the primary structure, some chemical modification may occur, such as phosphorylation or glycosylation (post translational modification). In case of the enzyme carbonic anhydrase a zinc ion is added post-translationally as a cofactor. (The amino acid sequence can be seen here (scroll down to 'sequence' title).

Is the attachment of zinc regarded as a type of post-translational modification?
When carbonic anhydrase is denatured, is the zinc ion released in the medium?
Will the amino acid sequence (primary structure) be changed after denaturation? If yes, are amino acids removed after denaturation, if yes, which?
I guess Zinc will be removed after denaturation. Is the remaining structure the primary protein structure?

1) Is the attachment of zinc regarded as a type of post-translational
  modification?

It is not really considered a post-translational modification because the zinc atom is not covalently bound to the protein. Binding to zinc is adsorption.

2) When carbonic anhydrase is denatured, is the zinc ion released in
  the medium?

Yes, but it depends on the extent of denaturation too. Metal ions can be removed using chelating ligands like EDTA, without actually denaturing the protein.

3) Will the amino acid sequence (primary structure) be changed after
  denaturation? If yes, are amino acids removed after denaturation, if
  yes, which?

Denaturation does not include cleavage of covalent bonds. There won't be change in the amino acid sequence.

4) I guess Zinc will be removed after denaturation. Is the remaining
  structure the primary protein structure?

Yes; just the polypeptide.

So how the protein sequence will look like after denaturation (the sequence given in the link in my question)? How I know the letter corresponding to the Zinc (is it M?)?

@aneps It will look the same. M is methionine


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Could someone entirely absorb smells by smelling?
When smelling, your nose detects the smells by absorbing them.
Does this mean that, if you were in an enclosed space, you could smell so much all the smell goes, and there is none of that molecule left to smell?
Would it take so long it would never happen in reality, or does it happen?

It seems unlikely purely in terms of the amount of air which comes into contact with the nasal epithelium - the tissue which contains olfactory receptors.

Nose doesn't really absorb it. THe odorant molecules bind to olfactory recpetors that transduce that signal as action potentials. Even if some amount of odorant actually is irreversibly absorbed that would hardly affect its concentration in the air.

Besides, the odor rapidly diffuses across the entire available space - in your case this would be the room - so it is not possible to get rid of the odor until the source is removed and all the air recycled

On the contrary, your olfactory epithelium - the bit that does the smelling up at the top of your nasal cavity - doesn't absorb smells. The olfactory receptors bind small molecules reversibly.
However, the olfactory epithelium has a coating of mucus, and so small molecules dissolve in the mucus in order to meet the receptors. Molecules will also evaporate off this mucus, but some vanishingly small fraction of the odorant in a room may stay in the mucus of the nose and the upper respiratory tract long enough to be moved by cilia to the stomach.
I think that for water-soluble molecules, the surface area of mucus lining the airways that odorant can reach is a more relevant factor than the number of a particular receptor (which is very low); but depleting a room of an odorant (which is concentrated enough for you to sense in the first place) by breathing would surely take an extremely long time; as the concentration dropped the remaining molecules would become 'harder to catch', and you'd suffocate first in this enclosed space.
Interestingly, hydrophobic molecules that do not readily dissolve in mucus may be bound by soluble 'shuttle'-like proteins which bridge the gap to the receptors: http://www.ncbi.nlm.nih.gov/pubmed/12044155
These odorant-binding-proteins probably contribute to the diversity of molecules we can smell, and presumably also bind odorants reversibly and may release them back in to the nasal cavity.


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Protein Structure Parameters
I'm wondering about the minimal set of parameters necessary to define a protein's structure.  My understanding is that the backbone geometry is defined by the phi and psi angles (torsion angles), and then from this template the side-chain rotamers are defined.  Is this sufficient to yield a geometric structure, or are there other factors involved?
On a related note, how exactly are two protein structures compared? I often see references to percent similarity, but what does this really mean?  In the Protein Data Bank, atomic coordinates are given, but my intuition is that coordinates are only important relative to all the other amino acids in the chain.  In other words, absolute coordinate comparison would seem to be uninformative.

If you're going for bare minimum data length, you'd also have to consider commonly occuring structures - think Huffman coding. Alpha helices and beta pleated sheets, for example, are a lot of data that can probably be compressed quite readily. It also occurs to me that one could define very rough parameters which give many possible configurations, but only one stable one, amongst other shortcuts.

Ah, interesting point I hadn't considered (encoding).  I think I'm going more for geometric parameters.  Perhaps another way of saying it - are torsion angles and side chain rotamers sufficient to completely determine a protein's structure?

By "protein structure" do you mean the position of the atoms in a protein at a particular point in time?

@LuboAntonov Yes, exactly - specifically the folded state.

Your percent similarity is sequence identity.

It depends on how accurate you want the description to be. Ideal bond lengths are normally assumed, so the structure can be described using φ, ψ, ω (for the backbone) and χ1-χ5 (for the sidechain) angles. This is what is used in most cases. However, the positions of the hydrogens in the sidechains are not uniquely defined by this description. This also does not describe hydrogen bonds and disulfide bridges, but those could be deduced from the relative positions.
You can get more information here: http://kinemage.biochem.duke.edu/teaching/anatax/html/anatax.1b.html
This description should be enough for most applications, though.

Comparing Protein Structures
There are a number of things you can look at such as root mean square deviation. This method compares the co-ordinates of two structures by superposing them on top of each other.

RMSD: This is implemented in the modelling Modeller or can be used in USCF Chimera

RMSD will provide a number in angstroms squared, with higher values indicating structural differences. A RMSD of 0.0 would indicate the structures are identical. There are different types of RMSD calculations such C-alpha, backbone and all-atom. C-alpha RMSD will only look at the C-alpha atoms to calculate the RMSD. Backbone RMSD will look at the backbone only and all-atom will take into account all the atoms to calculate the RMSD.

Other Things to Look at

Assuming the structure was created yourself, was the structure minimised? To remove clashes?
In addition phi, psi angles and mentioned above have you checked for clashes in your structure? Clashes can be checked in USCF chimera which checks for clashes with a default value of 0.6 Angstrom van der Wall radii overlap.


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Do plants need O₂ to consume energy they've stored via sugar?
This question came up as I work my way through the answers to another question I just asked.
My understanding is that plant photosynthesis looks something like this (though with lots more going on under the hood):
$$\ce{6 CO_2 + 6H_2O + light -> C_6 H_{12} O_6 (sugar) + 6 O_2}$$
(source)
and that the primary functions of the sugar are to store and transport energy. If that's true, then there's something fishy about the familiar view that plants need CO2 to breathe and produce O2, while animals need O2 and produce CO2. Doesn't a plant need just as much O2 as an animal would when it (the plant) gets around to consuming the sugar it has produced? Doesn't consumption of the sugar take you back to the original reactants?

Yes, plants require oxygen to generate ATP from sugar. However, they generate far more sugar (and O2) than they use.

OK, produced one further follow-up, Why do plants produce so much more sugar than they use?

Plants need sugar not only for energy but also for synthesizing essential metabolites and building blocks including cellulose (used in cell wall), glycoproteins and 5-carbon sugars for nucleotides.
As already mentioned by canadianer, plants respire by oxidizing sugars. This happens mostly during the night. However photosynthesis also produces ATP and therefore plants are not strictly dependent on respiration for energy. Moreover the fixed carbon in the form of starch makes up an energy reserve (like fats and glycogen in animals).


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Why do plants produce so much more sugar than they use?
I recently asked the question, "Do plants need O2 to consume energy they've stored via sugar?" to which @canadianer responded, "Yes, plants require oxygen to generate ATP from sugar. However, they generate far more sugar (and O2) than they use." Why do plants produce all that extra sugar, especially given that sugar is thermodynamically expensive?
One reason, I believe, is to produce fruit and so recruit animals to help with reproduction. But are there others?

Plants store sugar as starch and use it to make cellulose (for their cell wall). It's also important to realize that sugar is only one of the products of photosynthesis. The Calvin cycle produces 3 carbon molecules which can feed into other metabolic pathways such as for amino acid or nucleoside synthesis. Basically it's the source of all carbon in plants.

I just realized my other comment may have been misleading. Of course they use all of the sugar they produce, just not as energy.

@canadianer, you write, "They use all of the sugar they produce, just not as energy." Why use such an energy-expensive substance for cell walls? Doesn't the high energy content make it more appealing for animals to eat the plant?

possible duplicate of Do plants need O₂ to consume energy they've stored via sugar?

@kuzzooroo Building anything is energy expensive. Anabolic processes are energy expensive but they are essential for survival. Cellulose cannot be digested by all animals. Herbivores got the ability to metabolize cellulose in animals much later than the development of cellulose cell walls in plants, in evolution. (Actually herbivores rely on bacteria to do that)

Almost no higher animal has cellulase. Some rely on intestinal bacteria to digest the cellulose. Some animals ingest their feces to get the carbohydrates obtained by broken cellulose as the actual digestion of cellulose is in the colon where glucose can't be absorbed.

@WYSIWYG There are insect herbivores that produce cellulase themselves. It is rare overall (most rely on symbionts, both bacteria, fungi and protozoa), but spread in many insect orders.


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How does food intake affect medicine? Why pill instructions recommends taking them before (after) meal?
Even simple vitamins seem to have this in the instruction. Why is is so? Is there some simple model of how do pills interact with food? Does it depend on the food type? (What about drinks?)
Should not eating at all on some day be considered "before food" or "after food"?

This question is asking for medical advice, which is off-topic on all Stack Exchange sites, including Biology. Please consult with your physician if you have questions about any medications you may be taken, and when/why they should be taken. We cannot safely give you advice without knowing your full health situation.

@closevoters This can be taken as something that deals with pharmacokinetics.

@MattDMo I don't have any doctor around; the question is not about me and my pills, but about pills in general. Inconvenient "before meal" is just stated in the instruction, but not explained.

@anonymous If you remove your last question (sentence) about higher dosage, I think people will vote to reopen this question. As such the people here do not want to be responsible for something bad happening because of health related answers from SE

I'll vote to reopen if this is changed into a purely pharmacokinetic question.

I can tell you why you should take iron with food. Because you need something with it to "buffer" it so that you don't get a stomach ache!

From the Merck website :

Drug absorption is the movement of a drug into the bloodstream after administration.
Absorption affects bioavailability—how quickly and how much of a drug reaches its >intended target (site) of action. Factors that affect absorption (and therefore >bioavailability) include
1.The way a drug product is designed and manufactured
2.Its physical and chemical properties
3.Other ingredients it contains
4.The physiologic characteristics of the person taking the drug
5.How the drug is stored
If a tablet releases the drug too quickly, the blood level of the drug may become too high, causing an excessive response. If the tablet does not release the drug quickly enough, much of the drug may be eliminated in the feces without being absorbed, and blood levels may be too low. Drug manufacturers formulate the tablet to release the drug at the desired speed.

Essentially, most drug's absorption rates are slowed down by food in the digestive tract, which is beneficial for various reasons depending on the drug.
Some pills are irritants to the stomach, in which case they usually have a coating that may need an acidic environment to break down. Food would assist in this, as well as serving as a sort of diluting agent and even a physical barrier for the stomach.
Conversely, some nutrients (and certain pharmaceuticals) are absorbed by the stomach lining and small intestine much more efficiently when the body is actively digesting food, which is why vitamins and other supplements have the food recommendation.
I think that 'before or after' food should be read as 'shortly before or after', i.e., so food and pill are digested simultaneously. Otherwise, I believe they just don't mention it. Of course, this is a simplistic rendering of pharmacological absorption vis a vis food (there are some very specific interactions; grapefruit and various blood pressure medications come to mind), but this is the general answer to your general question, I believe.


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Relationship between nerves and axons
I just wanted to get a realistic viewpoint of our nervous system. I understand arteries and veins, but I wanted to know how similar our nervous system is to that?
I understand we have neurons (please correct me if I am wrong) all over the surface of body. Whenever we feel a touch a neuron fires a response, and that response travels through axons (myelin sheath).
My main question is what a nerve exactly is. Is it a long axon? How many axons (same thing as neuron body?) are in a nerve? I am sure it depends on different nerves.

I vote to re-open - this question is not too broad. On the contrary, it is a set of highly specific questions, basically boiling down to terminology. I edited the question previously when the close-votes were already pouring in, and hence I vote now to re-open without editing any further. I think it is fine as is. Furthermore, there is background info, so there is no ground to 'leave-close' due to homework :-)

I forgot to message you, but I edited your question to make it more compatible with Biology Stack Exchange. At Biology we like clear questions. Nice question +1

Chris, this was my first question on this website. I only knew of one rule and that was to be as specific as possible. I tried. I am not very familiar with the format of this website so I am not sure what "close-votes" or "re-open" you were talking about. I barely found out that my question was answered :) which I really appreciate.

@ChrisStronks I see a number 4 next to my question. What does that mean? Net positive votes I got?
Also, can anyone edit my question? Or do you run this website?

The close-vote and re-open comments were directed to others that close-voted this question. It may help you to read through the help site and see what a good question looks like and what can happen when people not agree with the question content.

The +4 means that 4 folks liked your question. I can edit it among many others. I am just one participant among many others with enough reputation to edit questions.

I will go through your list of questions below:

I wanted to know how similar is our nervous system to [the circulatory system]?
They are very different, but as in every comparison of very complex systems, there is some overlap. The circulatory system carries fluids, the nervous system electrical signals so they are functionally not alike. However, both systems run throughout the body and have a more or less central control unit (the brain and heart respectively). So there is a structural similarity. I reckon they are as much alike as a city's sewer system and electricity grid.
I understand we have neurons (please correct me if I am wrong) all over the surface of body.
That is correct
Whenever we feel a touch (stimulus arises) a neuron fires a response, and that response travels through axons (myelin sheath).
Tactile stimulation may result in firing of one or more neurons, dependent on the intensity of the stimulus. Larger stimuli will, obviously, recruit more fibers. Stronger stimuli will evoke stronger responses (increased firing). Axons indeed conduct the neuronal responses, like an electrical wire conducts electrical current. Longer axons are often myelinated (insulated). Not all neurons related to touch are myelinated, however.
So my main question is that what exactly is a nerve?
A nerve is a bundle of axons that carry related functional information. Typically, nerves conduct information originating from locations closely located together in the body, and generally they convey this information to a localized spot in the body as well. For example, the optic nerve carries information from the photoreceptors (related information) from the retina (localized source) to the brainstem (localized target).
Is [a nerve] a long axon?
A nerve contains many axons. 'Long' or 'short' is rather subjective.
How many axons (same thing as neuron body?) are in a nerve? I am sure it depends on different nerves.
Neuronal cell bodies are typically located outside a nerve. Nerves contain varying numbers of fibers. For example, the auditory nerve harbors the axons of the spiral ganglion cells that transmit auditory information from the inner ear to the brain. It contains between 31k - 32k (myelinated) fibers in normal-hearing humans (Spoendlin & Schrott, 1989). In contrast, the optic nerve, which carries visual information from the retina to the brain, contains some 1.3 million (myelinated) fibers in young human adults (Jonas et al., 1992)

References
- Jonas et al., IOVS 1992;33:2012-8
- Spoendlin & Schrott, Hear Res 1989;43:25-38

Chris, I deleted my answer. Plus this is the source of the picture:http://dtc.pima.edu/blc/182/lesson12/12step6/12step6page1.html

Thank you, Chris for answering the question. I really appreciate it.


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Does DNA Ligase look for complementarity in sticky ends?
Can DNA ligase seal two non-complementary sticky ends if the reaction is incubated at the optimum conditions ? I do almost 100% double digestion in the lab. However, during ligation, when I do a control without the insert, I still get many circularized vector and they cause massive false positives during transformation. Can ligase sealing two non-complementary sticky ends be a possible reason behind this ?

Since DNA ligase can ligate blunt cut DNA, it can probably ligate incorrect sticky ends, but the probability is low. Are you doing an antarctic phosphatase reaction to remove the 5' phosphate on your vector? That would reduce the liklihood of bad ligations.

Unfortunately I am not doing that because some people can make cloning work without phosphatase treatment in our lab and I am mostly following their procedures. At least so far.

I'd definitely try a phosphatase control and see if that's the issue.

You may be getting false positives because of incomplete digestion too. Did you check the digested plasmid on the gel? Also use very little of the plasmid (≤500ng) in ligation

I would also suspect incomplete digest. Depending on your transformation method a few hundred undigested plasmids are enough to get false positives and you will not see these in a control gel. You could try to extract only the band of interest from a gel.

I use around 300ng plasmid for transformation. Some say use less but they have no logical explanation unfortunately.
Regarding incomplete digestion: I have thought of it too. However, since the sites of two enzymes are very close (only 31bp in between the sites whereas the vector is around 6kb) when I extract the cut band from the gel, I also extract single digests and there seems to be no way to be sure if I am extracting only the double digests or not. I can give phosphatase treatment a shot but do you have any idea about the question regarding ligase ?

They found here the T4 Ligase can effectively ligate mismatched ends resulting in up to 5 mismatched bases. Which ligase are you using?

If I understand correctly you are preparing your cloning vector by digesting it with two enzymes that are 31 bp apart. If you have a high background of recircularized vector see if there is a unique restriction enzyme site within that 31 bp.  If there is, and if the fragment you are trying to insert also lacks that site, then a simple approach would be to inactivate the ligase, and digest the reaction with the third enzyme.  That should drastically reduce the background of recircularized vector.
If after gel purifying the vector backbone after the double-digestion, you get a  significant background of recircularization, then you can easily test your hypothesis about ligase ligating mismatched sticky ends: both of the starting sites should be gone and any sites in-between them should be gone.  Have you tested this?

I have solved the problem by increasing the time of digestion and preparing new plates. Now I get only a few colonies when there is no insert  - probably there are still some single digests and ligase repairs the nick- and it is not a major problem anymore. I have read about your suggestion elsewhere but there was only one such site between my sites and the enzyme for that was rare & expensive so I followed another approach as I mentioned. Apparently I got false positives because my enzymes were sloppy and my plates were a bit old.


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How close to Earth's core can organisms live?
We don't to know much about organisms living deep below the Earth's crust. Recently a team led by S. Giovanni discovered some microbes 300 m below the ocean floor. The microbes were found to be a completley new and exotic species and apparently they feed off hydrocarbons like methane and benzene. Scientists speculate that life may exist in our Solar System far below the surface of some planets or moons. This raises some questions:

What is the theoretical minimum distance from Earth's core where life can still exist. Please explain how you came up with this number. For example, there are temperature-imposed limits on many biochemical processes.
Is there the potential to discover some truly alien life forms in the Earth's mantle (by this I mean, life which is not carbon based, or life which gets its energy in ways we have not seen before, or non DNA-based life, or something along these lines)?
What is the greatest distance below the Earth's crust that life has been discovered? I believe it is the 300 m I cited above, but I am not 100% sure.

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

Are you serious? I am in high school, and I don't take a biology class. This is not homework and I doubt any professor would assign a homework question like this? I don't know much about biology, especially about organisms living deep below the Earth's crust, which is why I'm asking the question...How in the world do you expect someone who knows nothing about biology to "show an attempt at an answer". In my opinion this is a totaly valid question and its not homework.

@JoshuaBenabou Homework does not mean homework in school. Homework refers to your personal effort in the sense "doing your homework before asking others". Showing an attempt means looking up or at least doing a google search. And please dont give this "I don't know biology" argument. When I ask questions in stackoverflow I make sure that at least I read the manual page once. If you don't know any biology then start by learning some.

It is a good question. If you can add some evidence for your research, it will not be closed. Please be polite too! The message by Matt is a standard format "one reply for all" sort of message.

Alright I've edited the question to include some background information. Is it good now?

@JoshuaBenabou Can you provide some link to that experiment done by Giovanni and colleagues

http://www.eurekalert.org/pub_releases/2003-01/osu-rfl123102.php

I think the second subquestion should be removed, since it is rather nonsensical. It can be restated as: "What is the potential of discovering something completely unknown?". Of course we can discover something entirely new and alien, but to evaluate the possibility of this is far too speculative.

I bet the closest life can get to the core is 6377.1 km plus or minus 1 km.

How do you figure?

That is the radius of the earth. If you get 6370 km into the earth, you will be almost in the center of the core

@user137: But extremophile life has been found several miles deep in mines, so knock at least a few km off your number.  One example here http://proceedings.spiedigitallibrary.org/proceeding.aspx?articleid=928683 or search for "deep biosphere".

we have found life 7km down in the kola superdeep bore hole, the answer may well be as deep as liquid water can exist. which admittedly is not that far.

There's a lot we don't know about life in deep caves, but we can bound the deepest living organism to at least 3.5 kilometers down, and probably not more than 30 kilometers down.
The worms recovered from deep mining boreholes are not particularly specifically adapted to live that far down: they have similar oxygen/temperature requirements as surface nematodes.
The Tau Tona mine is about 3.5 kilometers deep and about 60˚ C at the bottom. Hydrothermal vent life does just fine up to about 80˚C, and the crust gets warmer at "about" 25˚C per kilometer. It's entirely reasonable to expect life to about 5 kilometers down, but further than that is speculation.
Increasing pressure helps to stabilize biological molecules that would otherwise disintegrate at those temperatures, so it's not impossible there could be life even deeper. It may even be likely, given that the Tau Tona life breathes oxygen.
I am certain no life we might recognize as life exists in the upper mantle.

At least 283 bacterial species (as of June, 2017) have been found in deep mines, deep seas, or deep-sea sediments; for example:
Abyssivirga alkaniphila, 2.3 km; Alcanivorax dieselolei, 5.0 km; Alcanivorax marinus, 2.5 km; Alcanivorax nanhaiticus, 2.1 km; Alkalimonas collagenimarina, 4.0 km; Alkaliphilus transvaalensis, 3.2 km; Altererythrobacter atlanticus, 2.6 km; Altererythrobacter marinus, 1.5 km; Amycolatopsis albispora, 2.9 km; Anoxybacter fermentans, 2.9 km; Arthrobacter ardleyensis, 5.0 km; Aurantivirga profunda, 1.0 km; Arthrobacter subterraneus, 0.5 km.

For links to the articles describing these bacterial species, see:
https://www.researchgate.net/publication/310900732_Bacteria_I_Names
http://bacteria.martinklvana.com/


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Has the protein composition (with identification) in honey and other honeybee byproducts been studied?
I am interested in studying honey and other honeybee byproducts.  I have not been able to find sequence or structure records for any of the contents of honey.
In particular, I want to study the protein sequence and structure and the amino acid compositions within honey.
Has any of this data been produced and published in any databases or research papers?

First of all: Honey is not a byproduct of bees - it's their main and most important product which stores energy for the bee hive for the time when no flowers are available.
Honey itself consists (according to the USDA database) to about 99.5% of water and sugars (82.5% sugars, 17% water). The sugars are mostly fructose and glucose, but also some other mono- di and tri-saccherides in traces. See reference 1 for details. It also contains trace amounts of vitamins and minerals, see table from the Wikipedia on Honey:

The protein content varies between honey sample but is somewhere in the range between 0.2 and 0.5% (see also reference 1). The proteins come from flowers (pollen incorporated into the honey) as well as from the bees (see reference 2). Paper 1 lists a number of enzymes as most common bee proteins in the honey, but doesn't go into much more details here. These are invertase, diastase, glucose oxidase and catalase.
You could now go into the sequence databases (Apis mellifera has been complete sequenced) and look up the sequence information of the enzymes. Information can be found here and here.
References:

A review of the analytical methods to determine the geographical and
botanical origin of honey
Source of the honey protein responsible for apple juice
clarification


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Is it possible for a human to get rabies from a rabies vaccine meant for dogs?
What would happen if a human was injected with a rabies vaccine meant for dogs? I know vaccines can contain weak or dead strains of the virus, but is it possible that the human could become infected with rabies from a vaccine meant for dogs? My thinking is that maybe a dogs' immune system is more suited to deal with a weak strain of rabies that would otherwise infect a human.

The question here is if the vaccines used in human and dogs are different. Or if there are really big differences between the immune systems of both, which I doubt. Generally living strains are weakened so that they trigger an immune response but not the full blown disease, which would be fatal in the case of rabies.

It would depend on which vaccine you're talking about, as there are several. Some use attenuated strains of the Rabies virus, others use killed, and some are recombinant glycoprotein vaccines. Here is a list from the CDC of all the rabies vaccines available in the US in 2011 (I wasn't able to find anything newer). Generally speaking, through, one would expect the FDA in the US and the relevant authorities in other companies to require vaccine manufacturers show that their product is safe in other species, in case of accidental exposure, such as you are talking about here. This is especially true of something being given to an animal that is quite often a family pet.
If you think you've been exposed to any type of medication which has not been prescribed for you, including dog rabies vaccine, you should seek medical attention immediately, if not sooner, but based on my experience in the pharmaceutical industry and dealing with regulatory agencies, you should be pretty safe, as the regulations surrounding vaccines are quite stringent.

Vaccines can generally be considered safe for this case. The charges are tested individually and are not released if there is any doubt on their quality or safety.

@Chris, I think the question then becomes: Is it possible for humans to get rabies from human attenuated rabies vaccine?

@CRags that's what I was trying to address, in part - pet vaccines have to be tested for possible transmission to humans. They wouldn't possibly use potentially contagious vectors in a vaccine meant to prevent disease in both species.


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How can action potentials be generated through thoughts?
I think I understand how a signal is transferred from neuron to neuron (from  How do the brain and nerves create electrical pulses?).
My question, however, is not about the standard textbook material on neuronal transduction. Instead, I am wondering how an electrical impulse starts in the first place in the brain. In other words, how can an action potential be generated de novo from a conscious thought? I am wondering primarily about a signal like a movement of an appendage or something similar.
So in short, my question is:
How is the 'first' action potential generated in the cortex when one consciously/voluntarily decides of moving a limb (or comparable action)?

You can have a look at this article. It is not accessible to me right now. When I get to read it then I'll post an answer.

@WYSIWYG interesting article! Waiting for your answer!

Where are my comments? Is this your doing @CRags lol?

@ChrisStronks not mine. Some moderator cleaned up!

This paper addresses the question that you are asking. The study is based on conscious decision making in rats.
Performance of rats were assessed in the following task:
The rats have to poke their snout into a waiting port until a auditory signal (beep) is heard.
After first beep the rats can get a small reward (small amount of water) in the reward port. However if the rat waits for a second beep it gets to have a bigger reward.
So there were three behavioral outcomes in the experiment done with 37 individuals:

Short-poke trials: Those that didn't wait for the signal (8.3 ± 4.6%)
Impatient trials: Those that waited for the first beep but did not wait for the second beep (58.8 ± 3.9%)
Patient trials: Those who successfully got the bigger reward. (32.9 ± 1.4%)

The impatient ones did not usually quit immediately after the first beep. This was not a lethargic response to signal but a moment of conflict between two decisions. There was a distribution of waiting times. The patient ones immediately responded to the second beep and took their reward.
Neural activity was studied in the M2 (secondary motor) cortex of impatient rats during the tasks and two kinds of neural activity was observed:

Ramp-to-threshold: Firing rate kept increasing till the end of waiting time suggestive of a neural threshold to quit waiting. (Fig 1)
Steady-transient activity: Firing rate correlated with waiting time i.e. higher firing rate higher the waiting time. This could constitute the neurons that are making the rat wait. (Fig 2)

Figure 1: Ramp-to-Threshold.  Reproduced from Murakami et al. (2014) Nature Neuroscience 17,1574–1582

Figure 2: Transient activity.  Reproduced from Murakami et al. (2014) Nature Neuroscience 17,1574–1582

It was also observed that this activity is task specific. The neurons that showed a certain activity in the above tasks did not behave the same way in the same rats performing a slightly different task.
So action potential is generated in the brain by "thoughts". However these thoughts are not generated de-novo. Any conscious decision is based on memory of past events and similar events evoke those memories, which in cellular terms is generation of action potential. In this case the action potential is generated in response to the rats' sensory input in the form of a beep. Other kinds of responses are instinctive and the brain circuitry has evolved to generate these kinds of responses to certain stimuli such as fear. The above example is a study of conscious decision making based on an acquired memory.

Does neurons that fire on their own (like the reticular activating system) have any role in thought generation?

@CRags Thoughts are essentially memories that are developed out of conscious actions and perceptions. The neurons that "fire on their own" are either controlled by an inbuilt oscillator (look at FHN model) or regulated by visceral stimuli. Then there are reflexes and other instinct driven responses which are basically preformed circuits. I am not sure how the autonomous nervous processes can affect conscious response- perhaps in an indirect way but I guess they don't have a direct role.

What about say, you come across an interesting formula for the first time and you start to think on how that formula was derived. In this case, would the short term memory be responsible for the string of thoughts that follow?

Very interesting answer though. +1 for that

@CRags I think when you are thinking about the derivation of that formula then you are essentially recalling similar formulae and trying to work it out in a similar fashion.

Wow, this is really cool! What a great article! Thanks for that awesome answer! So is the order/rate in which those memories are recalled totally random or is there some sort of mechanism behind what memory is 'remembered'? For instance, if an organism has two memories of an event that correlates with a situation it is currently in, what controls which memory 'shows up'? This is probably a stupid question and the answer is probably right in front of my nose, but still...

@CDB I can't say anything for sure but the strongest memory should be recalled first even though the temporal order of the memory registry might be different. How temporal information is stored in the brain is still under research.

There's a philosophical issue here: if you believe "thought" originates outside of the physical brain, you are probably some sort of dualist. However, I believe it is more likely that the brain is the machine that enables (apparent) consciousness and thoughts. If you believe "thought" causes neurons to fire, you might not be able to find a scientific answer, unless you can measure that "thought" external to the brain...
There are spontaneous activity in the brain. That is, neurons will fire by themselves with or without any external input at random times. See this question and my answer there in. Brain is surprisingly noisy. Perception and behavioral variability is often correlated with such noise, and studied in neuroscience. For example, see

Nienborg, H. and Cumming, B. G. (2009). Decision-related activity in sensory neurons reflects more than a neuron’s causal effect. Nature, 459(7243):89-92.

While I'm not a dualist myself, how do you address causal mechanics originating thought when quantum physics has ruled out local determinism? Global determinism could still exist technically, but that would be an infinitely more complicated model of neuroscience.


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Is it possible that weak memory is due to interference between signals in the brain?
"Weak memory", as used in this question, refers to the inability to retrieve a memory that a person otherwise knows he has memorized earlier. An example of this is some fact snippet that the individual memorized as part of a training exercise 2 weeks earlier.
Is there scientific consensus for the cause of this type of weak memory? Or is the consensus that there are multiple causes?
Is it possible that this type of weak memory is caused by interference between various signals in the brain, or what does the known evidence say (if anything)?

It is better to use the term "weak memory" because people might think "bad memories" refer to memories of unpleasant events.

Weak memory can be either because of synapses not strengthened enough by LTP or actual weakening because of LTD, synaptic pruning, amnesia or even neurodegeneration.

Was reading about something along this topic earlier, kidney failure can result in poor short term memory -http://www.ncbi.nlm.nih.gov/m/pubmed/2088591/.  Otherwise I would assume there are myriad causes for memory dysfunction

I would also add that cholinolytics which inhibit he action of choline cause memory loss and inability to retrieve memories of various levels. For example, the well-known cholinolythic trihexyphenydil causes one to forget the beginning of a sentense before the person comes to the end of the sentense and causes other memory losses. On the other hand, drugs that potentiate choline (like pramiracetam) cause significant memory improvements, even massive sudden recovery of long-lost child memories. This information is somewhat orthogonal to what you're asking, but I thought you might be interested.


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what does Pro→Glu substitution mean?
Considering the paper:
A single amino acid in E-cadherin responsible for
host specificity towards the human pathogen
Listeria monocytogenes
in the abstract portion, what does Pro→Glu mean? Does it mean that, in place of Glu(glucose), pro-16 is placed?

Proline is replaced by Glutamic acid. Pro16 indicated a position on the protein.

You are looking at a protein here, which is mutated in the higher host specificity, so glucose is not involved here. What is written here are the amino acids in the three-letter-code, the notation Pro→Glu means that Proline (Pro) is replaced by Glutamic acid (Glu).
The notation Pro16 means the proline on amino acid position 16 in the protein. You often find this replacements noted as Pro16Glu or P16E (in the 1-letter-code)

oops.. I shall remove my answer


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Why does an complete molar pregnancy not result in a clone?
Complete molar pregnancy is one where an ovum devoid of nucleus is fertilized by a sperm after which the haploid set of chromosomes double to form a diploid set.
As far as my understanding extends if the sperm had Y chromosome the embryo will not survive.
However if the sperm has X chromosome the zygote will survive to have the 46 XX karyotype and will start to grow as molar pregnancy (which is basically trophoblastic tissue with no fetal parts, as answered by Anongoodnurse).
Why is there no proper fetus? Why can't a "female clone" of male parent form instead? Where is the defect as such?

The Question pointed out by WYSISYG contains data only from animal studies. Although it answers my question, I want more data obtained from study of human trophoblastic tissue (from the molar pregnancy).  Papers on imprinting which are linked in those questions have no mention of molar pregnancy although Prader-Willi and Angelman syndromes are mentioned (as cases seen in humans).

Oops, I corrected my question thanks to anongoodnurse. I mixed up complete and partial moles with each other.

Imprinting issues: possible duplicate of Does a man contain all the genes needed to make a woman? and Could a sperm be altered to contain a female's genetics?

"However if the sperm has X chromosome the embryo will survive to have the 46 XX karyotype and will start to grow as molar pregnancy."

Complete molar pregnancy is diploid, and there is no fetal tissue identifiable. It is a disease of the placenta, a uterine tumor (cancerous in some cases, non-cancerous in others); fetuses do not develop from such pregnancies, not haploid or diploid (though they are usually 46, XX). A male haploid 23,X replicates, but only trophoblastic (what should be the placenta) tissue results.
Partial molar pregnancies are triploid, and a fetus can sometimes be identified. However, it is non-viable, as polyploidy is non-viable in humans. Even if it were, the abnormal placenta could not support it.
Molar Pregnancy
p57KIP2 immunohistochemistry in early molar pregnancies: emphasis on its complementary role in the differential diagnosis of hydropic abortuses

This should be a comment rather than answer. It does not answer the question in any way.

Yes this should be converted to comment.


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Are sensory receptors neurons?
Background
There are many receptor types in the body, with various functions and various mechanisms of transduction. Receptor cells are considered to be part of the peripheral nervous system, as they are the first step in conveying information from the periphery to the brain.
Many receptor cells do not fire action potentials. Action potentials are widely considered to be a key property of neurons. Instead, receptors often operate by graded responses. For example, upon illumination photoreceptors gradually hyperpolarize. Cochlear hair cells gadually depolarize when the stereocilia are bent into one direction and hyperpolarize when they go in the opposite direction. Hence, many receptors are in fact analog sensors, whereas spiking neurons can be considered to be operating in binary (all-or-nothing) mode.
Given their similarities and differences, are receptor cells classified as neurons?
Credits: This question was formulated after a discussion with @OneFace on the question "Relationship between nerves and axons"

Lol I was planning to ask this! Good question though. I am specifically interested in knowing if mechanoreceptors can be considered neurons.

Lol - I thought to ask and answer. so it allows more input here. It is a question that has been on my mind for ages.

Short answer
Receptor cells are specialized neurons

Background
There are, globally, three types of neurons (Eckert's Animal Physiology):

Sensory neurons: these cells transmit information from external stimuli (e.g., sound, light, pressure), or from internal stimuli (e.g., blood oxygen level or head orientation);
Interneurons: these cells connect other neurons within the central nervous system;
Motor neurons: these neurons carry effector signals to effector organs, causing contraction of muscles or secretion by gland cells.

To illustrate these classes of neurons let's consider the visual peripheral system. Fig. 1 shows a schematized representation of the retinal circuitry, connecting the photoreceptors to the ganglion cells of the optic nerve (interneurons):

Source: Instituto Balseiro
The photoreceptor's response is graded. Notably, the bipolar cell, being an interneuron has also a graded response. The bipolar cells convey the signal, in turn, to the ganglion cells that translate the analog, graded signals into a binary, neural spiking code that enters the optic nerve.
Receptor cells are considered neurons, but they are highly specialized. Although interneurons may come in various shapes and sizes, they are not so specialized as receptor cells. The photoreceptor, for example, has a highly specialized dendritic region containing the photosensitive pigment and membrane stacks that capture light.
Another receptor is the Pacinian corpuscle, a vibrotactile mechanoreceptor of the skin:

Source: Pixgood
In this case, the receptor cell is in fact a myelinized and spiking neuron that functionally much resembles an interneuron. Just as the photoreceptor, the dendritic part does not connect to another neuron, but is highly specialized structure designed to sense a physical external stimulus. In case of the Painian corpuscle, it is an onion-like structure consisting of many lamina. These lamellar structures substantially change the receptor's response to mechanical stimuli. Specifically, it allows the corpuscle to respond rapidly to pressure changes and allow it to faithfully transmit vibratory stimuli.

Reference

Eckert, Animal Phsyiology:
 - Chapter 5 - The Physiological basis of Neuronal Function
 - Chapter 7 - Sensing the Environment

I think there are more types of neurons. Several cortical/hippocampal neurons cannot be called interneurons (a term generally used for modulatory neurons)

I agree with you that interneurons are often said to be inhibitory. However, I extracted this info from Eckert. A quick Google search indicates it is an ambiguous term, but Eckert's definition is pretty widely used.

I think you can add a statement that the gene expression profiles of these cells closely match that of other kinds of neurons (compared to other excitable cells). They also have the same developmental origin and therefore they can be classified as neurons. Regarding point#1: I had looked at expression data from retina as well as brain; I am just telling an observation from the back of my mind. Need to verify that.

Neither hair cells (fig 1) in the inner ear nor taste receptor cells are neurons. They are modified epithelial cells (i.e. during development, they come from non-neural ectoderm). Additionally, Merkel cells in the somatosensory system (which might or might not be doing the actual transduction) are also derived from skin.

@alexforrence - thus you are saying that embryonic germ layer defines what a neuron is? In the end, neural tissue comes from the neuro-ectoderm, which is basically derived from ectoderm. Hence, neurons arise from the ectoderm.

That's why I emphasized non-neural ectoderm. It seems like a pretty good place to draw a line in the sand. I don't think that this answer addresses the question completely; I'll try to write up one in the next couple of days.

@alexforrence - I am looking forward to your answer!

@alexforrence Question is what is the right classification method- gene expression profile or developmental origin. I don't think the latter makes sense when we now know about iPSCs. Even though these cells may originate from epithelial cells, I guess they are functionally neuronal.

@WYSIWYG I think that's where part of the confusion is coming from. Non-neural cells are allowed to do a lot of the things that neurons do (release neurotransmitter, de/hyperpolarize, etc.). Developmental origin and gene expression go hand in hand; the signaling during development (based on location of the cell) can drive or suppress expression.

@alexforrence - One of the main reasons I think receptors are classified as neurons is that their connecting afferents are called secondary neurons: http://en.m.wikipedia.org/wiki/Spinal_cord, meaning receptors are primary neurons

It's just confusing semantics. That refers only to the somatosensory system, where the primary sensory neurons sit in the dorsal root ganglion. Making a blanket statement across all sensory systems is the problem.

@alexforrence - it is the same in the retina (photoreceptors connect to secondary neurons) and likely this applies to other sensory systems as well.

I am confident receptor cells are neurons. Whatever their gene expression profiles or origin in embryonic tissue.

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


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Why sudden stresses cause stuttering and/or other impairs in children?
The question is simple: Why sudden stresses cause stuttering and/or other temporary or permanent impairs in children (and even adults)?

The stuttering issue has an answer on http://cogsci.stackexchange.com/questions/8895/why-do-some-people-stutter-only-when-they-are-nervous/8911#8911.


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Do all sources supply all sinks on a plant?

Sources include any exporting organs, typically mature leaves, that
  are capable of producing photosynthete in excess of their own needs.
Sinks include any nonphotosynthetic organs of the plant and organs
  that do not produce enough photosynthetic products to support their
  own growth or storage needs. Roots, tubers, developing fruits, and
  immature leaves, which must import carbohydrate for normal
  development, are all examples of sink tissues.

Sinks are always supplied by sources. Now, I want to know do all sources transport their photosythetic to all parts of plant or some sources just supply some especial sinks.
This is a question for me:
Do all sources supply all sinks on a plant?

Welcome to Biology S.E.! If you need additional assistance, please visit The Help Center.

I really can't understand your question.

@WYSYWYG let me describe i this way. there are some sources and sinks in a plant. sources supply sinks. Now, I want to know do all sources transport their photosythetic to all parts or some sources just supply some especial sinks.

@Stack I had written my answer according What you said in your comment.

What you think about phloem is not correct, actually there are a lot of phloem which transport the photosynthetic. Although the overall pattern of transport in the phloem can be stated simply as source-to-sink movement, the specific pathways involved are often more complex. Not all sources supply all sinks on a plant; rather, certain sources preferentially supply specific sinks. In the case of herbaceous plants, such as sugar beet and soybean, the following generalizations can be made.

Proximity. The proximity of the source to the sink is a significant factor. The upper mature leaves on a plant usually provide photosynthetic to the growing shoot tip and young, immature leaves; the lower leaves supply predominantly the root system. Intermediate leaves export in both directions, bypassing the intervening mature leaves.
Development. The importance of various sinks may shift during plant development. Whereas the root and shoot
apices are usually the major sinks during vegetative growth, fruits generally become the dominant sinks during
reproductive development, particularly for adjacent and other nearby leaves.
Vascular connections. Source leaves preferentially supply sinks with which they have direct vascular connections. In the shoot system, for example, a given leaf is generally connected via the vascular system to other leaves directly above or below it on the stem. Such a vertical row of leaves is called an orthostichy. The number of internodes between leaves on the same orthostichy varies with the species.
Modification of translocation pathways. Interference with a translocation pathway by wounding or pruning can alter the patterns established by proximity and vascular connections that have been outlined here. In the absence of direct connections between source and sink, vascular interconnections, called anastomoses (singular anastomosis), can provide an alternative pathway. In sugar beet, for example, removing source leaves from one side of the plant can bring about cross-transfer of photosynthetic to young leaves (sink leaves) on the pruned side. Removal of the lower source leaves on a plant can force the upper source leaves to translocate materials to the roots, and removal of the upper source leaves can force lower source leaves to translocate materials to the upper parts of the plant.


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What is biological dark matter?
I recently stumbled upon the Biological Dark Matter wiki page. Its pretty light on details, but it appears to be genetic material found in humans that doesn't fall into currently classifications.
But what do we know about it? Is it really a big black box that we know nothing about? The article claims that it can make 40% of the genetic material in our gut, and I find it hard to believe that we really know nothing about it.

Interesting, I've never heard the term before. First, that Wikipedia page does not cite any peer reviewed research so it's not really informative at all. That said, the term seems to refer simply to the presence of genetic material that does not belong to known organisms. This article may interest you: http://www.nature.com/nature/journal/v499/n7459/full/nature12352.html

There are multiple answers to this question depending on who you ask (meaning, what their field of expertise is).
The biological dark matter from the wikipedia article in question seems to mean sequence from metagenomic samples which was not assigned to any of our commonly known domains of life. That might not necessarily mean that it does not belong to them. Sometimes it is hard to decide where a small particle of sequence informations belongs to, because it does not match anything we know. Still, it might be from a perfectly "normal" bacterium. Or it might be a result of sequencing errors.
Additionally, depending on how you assign a taxonomy to the sequence, there might be cases where there are so many different possibilities for where this sequence came from (because it is very conserved in a lot of different organisms, even from different domains of life), that this sequence will not get any taxonomy assigned. Not because there is none, but because we cannot safely decide which it is.
Some people also speak of this information as "dark matter".
There is for example this project which specifically is designed to study the dark matter we can (or at least for some reason do) assign to be microbes, but not more specifically.
Basically, any decision of where to place potential dark matter sequence is guided by our previous knowledge about the domains of life and the genomes of all those organisms. This knowledge is very incomplete.
I am sorry this answer lacks some more nice sources. Most of the information is based on my knowledge as a person working with datasets that might include "dark matter", if I would call it that. (I call it "not assigned sequence".) I don't have the time right now to add more sources, but if needed I can maybe add some later.
Edit:
As a fast add-on after re-reading your question: How much of the sequence is unassigned for example if one would study your gut depends a lot on what is actually there in you gut that we know, how diverse the community in your gut is, what database is used for comparison and how old this database is, how the data is preprocessed and analysed, and so much more. But yes, there is still a lot of genomic information in nature that has not made it into any database.

Take a look at this article: http://phys.org/news/2014-01-scientists-biological-dark.html
Is this the same "biological dark matter" you're asking about? If so, it sounds like what used to be called "junk DNA" or "non-coding DNA", which is what it was referred to as up until a few years ago when scientists discovered it is actually regulatory DNA, very interesting stuff, but basically it regulates gene expression, thus why it is usually in the form of RNA instead of a protein.
I hope this answers your question, I would strongly urge you to do some research on regulatory DNA, it's very intriguing.


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What creates the feeling of 'excess' blood pressure to an area of the body?
If I hang upside down, and feel blood rushing to my head, what structures are actually responsible for me "feeling" this excess flow of blood? Baroreceptors? Mechanoreceptors? Something else?
Regardless, how does this process actually work? How do I "feel" excess blood pressure to a certain area of my body?

Thanks @WYSIWYG (+1) I appreciate the help but must request that you remove the "possible dupe" label on this question.  If you really read both questions, I am actually asking 2 different things. Here I am asking for root causes of the feeling of pressure to any area of the body. The other question is specifically about ears and what types of structures cause the sensation of pressure. I argue these are 2 separate questions. Thanks again!

Ok removed my vote.

Arterial Baroreceptors felling the pressure.

Arterial blood pressure is normally regulated within a narrow range, with a mean arterial pressure typically ranging from 85 to 100 mmHg in adults. It is important to tightly control this pressure to ensure adequate blood flow to organs throughout the body. This is accomplished by negative feedback systems incorporating pressure sensors (i.e., baroreceptors) that sense the arterial pressure. The most important arterial baroreceptors are located in the carotid sinus (at the bifurcation of external and internal carotids) and in the aortic arch (Figure 1). These receptors respond to stretching of the arterial wall so that if arterial pressure suddenly rises, the walls of these vessels passively expand, which increases the firing frequency of receptor action potentials. If arterial blood pressure suddenly falls, decreased stretch of the arterial walls leads to a decrease in receptor firing.
The carotid sinus baroreceptors are innervated by the sinus nerve of Hering, which is a branch of the glossopharyngeal nerve (IX cranial nerve). The glossopharyngeal nerve synapses in the nucleus tractus solitarius (NTS) located in the medulla of the brainstem. The aortic arch baroreceptors are innervated by the aortic nerve, which then combines with the vagus nerve (X cranial nerve) traveling to the NTS. The NTS modulates the activity of sympathetic and parasympathetic (vagal) neurons in the medulla, which in turn regulate the autonomic control of the heart and blood vessels.

Of these two sites for arterial baroreceptors, the carotid sinus is quantitatively the most important for regulating arterial pressure. The carotid sinus receptors respond to pressures ranging from 60-180 mmHg (Figure 2). Receptors within the aortic arch have a higher threshold pressure and are less sensitive than the carotid sinus receptors. Maximal carotid sinus sensitivity occurs near the normal mean arterial pressure; therefore, very small changes in arterial pressure around this "set point" dramatically alters receptor firing so that autonomic control can be reset in such a way that the arterial pressure remains very near to the set point. This set point changes during exercise, hypertension, and heart failure. The changing set point (response curve shifts to right) explains how arterial pressure can remain elevated during chronic hypertension.
Baroreceptors are sensitive to the rate of pressure change as well as to the steady or mean pressure. Therefore, at a given mean arterial pressure, decreasing the pulse pressure (systolic minus diastolic pressure) decreases the baroreceptor firing rate. This is important during conditions such as hemorrhagic shock in which pulse pressure as well as mean pressure decreases. The combination of reduced mean pressure and reduced pulse pressure amplifies the baroreceptor response.

Although the baroreceptors can respond to either an increase or decrease in systemic arterial pressure, their most important role is responding to sudden reductions in arterial pressure (Figure 3). This can occur, for example, when a person suddenly stands up or following blood loss (hemorrhage). A decrease in arterial pressure (mean, pulse or both) results in decreased baroreceptor firing. Autonomic neurons within the medulla respond by increasing sympathetic outflow and decreasing parasympathetic (vagal) outflow. Under normal physiological conditions, baroreceptor firing exerts a tonic inhibitory influence on sympathetic outflow from the medulla. Therefore, acute hypotension results in a disinhibition of sympathetic activity within the medulla, so that sympathetic activity originating within the rostral ventrolateral medulla increases. These autonomic changes cause vasoconstriction (increased systemic vascular resistance, SVR), tachycardia and positive inotropy. The latter two changes increase cardiac output. Increases in cardiac output and SVR lead to a partial restoration of arterial pressure.
It is important to note that baroreceptors adapt to sustained changes in arterial pressure. For example, if arterial pressure suddenly falls when a person stands, the baroreceptor firing rate will decrease; however, after a period of time, the firing returns to near normal levels as the receptors adapt to the lower pressure. Therefore, the long-term regulation of arterial pressure requires activation of other mechanisms (primarily hormonal and renal) to maintain normal blood pressure.
This information from PhD Richard E. Klabunde lecture, that based on his book Cardiovascular Physiology Concepts (chapter 5, pages 93-123)

+1 for a good detailed answer, but I was just wondering, shouldn't venous baroreceptors also play a part in this, since the veins are more likely to change their internal pressure due to gravity (as compared to arteries?)


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I found these skulls in a old bottle in the woods. Can you tell me what they are?

Can you help me identify these skulls I found in an old bottle in the woods?

That top photo looks like a shrew skull.

Where and in what type of environment did you find them?

I found them in a bottle that I picked up in the woods in Illinois.

Why they were put inside bottle? Could there be archaeological significance?

Its a Shrew skull.

Hainault Forest Website
Photographs by © Brian Ecott