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What is ear wax?
A human, at some time in life or the other, must clear the auditory canal. This is usually achieved using soft-cotton buds, or such similar device.
Where does this wax come from? What purpose does it serve? Is it really wax? Is it the inner fluid leaking out?

As quoted from the wikipedia page on Earwax:

Cerumen [earwax] is produced in the outer third of the cartilaginous portion of
  the human ear canal. It is a mixture of viscous secretions from
  sebaceous glands and less-viscous ones from modified apocrine sweat
  glands. The primary components of earwax are shed layers of skin,
  with 60% of the earwax consisting of keratin, 12–20% saturated and
  unsaturated long-chain fatty acids, alcohols, squalene and 6–9%
  cholesterol.

It's purpose -- further quoted -- is that it:

protects the skin of the human ear canal, assists in cleaning and
  lubrication, and also provides some protection from bacteria, fungi,
  insects and water

Some interesting (and stomach churning) earwax trivia:

In medieval times earwax, and other substances such as urine, were
used to prepare pigments used by scribes to illustrate illuminated
manuscripts.
The 1832 edition of the American Frugal Housewife
said that "nothing was better than earwax to prevent the painful
effects resulting from a wound by a nail [or] skewer"; and also
recommended earwax as a remedy for cracked lips.
Before waxed thread was commonly available seamstresses would use their own earwax
to stop the cut ends of threads from fraying.

in case  you want some more nitty gritty details: this boingboing post records some actual TLC of earwax (original link is off line). note the huge squalene/cholesterol ratio.http://boingboing.net/2006/08/08/scientist-analyzes-t.html

Gnarly! P.S.: Good news:  thanks to the invaluable Archive.org, we can view the original article here: http://web.archive.org/web/20060829233236/http://blog.tenderbutton.com/?p=187


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Would two species of yeast with similar genome sizes have the same number of genes or chromosomes?
Similar organisms generally have similar genome sizes. Given this, would two species of yeast have the same number of genes and chromosomes?
Edit: Fixed with thanks to @daniel-standage

I'm doubtful regarding your premise. See my related comment on this thread.

This question appears to start from the premise that different species of yeast are closely related, but they aren't. Saccharomyces cerevisae and Schizosaccharomyces pombe, both Ascomycetes, are thought to have diverged at least 300 million years ago (c.f. the mammalian divergence from other vertebrates was about 200 million years ago).
S. cerevisiae has a genome size of 12.1 Mb, with 5821 protein coding genes (plus another 786 dubious ORFs) spread over 16 chromosomes.
S. pombe has a genome size of 12.6 Mb with 5124 protein coding genes on just 3 chromosomes.
Filamentous fungi have larger genomes and gene numbers. From memory, Aspergillus nidulans has 8 chromosomes and over 9,000 protein coding genes. So, the similarity in gene numbers in the two yeasts probably reflects their broadly similar lifestyles.

source: Stack Exchange

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

sort: votes


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Colonial Cells Demonstrating Cell Specialization
Are there any living examples of cellular colonies demonstrating very primitive cellular specialization?  If so, what do we know about how they assimilate?  How independent are the individual cells and what do we know about their behavior (for example, do they, perhaps, migrate to different colonies in certain proximities)?

Probably not what you are looking for but the protozoan slime mold Dictyostelium discoideum lives as free amoebae which can coalesce into a multicellular migratory slug that eventually forms a fruiting body in which some cells form the stalk while others form spores.
Slug formation is by chemotactic signalling with cyclic AMP as the signal. I seem to remember that there is a predatory species of slime mold which uses cAMP to attract D. discoideum as prey, but I can't bring the name to mind and have failed to find it online.

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


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How does ethanol interact with insulin?
I know that ethanol increases insulin secretion--could someone explain why?
All I have found till now is experimental data analyses.  I am interested in mechanism of alcohol consumption.

Consumption of ethanol? Injection of ethanol? ethanol secreted by the body? Could elaborate a bit and possibly give us some links to your claim of "ethanol increases insulin secretion"?

@Manishearth Thank you for your answer! Here is my source of information: http://www.medicinenet.com/alcohol_and_nutrition/page4.htm , and I am interested in mechanism of peroral alcohol consumption.

Maybe this should migrate to biology? To my knowledge, main results  of ethanol consumption are changes of lipid membranes (ethanol dissolves in the membranes), synthesis of acetaldehyde that can modify structure of many molecules via condensation and slowly oxidized into acetic acid with change of internal pH. This changes are nonspecific and results in numerous responces in metabolism. It is especially true for change in properties of cell membranes, where all cell receptors are located and which are place where neural signal run.

@permeakra Thank you for participation! I won't be against, if my question will be moved to biology SE, if it will more likely receive answers there. As you see, that is my first question here, so I am not sure about local foundations.

Alcoholic beverages, ingested casually, deliver two main nutrients the body will metabolize: sugar and ethanol. The body's natural response to a rise in blood glucose will be stimulated secretion of insulin (from B cells of the pancreatic islets). Alcohol is metabolized primarily by the liver, being first converted to acetaldehyde by alohol dehydrogenase and a coezyme NAD+. Acetaldehyde metabolism quickly converts this to acetate. Acetate is then eventually metabolized elsewhere in the body to carbon dioxide and water. The interesting effects are mediated by acetaldehyde, which can accumulate to toxic levels in some people. This ties into insulin because this article suggests that alcohol consumption changes blood flow from exocrine pancreas (responsible for digestive enzymes) to endocrine pancreas (responsible for secreting homrones, such as glucagon, insulin, somatostatin). Alcohol seems to modulate the late-phase of insulin secretion, increasing secretion, which leads to exaggerated glucose disposal and at least for diabetics causes hypoglycemia.

Huang Z, Sjöholm A. Ethanol acutely stimulates islet blood flow, amplifies insulin secretion, and induces hypoglycemia via nitric oxide and vagally mediated mechanisms. Endocrinology. 2008 Jan;149(1):232-6. Epub 2007 Oct 4.

Thank you for explanation and link, I read the article from endojournals and my interest was absolutely satisfied. :)


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Is eating salt dangerous for the brain?
I read somewhere that eating a lot of salt will raise blood pressure, which will in turn damage brain tissue. This is because water molecules gather around salt ions, thus making it harder for the body to remove the excess water from the blood.
Is this true? How much salt is actually dangerous?

This thread may be helpful.

Eating salt raises blood pressure that is true.  Increased blood pressure is a risk factor in a variety of diseases.  Sodium however is also essential in the diet, as sodium and potassium are the key elements involved in generating action potentials in neurons.

I have recently read about a murder by force feeding salt to a kid. Tragically, the kid went crazy and then died...See also http://en.wikipedia.org/wiki/Hypernatremia and http://www.hawaii.edu/medicine/pediatrics/pemxray/v3c14.html

Good question. The answer really depends. There is a normal range of plasma sodium concentration that ranges from about 135 to 145 mM. You body has multiple endocrinologic and neurological mechanisms to closely regulate this concentration. So even if you went out and ate a ton of salty snacks, your body would still keep your plasma sodium concentration within this range. A salt concentration much lower or greater than this can start to cause problems depending on how fast it happens and how far from the normal value. Brain surgery patient are often given lots of extra salt to keep their brains "salty" as this protects from cerebral edema and counteracts salt wasting that often occurs with brain injury. However, the opposite or very high sodium concentrations are also not good. As you said, a diet high in salt can lead to high blood pressure and chronic high blood pressure can cause damage the small blood vessels in the brain and cause small strokes over time or very high blood pressure can cause larger bleeds. Usually we see this in patients with very high uncontrolled blood pressures in the 170-200s systolic range. I'm kind of pulling those numbers out of my memory and you would have to check the literature to verify.

Thanks for the answer. I have a very frequent and apparently strong pulse, but low blood pressure. Does low blood pressure mean that I'm 'safer' when eating salt than other people? Also how do I detect small strokes?


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What are the advantages and disadvantages of using beta-galactosidase compared to luciferase as a reporter gene?
In the University labs, we have used Beta-galactosidase as a reporter gene to quantify the expression initiated by the stress-response promoter in yeast. This was done by exposing one of the two groups to osmotic stress (high salt concentration) whilst the other was unstressed. Then the levels of beta-galactosidase were compared.
A question given to us afterwards asked to give advantages & disadvantages of using Beta-galactosidase compared to Luciferase as a reporter gene in this experiment. And which one would be, overall, more suitable?

Beta-galactosidase (B-gal for short) is an enzyme that will process the substrate lactose. In applications using B-gal as a reporter (lacZ gene), two lactose analogues are commonly used: X-gal or ONPG (as pointed out by @Alan Boyd). Both substrates are colourless, becoming coloured once hydrolyzed by B-gal. The formation of this colour allows B-gal to be assayed by means of either visual inspection, or more accurate means by using a spectrophotometer or camera.
When X-Gal is hydrolyzed, an insoluble blue dye is formed. Evolution of blue colour is intensified as more substrate is hyrolyzed, allowing for quick blue/white screening by visual inspection in common applications of cloning and gene expression. Using the X-gal substrate, B-gal assays are more sensitive to gene expression (the dye precipitates out and retains colour very well), however X-gal is not quantitative (Möckli & Auerbach. BioTechniques 36:872-876 (May 2004)). In contrast, ONPG hydrolysis evolves a soluble yellow dye. This colour developement is quantitative, however is less senstive than X-gal because the linear relationship betwen light absorption (at 420 nm) and substrate concentration is small. Using ONPG as a B-gal substrate allows for quantitative measurement of B-gal activity (and therefore promoter activity). (Note that ONPG itself is not capable of inducing the lac promotor, unlike X-gal.)
Luciferase reporters (there are actually a few different luc genes) operate in a similar fashion. The enzyme cleaves its substrate, however instead of yielding an insoluble blue dye, emits a characteristic photon. Luciferase activity must be measured using specialized camera hardware to detect and count photons emitted from your yeast clones. This assay will still answer yes/no reporter questions, but can also be quantified to look at how much the reporter was activated. Luciferase activity is a quantitative reporter while also yielding spatiotemporal information.
The choice of reporters depends largely on the question you wish to answer. If promoter induction is relevant (eg, the stress-response promoter was activated), then luciferase or B-gal with X-gal are best suited for their higher sensitivity. Given that luciferase requires a special camera and optical filter (such as a gel documentation system), X-gal is ideal because it may be screened by eye. If promoter activity is being assayed, then B-gal+ONPG or luciferase will yield quantitative measurements of reporter gene activity, and require at least a spectrophotometer.
Given these are university labs, I assume that materials costs are to be minimized and ease of experimental protocol to be maximized, B-gal is the ideal reporter. Luciferase requires: more costly substrate; specialized equipment; careful handling of materials, and more time (as screening necessarily takes longer, therefore lower throughput for a lab demo setting).

I'm pretty sure that Xgal isn't an inducer of lac expression otherwise we wouldn't add lots of IPTG in blue-white screen plates. And in any case this really wouldn't matter if we are talking about using reporters for measuring the activity of other promoters, because a lac inducer would be irrelevant.

@AlanBoyd the induction of lac is irrelevant to the discussion, but I've included it for completeness. IPTG is only required if lacZ repressor is overexpressed. For example, blue/white screening is easily achieved with X-gal alone for DH10B (TOP10) strains, Mach-T1, DH5A-T1, but not others (see page viii: http://tools.invitrogen.com/content/sfs/manuals/topota_man.pdf ).

Here a list of other luciferase assay shortcomings.

I think that @leonardo has this backwards. β-galactosidase can be assayed accurately and cheaply using ONPG as a colorimetric substrate with no solubility problems. All that is needed is a spectrophotometer: my guess is that this is the assay the OP used in their experiment. So my answer is - use β-galactosidase for inexpensive quantitative analysis - no need to add luciferin and ATP or to worry about oxygen availability. I'm struggling to think of a disadvantage for β-galacosidase - maybe there are higher background levels from other cellular glycosidases, whereas there will be no background luciferase activity?

I was unaware of ONPG as a substrate for B-gal. Indeed, the problem with X-gal is that after hydrolyzation, the blue dye formation is not sensitive enough for quantitation (eg, PMID: 17957822). Whereas with luciferin, evolution of photons gives sensitive spatial and temporal information with no background (relative to B-gal). There is still a big cost differential between the two, which can be a concern for university labs.

Edited my answer to reflect info in your post.

I realize this question is about yeast, but I'm afraid that people may try to expand the answer to all systems, and beta galactosidase is not good for all systems, particularly for animal studies. I've seen too many gene therapy papers try to get away with using it.
Beta galactosidase is not a good reporter gene for in vivo gene delivery studies. There is too much endogenous activity in most tissues to distinguish the exogenous activity. When doing non viral gene delivery, the amount of DNA expressed is often so low that you cannot overwhelm the endogenous activity and therefore cannot conclusively say the enzyme activity you detected is from your new DNA.
Luciferase is far superior for in vivo work. First, there is no endogenous luciferase activity in most animals ( you're out of luck if you're doing work on fireflies ) so you can be sure that any luciferase activity you detect is real. Luciferase activity can be determined noninvasively though bioluminescent imaging, allowing for repeated measurements on the same animal. Beta glucosidase can require killing the animal, dissecting the tissues, preparing microscope slides, and then analysis, so doing a time course study will require using many more animals.
The only advantage I can see beta glucosidase having over luciferase is if you want to see what percentage or precisely what type of cells are expressing the reporter gene. However, I think GFP or another fluorescent protein would be more appropriate because of the endogenous activity issue I described earlier.
Again, my answer applies for animal use. If you're just growing yeast on a plate, the beta galactosidase is probably the cheaper way to go. We did some 384 and 1536 well plate assays on primary hepatocytes with luciferase, and the luciferase reagent was about $250 for 10mL. You might also consider fluorescent proteins for screening. I've made bactieral colonies with RFP that were visibly red, so no need for UV, but even if you need UV light to see the fluorescence, a standard UV transluminator for viewing gels will be good enough, and no extra reagents to add.


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What happens when we know that there is something that we forgot but we can't remember what it was?
I think it happens for everyone that sometimes we go to a room and forget why we went there. Is there any research or article on this?

It is a phenomenon known as room amnesia, some research has shown that your brain may use physical barriers like the room and doorways as a way to compartmentalize thoughts.
One article summarizes it here:

The researchers say that when you pass through a doorway, your mind
  compartmentalizes your actions into separate episodes. Having moved
  into a new episode, the brain archives the previous one, making it
  less available for access. It’s as if you slam a mental door between
  what you knew and…what was I saying?

This is the research.

Nice! I wonder if this works with transparent walls. Perhaps Japanese style semi-transparent paper walls?

Try it! Go to your local garden centre, stand in a display greenhouse, think of something to go and buy, then walk out of the greenhouse and see if you remember!

Thanks for the concise yet comprehensive answer.


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How are lysosome membranes protected from the attack of hydrolases?
Lysosomes are a bit like the suicidal bags of cells. They help to clean cells, have an acidic pH and contain a large number of hydrolyzing enzymes.
But why don't these hydrolyzing enzymes attack and destroy lysosomes' membranes?

Early histochemical work indicated that the internal surface of the lysosomal membrane has a glycocalyx - a layer of polysaccharide, presumed to have a protective role.

Neiss, W. F. (1984) A coat of glycoconjugates on the inner surface of the lysosomal membrane in the rat kidney. Histochemistry 80, 603–608

Subsequently it was found that major membrane proteins of the lysosomal membrane are protected from proteolysis by glycosylation:

Kundra, R. and Kornfeld, S. (1999) Asparagine-linked oligosaccharides protect Lamp-1 and Lamp-2 from intracellular proteolysis. J. Biol. Chem. 274, 31039–31046

See this paper for a more recent study of another lysosomal membrane protein:

Schieweck O. et al. (2009) NCU-G1 is a highly glycosylated integral membrane protein of the lysosome. Biochem. J. 422: 83-90

NCU-G1 is the mouse orthologue of the human C1orf85 protein. The NCU-G1 gene encodes a 404 amino acid protein. This is a Type 1 transmembrane protein - i.e. the N terminal domain is directed to the extracytoplasmic surface of the membrane. In vivo the protein is detected in 70 kDa and 80 kDa forms. The discrepancy between the polypeptide size and the molecular mass is shown to be due to extensive glycosylation. The protein sequence includes 9 potential glycosylation sites.


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How much weight/volume do microbes occupy within the human body?
Microorganisms constitute the bulk of all the biomass on Earth. I weighed myself yesterday, and wondered how much less I would weigh if I were completely free of bacteria and microbes, inside and out.
Approximately how much weight and volume do microbes occupy within the average human body? How were these values obtained?

@AlanBoyd's calculations are reasonable, I think the estimate is off though.  The human microbome includes other bacteria which are not necessarily E.coli equivalent.
The human microbome projects give estimates that microbes are 1-3% total body mass.  i.e. several pounds of bacteria.
The GI tract alone has most of the microbome mass - faeces is ~60% intestinal flora/fauna by dry weight, which for many adults alone must be hundreds of grams at any given moment.

The bacterial flora weighs approximately 90 g and, assuming bacterial cell density is approximately 1 g ml-1, occupies a volume of 90 ml.
The human body has 1013 human cells and hosts 9x1013 bacterial cells.
One E. coli cell has a mass of 0.95×10−15 kg (wet weight).
Assuming that E. coli is typical with respect to mass of human microbial flora:
mass of bacterial cells in one human body = (0.95×10−15 * 9x1013) kg
 = 0.0855 kg = 86 g

Just human intestines have over a kilogram of bacteria! A good enema will leave you 2kg lighter and that's mostly bacteria.

The number I read where more like 1-2 orders of magnitude more bacterial cells than cells in our body.

According to this source, it's about 2 kg:

Our gut microbiota contains tens of trillions of microorganisms,
  including at least 1000 different species of known bacteria with more
  than 3 million genes (150 times more than human genes). Microbiota
  can, in total, weigh up to 2 kg. One third of our gut microbiota is
  common to most people, while two thirds are specific to each one of
  us. In other words, the microbiota in your intestine is like an
  individual identity card.

Other source, confirm it:

Le chiffre a de quoi surprendre. Il s’explique par le fait que les
  bactéries sont en général beaucoup plus petites que les cellules de
  notre propre organisme. Il y en a donc une quantité énorme dans un
  volume restreint; enfin sachez quand même que nous portons en moyenne
  1 à 2 kilos de bactéries, pour la plupart localisées dans notre colon.
  Il semblerait d’ailleurs que le colon humain soit l’un des écosystèmes
  les plus denses que l’on connaisse.


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What types of archaea have been found in animals?
I am curious as to the species or "types" of archaea that have been found to reside within animals symbiotically. One of the only ones I can think of off the top of my head are methanogens, which live in the gut of ruminants for example.

Humans:
A pioneering study using 16S RNA primers found only Methanobrevibacter smithii in the human intestine.

Eckburg PB et al. (2005) Diversity of the human intestinal microbial flora. Science 308 1635-1638

In a recent review there is a comprehensive Table of archaea found in humans (this includes non-intestinal flora):

Dridi B et al. (2011) Archea as emerging organisms in complex human microbiomes. Anaerob2 17: 56-63

Much of the work that is catalogued by Dridi et al. is repeated identifications of Methanobacteriales (Methanobrevibacter smithii, Methanosphaera stadtmanae and Methanobrevibacter oralis), but there are others from the Thermoplasmateles, the Halobacteriales and the Sulfolobales, plus some that are thought to be members of unknown archaeal orders.


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How much energy does human body fat contain?
I have been reading the Wikipedia article about food energy, but as I'm not a biologist, I don't really understand it properly, so I came here to ask you guys.
My question is: If a human body needs X kcal of energy and it's taking it from the stored fat, how much fat (weight/kg) does it need to burn?
I know that 1 gram of fat represents 9 kcal of energy, but according to the food energy article, the efficiency of getting that energy isn't 100%, so the formula might be a lot more difficult.
I'm not sure what is the real efficiency value here. The article mentions more values, ranging from 18% to 40%.
P.S.: If this belongs to Chemistry.stack, please, tell me or move it there.

For your question, the body would never just burn fat - that physiologically impossible. Your question, however, is common for people trying to lose weight. Most answers are oversimplified. In the literature and on my public websites you can find values for "one pound" of fat being approximately 3500 calories. Thus, people try to make the statement - "I want to lose 5 pounds, so that means I need to burn 3500 x 5 = 17,500 excess calories". It doesn't really work that way, because they body does a great job at adjusting and conserving energy though adjustment of energy expenditure.

I am not sure if I am able to answer your question, but I will give it a try and hope that someone tells us if I'm wrong.
Biologists talk about different kinds of energy depending on where you measure it. The first measurement is the gross energy (GE) which is measured through bomb calorimetry and is basically how much heat a substance gives off when completely burnt. I have recently read in a compendium that the GE value of fat is ~9,4 kcal/g.
The next stage is digestible energy (DE), which is how much of the forage you actually can digest, which would exclude for example fibres.
Next stage is the metabolizable energy (ME), the energy which can be used in actual metabolism (DE - energy losses from transporting nutrients etc). This are the value you reported. (I don't have a source, but I've heard the same values from multiple recognized sources.)
Now is the part where it gets a bit trickier, as the final measurement of energy is the net energy (NE). This is defined as the metabolic energy minus the heat increment, which could be simplified as the energy losses through the conversion between different types of energy (ie. from long carbohydrates into glucose etc.) within the body. Even more simplified it can be said to be the difference between the heat production in a fastened person and the heat production in a fed person, thus being the heat produced by eating, digesting, absorbing and transporting food.
I argue that because the fat already is incorporated in the body it has a very efficient value, and very little transportation within the body is needed. And because the energy (ie, the fat) is internal, it is not accounted for in the heat increment and therefore the NE of internal fat is the same as ME.
And according to the wikipedia-article you linked to United Nations recommendation of the average minimum energy consumption per person is 1800 kcal/day. Thus the amount of fat required to meet the minimum energy requirements of a person would be 1800/9=200g of fat per day.
If you want to read more about the different energy-measurements and the heat increment here is a good link. And don't forget that energy alone is not sufficient for a person as we need protein, vitamins, minerals etc...

Does fat tissue contain any water? Because if it does, than you will not get 9*200 calories from 200g of fat.

Fat does contain water - just like every other cell in the body. Relatively speaking, it just has a lot less given that it's storing a bunch of triglyceride.


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Will a completely removed cat whisker grow back?
I just accidentally pulled out, while playing, my cat's whisker entirely, follicle and all. I feel terrible as I know she is a kitten and whiskers are rooted deep in a place rich in nerves. I'm wondering if the whisker will grow back and if it will cause a lot of pain as it regrows.

If you're concerned about the pain aspect, approach your vet, as I'm sure they would be able to tell you how to treat it.

The short answer is that yes, they will grow back. Cats do regularly shed their whiskers and grow them back in time (reference). The thing is that if damage has been done to the root of the whisker, it may grow back in an irregular manner (reference). Wish for the best and by now I think the whisker should be back just fine.


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Is the amount of phosphoric acid added to colas enough to disrupt the function of the kidney over the long term?
Both Coca-Cola and Pepsi add phosphoric acid $H_3PO_4$ to their colas to give them a signature "bite".
The kidneys use a phosphoric acid/dihydrogen phosphate/hydrogen phosphate homeostasis as one mechanism to eliminate/excrete excess acid from the body.
The issue of whether sodas containing phosphoric acid can exacerbate osteoporosis and related conditions has been explored here and in some detail on Wikipedia, but I'm more interested in direct effects on the kidney.
I'm interested to know if the overall renal physiology is adversely affected by extra phosphoric acid that long-term moderate consumption (say a single 2L bottle per week for a year) of soda would introduce (including interrupting or saturating the Na-Pi transporter)?

Could you define "long-term"? Say, one 200ml can of soda/day for 10 years?

@nico That's a good idea.  I was trying to make it more abstract and less "medical advice"y.

It's just that I have the feeling that the result would vary a lot depending on the frequency of assumption (not that I have any data whatsoever regarding this issue. Very interesting nevertheless!)

The phosphoric acid in cola will contribute to dietary intake of phosphate. I may be missing something, but, since the transporter functions to reabsorb phosphate that has been filtered out at the glomerulus, excess phosphate will spill over into the urine.
According to Wikipedia the RDA for phosphorus is 700 mg and the tolerable upper intake level is 4000 mg. Coca cola contains 17 mg phosphorus (as phosphate) 100 ml-1 (which is 340 mg in 2 L)
According to this source,

in the United States, an average person drinks 412 8-ounce drinks — or 3296 ounces — of Coke per year.

This works out at 9 oz per day = 266 ml = 45 mg phosphorus
For comparison (from here):

white flour contains 595 mg 100 g-1
one boiled egg contains 220 mg
canned salmon contains 240 mg 100 g-1

No, you didn't miss anything, great answer!  I was thinking about the precision of the acid-base balance of that particular system being disturbed (realizing, of course, that it potentially only handles "spillovers" from the bicarb system, I think).  It's interesting to see the comparison of the content with other foods, though I'd be curious about how much of that in the egg, etc., is AMP/ATP and others.

Brain fart on selecting this as the answer, sorry for the delay.


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Does finite rate of increase depend on mortality of individuals in a population?
As written in my lecture handouts, there two main factors in the Geometric Growth Model of populations:
$R_{0}$ is the expected lifetime reproductive output. This way, for unicellulars, for example, when time between division represents life time, if there is no mortality, $R_{0}$ is calculated as $R_{0}=1*2$, where 1 is 100% and 2 is the amount of daughter cells expected to be produced as a result of the mother cell split. We also define that for this isolated incident, $B$, the amount of births is 2, while the mother cell "dies", which leads to $D=1$.
The second factor is $\lambda$, which is the finite rate of increase, which in other words means that this is average per-capita multiplication factor per one time-step.
When we measure population growth in time-steps of 1 lifetime, we can conclude that $\lambda=R_0$. We actually look at $\lambda$ as at $\frac{N_{t+1}}{N_{t}}$, where $N_{t+1}=N_{t}+B-D$(1) and $N_t$ is the amount of individuals in the populations at time-step $t$. This way we define $\lambda$ using $b=\frac{B}{N_{t}}$ and $d=\frac{D}{N_{t}}$: $\lambda=\frac{N_{t+1}}{N_{t}}=\frac{N_{t}}{N_{t}}+\frac{B}{N_{t}}-\frac{D}{N_{t}}=1+b-d$.
All fine when we deal with ideal conditions, where all mother cells divide and there are no mortalities or mutations.
But suppose we're told that only 80% of the mother cells will divide, and the remaining 20% will die without division. In this case: $R_{0}=0.20*0+0.80*2$.
What I'm trying to understand, how will $\lambda$ be affected by this? Does $\lambda$ refers to ideal conditions only, or it depends on the natural situation?
(1) We ignore Immigration and the Emigration at this point.

*It's been several years since I've worked with similar equations. The following reply is based on memory, and if anyone has a firmer grasp of the materials, please modify or answer as you see fit.
I would assume λ is under ideal conditions or as an average of whatever species you're working with. Your modified lifetime reproductive output still leaves out many variables which can affect λ. By your own words it leaves out mutations and daughter cells that are dead-on-arrival. There could also be predation or conditions where the Mother-cell produces more than one Daughter-cell, resulting in R = 3 instead of 2 and your subsequent λ also being 3. UCLA Bioengineers have actually observed up to 5 daughter cells in cancer lines.
I'm not sure what you mean by "... or it depends on the natural situation?", but ultimately reality is always more complicated than basic equations usually describe. Either B or D can increase or decrease, depending on the species, environment, and how you define t.
Your equation still produces a population increase, just at a slower rate than your ideal conditions. If you're asking if there's a specific definition for "λ" referenced in your equation, I'm not aware of any specific definition for "λ" - it's not a Constant.
Your title question - does the rate of increase depend on mortality - is ultimately "Yes." If mortality is higher than the birth rate, then you will see a decrease of the population until extinction is reached if there isn't an equilibrium or rebound.
However, most populations change at an Exponential rate - NOT Geometric. To that end, you might be interested in the r/K Selection Theory and how they operate within Exponential equations (which are similar to your Geometric equations). In short, r-Selection is the reproductive strategy of producing extraordinary amounts of offspring with a very, very low survival rate. However, because so many are produced you only need a small overall percentage of survival to maintain or increase populations. The tapeworm I mentioned above is one of the stereotypical examples. K-Selection represents species that invest additional resources into raising a few offspring, usually just a handful that are carefully watched over and raised by the parent(s) until they are capable of reproducing themselves. Humans, elephants, most birds, and larger animals in general are K-selected.
For r-Selection your B and D will both be very high, and for K-Selection both B and D will be low. However, both will result in a positive λ simply because it's all about the ratios.

Thanks for your answer. I will look into r/K Selection Theory.

r/K selection is just as relevant for populations with discrete growth. However, the whole concept of r/K selection has also been challenged - for an overview see Reznick D, et al. 2002. r-and K-selection revisited: the role of population regulation in life-history evolution. Ecology, 83 (6): 1509–1520 and this nice blogpost Oikos blog: Zombie ideas in ecology: r and K selection.

The same relationship still holds, and $\lambda$ just describes the finite population growth rate under a particular set of conditions. 'Ideal' conditions (whatever that means) are not implied. Generally you can write: $\lambda = e^r = R_0^{1/G}$, where $G$ is the (average) generation time. However, $r$ (the instantaneous/intrinsic rate of increase) is not really relevant for an organism with discrete reproductive events (i.e. geometric growth)
So for your second example where $R_0$=1.6, assuming that $G$=3 timesteps, $\lambda$= 1.169. However, as hinted above an exponential model is generally a better fit for unicellular organisms.


text:
Do memories have mass?
If it were possible to live forever, would our brains grow infinitely with the number of memories that we store? Or would we remove old memories as we create new ones?

there is a related discussion on CogSci.SE.

Does your computer get heavier, the more data you store on its hard drive?

You would need to live a long, long, long, long time for this to become remotely problematic.
Your question seems to suppose that a memory is "stored" by a neuron, and since neurons have mass, then the more memories we have the more our brains will weigh. Actually, neurogenesis is pretty rare in the adult brain--most of the cortex is fixed, and new neurons do not grow. (The hippocampus is the best known counterexample, but it's important to note that contrary to lore, the hippocampus doesn't store memories per sé, though it is involved in the formation and retrieval of memories).
Memories are represented in the brain as patterns of firing neurons. Let's say, for simplicity, that each neuron can either be on or off. Since there are 86 billion neurons in the brain, we can experience 2^86bn possible brain states. That's a lot.
Of course there are a lot of simplifications here--most notably, there is a lot of structure to the brain, and so i'm not suggesting you can store 2^86bn memories--but the logic is the same. Even with only 1,000 neurons, we can store a ridiculous amount of information (2^1000).
I would like to comment on MCM's answer as well, because I don't think it's true that we "remove" old memories. Or rather, the topic is still being debated in cognitive science today. For an old take on it, see renowned memory researcher Endel Tulving's (1974) article, in which he says:

When we forget something we once knew, it does not necessarily mean that the memory trace has been lost; it may only be inaccessible

The idea is that some memories are suppressed (no, not repressed), being rendered inaccessible. Robert Bjork and John Anderson have (separately) done some nice work in this area.
So before you worry about this becoming a problem, I suspect you need to work out the secret of immortality first.

Tulving, E. (1974). Cue-Dependent Forgetting: When we forget something
  we once knew, it does not necessarily mean that the memory trace has
  been lost; it may only be inaccessible. American Scientist, 74-82.

The expected number of atoms in the universe is around 2^{266}, very far from your figure.

whoops, you're right. math error, should've noticed it. i've rolled back to the previous edit.

Why are you assuming that 1000 neurons give 2^1000 possible states? A neuron can be connected to multiple neurons, and certain connections are stimulatory and certain inhibitory, it is wrong to compare biological neuronal network to computational neuronal network, because that is not how things work in the brain. On the other hand, having 86 billion neurons is very different than having 86 billion neurons involved in memory formation...

as i said, i oversimplify things quite a bit. my point here is simply to show that if memories are represented as patterns of neuronal firing, the combinatorics is such that the brain has a vast amount of 'storage', even if only a miniscule fraction of those patterns could represent memories. im happy to edit if you have suggestions to make this more clear, but i'm not trying to make any claims about hard numbers.

We already remove old ones and create new ones. I doubt you remember most of Geometry, for instance.
As for capacity, this article from Scientific American gives a good overview of what we can estimate with our current knowledge.

For comparison, if your brain worked like a digital video recorder in a television, 2.5 petabytes would be enough to hold three million hours of TV shows. You would have to leave the TV running continuously for more than 300 years to use up all that storage.
The brain’s exact storage capacity for memories is difficult to calculate. First, we do not know how to measure the size of a memory. Second, certain memories involve more details and thus take up more space; other memories are forgotten and thus free up space. Additionally, some information is just not worth remembering in the first place.

So, there is an upper limit. Where is it? Well, probably a bit longer than our reasonable lifespan at the moment.

You've struck upon an interesting point with your example, actually, someone who is a surveyor would probably remember a lot of geometry.  Our ability to do so depends on context and usage of the information.

Two downvotes without a comment? Jeez. People, I implore you, if you think my answer is inadequate - say as much. I will happily do further research if I have the time and willpower.

I have not downvoted (nor upvoted) the answer but personally I really don't like when journalists amuse themselves speaking of petabytes of information, as if the brain was a computer. It is not and the reality is that we currently do not know enough about memory formation to give any meaningful answer to this type of problems.

@nico - The author is a Professor of Psychology, not a journalist.

@MCM: even if he was a Nobel Prize I would maintain my point...

@nico - Sure, but at least you voice your point. ;)

We already remove old memories (well, more properly unimportant ones) partially in order to make room for new ones
There are 3 different levels of storage, but none of them involve an increase of mass. (Distribution of mass, in one sense, but not amount thereof.) I'm not a neuroscientist, but there are one or two lurking around here who can correct anything wrong that I say, so don't take me as an authority. As I understand it: the first level is strictly electrochemical and very short-lived (except in some savants), such as what was the last word that you heard or the last time that you cracked your knuckles. Once the experience is over, it is forgotten. The second is just chemical, as proteins or whatever organize themselves into patterns that are essentially "books". That is what happens with stuff that you need to keep, such as school lessons, tax laws, or whatever. The third is DNA transcription, wherein a memory becomes an intrinsic part of your existence and might be inherited (as in "instinct" or even transplanted to another person.


text:
What mechanisms do animals living in groups (herds, packs, swarms) have against spreading contagious diseases?
While for example a wolf pack provides protection to a sick wolf, increasing its chance of survival, there is a risk of infecting other members of the pack, decreasing their total chance of survival.
Do animals have mechanisms for preventing that? For example the sick member leaving its group temporarily?

Diversity in immune genes within the population could be something.

Three proposed mechanisms:

altruistic self-removal (i.e., diseased individuals leave the group to prevent transmission to kin) has been documented in eusocial insects (ants and bees); Rueppell et al 2010 J. Evol. Biol. say:

altruistic self‐removal by sick social insect workers to prevent disease transmission is expected under most biologically plausible conditions. The combined theoretical and empirical support for altruistic self‐removal suggests that it may be another important kin‐selected behaviour and a potentially widespread mechanism of social immunity.

social distancing/avoidance: This is a commonly used term in human infectious disease epidemiology for the practice of avoiding contact with infected people. I don't know of any great references, but Loehle 1995 Ecology "Social Barriers to Pathogen Transmission in Wild Animal Populations" says:

Data on animal behavior in this regard [social avoidance] are sketchy. Sick individuals in cattle herds do seem to be isolated somewhat from the group (L. R. Rittenhouse, Department of Range Science, Colorado State University, and Ray Strickland, University of Maryland, personal communication 1988), though whether by chance (failing to keep up with the group due to listlessness), by voluntary isolation, or by avoidance on the part of others is not clear. Edwards (1988) found a higher degree of investigatory behaviors but a lower degree of touching between other group members and mice infected with Trichinella spiralis, though this disease is not transmissible by contact. This example would fit the proposed behaviors perfectly. More study is needed.

seasonal migration has been proposed as a way for group-living organisms to temporarily leave their habitat, allowing the built-up parasite burden in the environment to diminish before they return; it may also have a group-level effect of filtering out diseased individuals.

Folstad et al. 1991 Can. J. Zool. Parasite avoidance: the cause of post-calving migrations in Rangifer?

Intensities of warble fly larvae, Hypoderma tarandi (L.), were examined in slaughtered reindeer (Rangifer tarandus tarandus L.) from different summer grazing areas of Finnmark County, northern Norway. To test the hypothesis that larval abundance decreases with increase in post-calving migration distance (i.e., distance from calving grounds), herds with differing migration distances were sampled. The prevalence of infection in the total sample of 1168 animals was 99.9%. The study revealed significant differences in larval abundance among herds from different summer grazing areas. Herds with post-calving migrations have significantly lower larval abundances than herds remaining on or near the calving grounds for the whole summer. Between-herds variation in abundance of H. tarandi larvae is assumed to reflect differing densities of the infective stage (adult flies) on the herds' summer ranges. Larval abundance in a herd is in turn negatively correlated with the distance between the main larval shedding areas (i.e., calving grounds) and the areas of greatest transmission (i.e., summer pastures). These results are discussed in relation to transmission of other parasites common to Rangifer and suggest that this host's post-calving migration may be a behavioural adaptation that reduces levels of parasitic infections.

Loehle 1995 also discusses this (qualitatively/speculatively):

A more subtle effect results from migration. Consider a species that migrates seasonally some large distance. An area that becomes fouled and unsanitary during one season will become largely clean again by the following year. In between, nest and skin parasites such as ticks and fleas will have nothing to eat and will be greatly reduced in number. For example, wide spacing in rabbits results in reduced flea numbers (Mohr 1963) for these same reasons. Excrement piles will decompose between seasons and wash away. Significant benefits could thus accrue to migratory species, even though long distance migratory behavior is not likely to have arisen from this cause alone. (It may result from predator avoidance [Fryxell et al. 1988], or more commonly be due to weather and food supply factors.) Abandonment of rookeries during the non-mating season might, however, be the result of disease avoidance. Another consequence of migratory behavior is the effect on internal parasites ...  Consideration of epidemiology thus leads to some unexpected benefits of migratory behavior.

Hall et al. 2014 J. Anim. Ecol. "Greater migratory propensity in hosts lowers pathogen transmission and impacts" explore a theoretical model of migration effects.

Almberg ES, Mech LD, Smith DW, Sheldon JW, Crabtree RL (2009) A Serological Survey of Infectious Disease in Yellowstone National Park’s Canid Community. PLoS ONE 4(9): e7042. doi:10.1371/journal.pone.0007042

The authors found that the majority of Yellowstone wolves had been exposed to a number of different viruses (evidence from antibodies in blood samples).
They also found evidence for historical outbreaks of canine distemper virus in wolves, coyotes and red foxes in 1999 and 2005. These outbreaks correlated with peaks in wolf pup mortality.
This evidence suggests that wolves have no mechanisms for avoiding the spread of these viral diseases. Perhaps periodic episodes of increased mortality are the price that has to be paid for a longer-term 'herd immunity'?
Edit - in response to OP comment below:
The data indicate very high levels of seropositivity to the viruses. I would say that 'not 100% successful' is an understatement. But I must admit that I am way out of my area of expertise here!
From the abstract:

We found high, constant exposure to canine parvovirus (wolf seroprevalence: 100%; coyote: 94%), canine adenovirus-1 (wolf pups [0.5-0.9 yr]: 91%, adults [>or=1 yr]: 96%; coyote juveniles [0.5-1.5 yrs]: 18%, adults [>or=1.6 yrs]: 83%), and canine herpesvirus (wolf: 87%; coyote juveniles: 23%, young adults [1.6-4.9 yrs]: 51%, old adults [>or=5 yrs]: 87%) suggesting that these pathogens were enzootic within YNP wolves and coyotes.

That's very interesting. But I think the conclusion is not completely correct. I'd rather conclude that "based on the evidence, if wolves have mechanisms for avoiding the spread of those diseases, they're not 100% successful." It could be that they have such mechanisms, and without them, the mortality would be even higher. The last sentence is an intriguing point. Perhaps from evolutionary perspective it's better to let the whole pack/herd become infected and if it survives, all the survivors will be immune.

(This answer is still a work in progress, but I'll work more on it eventually...)
It's not terribly controversial to say that infected hosts may be more likely to be eaten by predators. However, at least one author (Smith Trail et al 1980; full reference below) has suggested that this could be adaptive; in some sitautions there could be a net gain to inclusive fitness if, by 'submitting to' predation, infected hosts are able to reduce the force of infection acting upon close relatives.
(Full reference: Smith Trail DR. 1980 Behavioral interactions between parasites and hosts: host suicide and the evolution of complex life cycles. American Naturalist 116, 77-91)


text:
Structures of cyclodextrin complexed with small ligands
For some structural study I am looking for cyclodextrin strucutures (in 3D format such as pdb, mol2, etc) complexed with small molecule ligands, such as cholesterol and even smaller. Right now I could only find on the PDB database some proteins complexed with cyclodextrin, but no structure of cyclodextrin with small ligands, could you help me?

I looked for relevant publications at Web of Science using 'structur* AND cyclodextrin' in the Title field. For the period 2011-2012 there were 56 hits including:

Racz et al (2012) Structure of the inclusion complex of beta-cyclodextrin with lipoic acid from laboratory powder diffraction data. Acta Crystallographica Section B 68: 164-170
Ali et al (2012) Structure determination of fexofenadine-a-cyclodextrin complex by quantitative 2D ROESY analysis and molecular mechanics studies. Magnetic Resonance in Chemistry 50:299-304
Lula et al (2012) Interaction between bradykinin potentiating nonapeptide (BPP9a) and beta-cyclodextrin: A structural and thermodynamic study. Materials Science & Engineering C 32: 244-253

I looked at some of the papers but I didn't find any specific case where a structure has been deposited in a database. There were, however, several mentions of the Cambridge Crystallographic Data Centre  as a source of small molecule structures.

this is great! I will check whether the structures have been deposited somwhere


text:
Where does the 'C' in exhaled CO₂ mostly come from?
When a human being exhales CO₂, what is, by the numbers, the main source of carbon atoms exiting the body in this way? I mean what class of cells, or which tissues are the biggest on a pie chart of where carbon atoms breathed out in the form of CO₂ molecules came from?

Duh, I just realized it's probably mostly from leftovers after the sugars that you eat are burned for energy. I've also heard that broken-down fat from weight-losers gets breathed out. Is that at all true?

yes, the CO2 is the product of various metabolic processes. I can expand if you want...

CO2 is a product of Cellular Respiration, which generally takes Glucose and molecular Oxygen to produce Carbon Dioxide, water, heat, and allows ADP to be regenerated into ATP (or other various oxidation reactions). The Carbon comes from wherever the acetyl-CoA used in the Citric Acid Cycle came from - either carboyhydrates or fatty-acids (saturated carbon chains).
Simplified reaction:   C6H12O6 (s) + 6 O2 (g) → 6 CO2 (g) + 6 H2O (l) + heat
So, you are correct. CO2 transferring out of the lungs is mostly the result of burning sugars (or fats) for energy (the regeneration of ADP/GDP with respect to human biology).
To that end, the tissues that produce the most CO2 will be the cell-types which constantly require energy. Nominally, muscle tissues.
Per your comment, broken down fat, or rather, the process of Fatty-Acid Catabolism, results in the production of acetyl-CoA, which is a primary player in the Citric-Acid Cycle. The Citric Acid Cycle, which you should recognize as the Cycle that Pyruvate - the end result of Glycolysis (the breakdown of Glucose into 2x 3-Carbon Pyruvates) - also goes into after being converted into acetyl-CoA by Pyruvate Dehydrogenase.
The sum of all reactions in the citric acid cycle is:
Acetyl-CoA + 3 NAD+ + Q + GDP + Pi + 2 H2O → CoA-SH + 3 NADH + 3 H+ + QH2 + GTP + 2 CO2
So, for a basic breakdown with respect to CO2:

Carbohydrates (Sugars, Starches) → Glucose → Pyruvate + ATP + NADH
Pyruvate → Acetyl-CoA
Lipids (fats) → Lipolysis → Acetyl-CoA
Acetyl-CoA + ... + H20 → ... + CO2

In the resting state it's the brain that is responsible for the largest proportion of cellular respiration: estimates vary but are usually in the 20-25% range. This is because even at rest the nervous system is working hard to maintain the ion gradients that are essential for propagation of action potentials.

At rest, the main sources of CO2 are the brain, liver and heart.
The original questions seems to me to be asking for information about which tissues or organs are responsible for producing most of the exhaled CO2. As other answers have mentioned, CO2 production by cells reflects the amount of oxidative metabolism that is being carried out. This means that we can answer the question by simply asking - which tissues/organs are responsible for consuming the most O2?
There are many sources of information about this, but the most succinct statement that I have found is here:

The average human body of 139 lb (63 kg) consumes 250 ml of O2 each minute. The major single-organ oxygen consumers are the liver, brain, and heart (consuming 20.4%, 18.4%, and 11.6%, respectively), while the sum total of all the body's skeletal muscles consume about 20%. In addition, the kidneys use up about 7.2%, and the skin uses 4.8%. The rest of the body consumes the remaining 17.6% of the oxygen. Oxygen use can also be measured per 100 gm of an organ to indicate concentrations of use; as such, heart usage is highest, followed by the kidneys, then the brain, and then the liver. During exercise, the biochemical oxygen demand increases for active tissues including the heart and skeletal muscles.

Other sources are in broad agreement with this. Note however that these are values at rest. As the quotation states, during active exercise the skeletal muscle will become the major source of CO2.

The chemical formula for glucose is C6H12O6. When the body needs energy, the glucose molecule is broken down to give CO2 and water:
$C_6H_{12}O_6 + 6O_2 => 6CO_2 + 6H_2O$
Therefore, I think "C" comes mostly from glucose molecules.

The two main chemical processes in the human body that generate carbon dioxide (CO2) are:

Basal metabolic process of CO2 (CO2m) produced by the combustion of sugar in organs and tissues of the body.
Bacterial decay processes occurring as a result of activity of the microbial fauna in the colon. This forms CO2 (CO2c), H2, CH4 and higher hydrocarbons, NH3, H2S and other mercaptans.

The total level of carbon dioxide in the blood (CO2b) is therefore the sum of the metabolic (CO2m) and carbon dioxide arising in the large bowel (CO2c). In certain circumstances CO2c arising in the colon may be resorb into the bloodstream.

Could you add a citation or two to provide readers of your answers the chance to do further reading? It is considered a prerequisite for valid answers at Biology.SE to include references.  I type-edited your answer a bit. Welcome to Bio.SE and thanks for your contribution! +1


text:
When running a gel, what could cause a standard to run "faster" than usual?
We are running a gel on the products of a restriction digest to determine the size of an insert. We know the vector backbone size should be ~2.9kb; however, the standard appears to be running too quickly (or our samples too slowly), causing the backbone size to be about 4kb (which distorts our results for the insert size).
What could possibly cause this? Thank you.

Are the salt concentrations identical or similar in your sample and the standard?

Are you sure you have complete digest of the vector?

If the salt content or pH is different than "normal," run time can be affected. After all, you're applying an electric current to the sample(s) and ion concentrations and pH are sensitive to that current. Of these two, salt/ion levels are more likely to have an effect as your samples/markers are likely to be adequately buffered.


text:
Can a human smell through the ears?
The title does, prima facie, appear absurd.
Performing a swallowing action whilst pinching the nostrils shut gives the impression of listening through a bucket filled with water around the head; audible sound levels are perceptibly reduced. Some humans may encounter a similar sensation blowing their nose - hard.
This makes sense give the ears connect to the mouth/nose through the eustachian tubes. Can an odour make its way to the olfactory sensors through the ears?

do you mean "are there olfactory receptors in the ears" or "can smelly things make their way through our ears to the nose". Cause in the second case, the eardrum is in the way.

@Shep: The latter; sometimes when i put drops in me ears, i get this weird taste too ...

@Everyone - It doesn't take a high concentration of aromatic compounds in the air to actually stimulate a smell (or taste) response. I'd bet that enough of the drops vaporize in your local head-space that you end up tasting the stuff. Happens with me and menthol all the time.

A quick diagram to point out to people who may not know what Eustachian tubes are (#2).

In order for the aromatic molecule to reach the olfactory bulb, it would first have to get through the Tympanic Membrane (#22) [a.k.a. - Eardrum]. The Tympanic Membrane is water/airtight unless pierced.
So, while it's plausible that an aromatic molecule could travel through the Eustachian tubes and enter the pharynx areas, there isn't any way to get into the middle-ear in the first place unless the Tympanic Membrane has been compromised.
In a healthy and intact individual, the answer should be No.

TY, clear, and to the point.
p.s. I'm doomed )+:

@MCM gave a succinct and accurate description of how a healthy and "normal" person will not be able to smell via olfactory sensing trough the Eustachian tube.
Here is an interesting concept in which the brain is able to confuse senses, or alternatively, use sensory input as a metaphor for interpretation via another sensory output. This is a condition known as synesthesia. The majority of known synesthetes have cross-talk between audio-visual sensory pathways. That is, one may interpret sounds as shapes or colours, while another may interpret specific objects (or symbols) as colours or sounds. There were a handful of synesthetes studied in the late 1980's (referred to in this article by Day S.) and one patient was able to interpret sounds as smells. In the review article, smell-interpretation of sound accounts for ~0.1% of known synesthetes, while sound-interpreting olfaction is more common at ~0.6% incidence. On some higher level, the neural information for two senses is confused, and synesthetes that may confuse smelling for some other sense, can not technically perceive scent (using olfactory receptors) through other sensory organs (like the eyes), so the answer is technically no.

Day S. Psyche 1996, 2(32).

This blending of the senses in their perception is happening at a higher level in the cortex, though, the synesthetes are not actually smelling with their ears.

Exactly. Just as it's impossible for eyes to perceive sound, or to smell colours.

It's a fine answer, I just thought some further clarification that it was a negative answer to the question might be helpful to the OP (but I suppose we now have it here in comments anyway).

Modified 6 Dec 2012: One approach to this question is to perform a sequence similarity search for genes encoding genes with a functioning in sensing external stimuli, be they
olfactory receptor, taste receptor or other such genes that are expressed in cDNAs or RNA-Seq data from library preparations of the appropriate ear tissue. While there is not likely at this point in time to be much data available in RNA-Seq format, one might find cDNA libraries from cochlea or neighboring tissue.
A "hit," meaning there is evidence that, for example, an olfactory receptor gene is expressed in cochlea, eg, only means that there is potential to smell through the ears. Taste receptors are expressed throughout the alimentary canal in humans, but tasting the contents - food or other - is not readily perceived as de facto taste outside the oral cavity. Nonetheless, there is no reason not to expect such sensors are expressed to relay information to the brain as to what is or is not present. "Smelling" in/by the ear for the purpose of detecting the presence of a given entity or molecule could serve a similar function.

You jumped the gun a bit. You're addressing the literal interpretation of the title, instead of the hypothetical situation addressed in the question. ;-)

And in any case, I am afraid that your data would not support your conclusion. The expression of an olfactory receptor gene in cochlea only means that an olfactory receptor gene is expressed in cochlea. It does not necessarily follow that the gene's product has the same function there as it does in the nasal canal.

@terdon I wrote that expression of a olfactory receptor means there is the potential for that function and not an absolute, defined function.

I know, but I am a horrible pedant and have recently been working on ways of predicting protein function and this is one of my pet peeves :). To my great annoyance I cannot use expression data to infer function.


text:
What is the length of anaerobic biodigestion stages?
I have built an experimental portable batch biodigester to process organic garbage. A 50L drum filled half with garbage, half with water and with some cow dung added for inoculation, is connected from the top to a truck tire, boxed into another, larger drum.
I consider filling the bin within a week, based on the amount of daily garbage my home is producing. After a week, the bin is filled in with water and inoculated, and connected to the gas-holder.
How long would the biodigestion take in average before I can disconnect the bin and use the remaining slurry?
I have looked at existing information regarding the biodigestion process. The stages of biodigestion are explained in Chapter 4 of the Biogas Handbook sample I have:

Aerobic
  Oxygen will inevitably enter with the raw materials put into the generator, and so aerobic bacteria use this oxygen up,
  meanwhile doing what they can to break the materials down. CO2 is
  released, and some heat is generated.
Extracellular enzymes
  In this stage, anaerobic bacteria release enzymes that attack large molecules which are still outside their own
  bodies (extracellular), so these molecules will be broken down into
  “bite sizes.”
Acid digestion
  The bite size molecules (still fairly large) are absorbed by the bacteria and digested. The main byproducts of this
  third process are simple molecules such as the short chain fatty
  acids, H2 and CO2. (We’ll get into the short chain fatty acids soon.)
  It’s interesting to note that at this stage, hydrogen gas, an
  excellent fuel, is evolved. Hydrogen does not often show up in the
  final biogas apparently because it is used by the anaerobic bacteria
  (in the next stage) in making CH4, methane.
Gas digestion
  Now comes the part we’ve been waiting for. The fatty acids are now gobbled up by the last group of bacteria, who turn them
  into H2O, CO2, and best of all, CH4.

Alas, the length of these stages is not explained. However, Biorealis suggests the length of the Acid Digestion and Gas Digestion in a critique of conventional continuous-feed biodigesters vs. the two-phased biodigester it has developed:

Conventional single-stage digesters are not only unstable, they are
  also relatively inefficient. For example, if the system is operated at
  a hydraulic retention time (HRT) conducive to growth of acidogens (2-3
  days), any methanogens present will be washed out of the system faster
  than they can reproduce, preventing them from ever becoming
  established. On the other hand, if the system is operated at an HRT
  conducive to growth of methanogens (20-25days), the faster growing
  acidogens will be maintained at the low growth rates of the endogenous
  growth phase - essentially at starvation level.

NB: I opted for a batch biodigestion system to avoid the complications mentioned by Biorealis here above and because Biorealis' two-phased biodigester is more expensive and less easy to build.
So far I have a rough biodigestion calendar of:

3 days of acid digestion
20-25 days of gas

But I still lack some information on the stages:

how about the length of the two previous stages mentioned in the Biogas Handbook?
on what do those stages depend and can I accelerate digestion somehow? (I already know about heat at 21°C, how about water ratio or anything else?)
how long does it take to digest a big chunk of food, say a 27cm² bit of carrot? (Important because I hope the garbage is completely processed before I toss the slurry in the garden as fertilizer)
in short after how much time can I confidently unplug the batch, knowing the biodigestion is complete?

Could you help me shed some light on the length of biodigestion stages? Thanks.

PS: couldn't find appropriate tags, please help on that if you can.

I'm sending this over to [biology.se], it fits in their scope much better than ours and probably will get a better answer there :)

To give timescales for the different processes is very difficult because the speed (in g/d product yield) depends greatly on the number of bacteria, so first you'd have to modl the bacteria growth. I assume you don't want to go that road.
Also note that not all of the substrate is in the same state of fermentation at the same time, more so if you have bigger lumps. Like whole carrots.
One industrial batch-style fermneter I know of uses total retention times of 3-4 weeks, and they mix half the digestate into the fermenter again to provide for inocculum.


text:
Insulin and monoclonal antibody production
When producing insulin, the gene for its production is inserted into the plasmid of a bacterium that is allowed to replicate freely.
Why can't the same thing be done with antibodies (as I understand it, currently cancer cells are fused with mammalian cells that produce these antibodies, and now the tumour is allowed to replicate, much like the bacterium, making more antibodies)?
What is different about these two proteins that means fairly distinct processes of production are required for each?

See http://en.wikipedia.org/wiki/Glycosylation

I recommend that you take a look at this:

Jeong KJ, Jang SH, Velmurugan N. (2011) Recombinant antibodies: engineering and production in yeast and bacterial hosts. Biotechnol J. 6:16-27.

This fairly recent view discusses the progress and prospects for producing functional antibodies in yeast and bacteria. As pointed out by @Nick in the comment to the OP, the main stumbling block in both cases is the engineering that would be necessary to ensure correct glycosylation in the heterologous expression systems. This quotation from the cited review sums up the situation:

The N-linked glycan structure in the Fc region of antibodies is indispensible for binding to receptors (FcγRs), but glycosylation has been one of the major limitations in choosing possible production hosts. Eukaryotic yeast as well as bacteria, including E. coli, have not been used as the main hosts for the production of recombinant antibodies (full-length IgG format) for use in humans because of glycosylation problems.

They do however go on to discuss some interesting developments such as the expression of a Campylobacter N-glycosylation pathway in E.coli, as well as strategies for the production of functional antibody fragments.


text:
How do prokaryotes perform cellular respiration without membrane-bound organelles?
In order to survive, prokaryotes such as bacteria need to produce energy from food such as glucose. In eukaryotic cells, respiration is performed by mitochondria, but prokaryotic cells do not have membrane-enclosed organelles. How do prokaryotic cells respirate without mitochondria?

This Wikipedia page has information on endosymbiosis a.k.a symbiogenesis https://en.wikipedia.org/wiki/Symbiogenesis

Mitochondria are very similar to bacteria and are thought to have originated from bacteria. This points you to the answer: bacteria produce ATPs the same way mitochondria do, with the oxidation machinery place in their plasma membrane (analogous to the mitochondrial membrane).

If you could add a diagram or a reference then it would be great.

An electrochemical gradient is needed to carry out cellular respiration. Compartimentalization is necessary for gradients to exist. Both mitochondria and certain bacteria possess a double membrane, between which a gradient can be kept. Essentially, they are acid-containing bags which in turn enclose cytoplasm-containing bags. Mitochondria can be thought of as bacteria living in permanent symbiosis with their eukaryotic hosts. Conversely, those bacteria can be thought of as their own mitochondria.


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Can animals that rely heavily on sonar sense colour?
Apparently there're species around as rely heavily on sonar to sense the world around them.
E.g. Bat, Dolphin, Whale ...
The humans, and other terrestrial beings in a lighted world are capable of distinguishing colour in varying degrees of acuity. Is this ability to sense colour in our environment applicable to species (terrestrial, avian, and marine) that rely heavily on sonar?

Are you asking whether they can see color with their eyes, or whether they can detect the properties of an object that would reflect light in the "red" wavelength with reflected sound waves?

Any animal using sound cannot sense color though sonar directly, though these animals are not entirely blind and can probably see colors in the infrared we can't.

Even on the darkest night there is some light around and all bats use this. Old World fruit bats have colour vision, which is useful to them as they are often quite active in daytime, roosting on trees in exposed positions, rather than tucked away in dark crevices like most microbats, which can see only in black-and-white.

Dolphins have additional senses in addition to seeing they can sense electrical fields.  So if an animal has its eyes covered, they will seem to be able to do things you would not expect.  Its not the same as seeing the color though.
Such animals using sonar can additionally sense density and hardness as well as other material attributes which would cause the acoustic properties of the material as well as movement.

A hard-bodied insect produces a different quality of echo from one with a soft body, so bats can distinguish between some different groups of insects in this way. They can also determine the size of the object.

What's really interesting is that even human beings can experience this unusual sense.  Blind people have learned to echolocate by making clicks with their mouth, and there is a movement to teach this skill.
Anyone can try it.  In just an hour or two I was able to tell how close I was to a wall, whether the wall was concrete.  I couldn't play video games (2:20 on the link) or see colors though.

Dolphins, seals and other sea mammals have a monochromatic view, only a green photoreceptor.
http://brain.mpg.de/fileadmin/user_upload/images/Research/Research_Units/Peichl/2001_MPG_whales_and_seals_EN.pdf
Most mammals have bichromatic B.G vision:
The evolution of trichromatic color vision in primates occurred as the ancestors of modern monkeys, apes, and humans switched to diurnal (daytime) activity and began consuming fruits and leaves from flowering plants.
Wiki evolution of color vision (see top ref to main article)
Humans see R.G.B. and bats see G.B.UV.
Some birds, shrews, tenrecs and rats can use simpler echolocation. (wiki)
Birds R.G.B.UV have five types of cones including four single cones, which support tetrachromatic color vision and a double cone, which is thought to mediate achromatic motion perception.
Rats Grey-UV (Rattus norvegicus) have two classes of cone, one containing an ultraviolet (UV)-sensitive photopigment and the other housing a pigment maximally sensitive in the middle (M) wavelengths of the visible spectrum.
Reindeer can see UV.
UV vision isn't possible with big eyes:
...the eyes of smaller birds were more UV transparent than the eyes of larger birds. This means that small birds, such as songbirds, can take full advantage of ambient UV light, while larger birds, such as swifts and raptors, block a lot of the UV light from reaching the retina.
"If you want to be highly UV sensitive — be a UV specialist — you have to be small," Lind said. "For me, that is quite thrilling because it means that your perception of the world is dependent on your physical size."
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0006390

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


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Eyelids interconnected?
I've seen a patient who had a Vitrectomy (eye surgery) done on a single eye manifest massive swelling on both eyelids.
That seems like having my left hand swell after punching a wall with my right one.
Is this example in the eyes rare? How and why does it happen in the eyes? Does it happen anywhere else?

I cannot obviously speak for the specific case you mention (and, anyway, I am not a medical doctor so I would not make a diagnosis in any case), but one thing that comes to mind is that eyes are part of the immunologically privileged sites of the body. This means that an inflammatory response is not elicited in case of the introduction of an antigen.
I quote from Immunobiology by Charles Janeway

Some body sites are immunologically privileged. Tissue grafts placed in these sites often last indefinitely, and antigens placed in these sites do not elicit destructive immune responses.
  Paradoxically, the antigens sequestered in immunologically privileged sites are often the targets of autoimmune attack; for example, brain autoantigens such as myelin basic protein are targeted in multiple sclerosis. It is therefore clear that this antigen does not induce tolerance due to clonal deletion of the self-reactive T cells. Mice only become diseased when they are deliberately immunized with myelin basic protein, in which case they become acutely sick, show severe infiltration of the brain with specific TH1 cells, and often die.
  Thus, at least some antigens expressed in immunologically privileged sites induce neither tolerance nor activation, but if activation is induced elsewhere they can become targets for autoimmune attack (see Section 13-25). It seems plausible that T cells specific for antigens sequestered in immunologically privileged sites are more likely to remain in a state of immunological ignorance. Further evidence for this comes from the eye disease sympathetic ophthalmia (Fig. 13.36). If one eye is ruptured by a blow or other trauma, an autoimmune response to eye proteins can occur, although this happens only rarely. Once the response is induced, it often attacks both eyes. Immuno-suppression and removal of the damaged eye, the source of antigen, is frequently required to preserve vision in the undamaged eye.


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Difference between Appendix and the Cecum?
What's the difference between an appendix and a cecum, and what are their functions?

In herbivores the Cecum is an area that stores plant matter and helps digest it via symbiotic bacteria. Carnivores have smaller Cecums because meat is easier to digest than plant matter. In humans the Cecum is also an anatomical landmark that delineates the change from small intestine (a digesting organ) to the large intestine (mostly a capacity/storage organ).
The Appendix is a small, previously thought "superfluous" fleshy worm-shaped organ at the junction between the small and large intestines. Recent research posits that the appendix is sort of a harbor for a person's gut flora that can re-populate the intestines should the existing bacteria die or get removed (diarrhea being the most common cause). It can also become infected, inflamed, and require surgery to remove (Appendicitis).

But, how do people survive then if their appendix is removed, if it has such a crucial function?

Its function (which is still being debated) isn't that crucial. Rarely ever is all of your gut flora wiped out, and there are other ways to repopulate. Because of its seemingly benign, if not particularly useful, existence it is only removed if it becomes a problem. However, if it is removed, practically everybody recovers fully and there are practically no side-effects.

Also see: http://biology.stackexchange.com/questions/1502/is-the-appendix-a-vestigial-structure-in-all-vertebrates

Appendix and cecum both are parts of the large intestine.
Appendix is the inferior extension of the cecum of the large
  intestine. It is a blind pouch-like structure that resembles a worm,
  hence the name ‘vermiform’.
and
Cecum is a small intraperitoneal pouch-like structure located on the
  right side of the lower abdomen.

Source - Knowyourbody.net

Multiple answers are usually appreciated because they can address different aspects of a question. However, simply repeating the point already stated by an existing answer is not really appreciated.

Hi Welcome to BIO.SE. Thanks for adding an answer. However, in addition to WYSIWYG's comment, we also discourage simply quoting large chunks of text. Instead, try to synthesize info from one or many reputable sources into your own words and formatted for this site. Thanks.


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Can compounds be predicted from Polyketide synthases gene clusters?
I've seen a few talks on the subject. From a gene cluster, there is some decent ability to determine which domains contribute to certain functional groups in the final metabolites. It sounds like this is largely what Warp Drive Bio is trying to do. How realistic is this technology?

I would love to talk to you about this subject after my final :-) Why are you interested?

@Gergana Vandova, we were talking about whether or not Warp Drive Bio and Radiant have a realistic pipedream or not. I think that if they focus on PKS type Is, they might pull it off.

I would say that for type I polyketide synthases (PKS), this is possible. These proteins are variations on fatty acid synthases which have modules, each of which adds a two carbon unit as well as a chiral methyl group to an extending chain which may be reduced to give anything from a ketone, an alcohol to a completely reduced carbon chain.  In the illustration below you can see these 3 options, but double bonds are also possible.

Other sorts of PKS pathways (type II and III PKSs) have proteins which are harder to predict in terms of what they produce since a single protein does the extending of the polyketide chain to cyclize it, typically into an aromatic compound.  All this happens in a single protein site, so careful modelling would be required and I'd be suprised if this has been done accurately.

Note the last arrow there 'tailoring steps' - accompanying the PKS genes themselves are often a slew of acetyl and methyl transferases, additional reductases, coupling enzymes, even delivery proteins... the list goes on and on.  These steps would be hard to predict because the substrate for an o-methyl transferase isn't easily determined.
I think there are several companies trying to leverage 'best guess' bioinformatics here.  They are likely to get a good idea of the backbone, but maybe won't place every methyl and acetyl group correctly.
There are definitely people out there who think this could work to deliver diverse candidates to drug discovery.  see Radiant Genomics as well.

Each module adds a two (not three) carbon extender unit to the growing polyketide chain. Pleas correct it in your text.


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Are all known germs benign in small enough quantities? i.e. Why do we wash our hands?
We know that we wash our hands because germs can get into our body through the nose, the mouth, the eyes, cuts, etc. But I doubt we can completely clean our hands of germs every time we wash them, down to the individual bacterium or virion, even if we use anti-septic soap. So chances are, even if we keep up with our hygiene, germs still get into our body, only in very very small quantities. So here are some questions:

In theory, is there a dividing line where we can say "ok, at this non-zero count of bacteria or virion, there is still (an arbitrary probability) that a normal healthy person won't get sick" for every germ known to man? If not, are there germs that are known to cause havoc in a healthy person even if he comes into contact with a single individual bacterium or virion?
Do we know a certain trend based on the classification of the germ?
How about the most commonly found germs (whichever they are)?
How about some of the most feared, but not so common, virii known to man, like HIV, ebola, SARS?

I think that without being able to answer some of these questions, especially #3, hygiene would be nothing but a ritual activity (because "it just works").

Kind of related: http://biology.stackexchange.com/questions/5395/how-much-weight-volume-do-microbes-occupy-within-the-human-body

the answer is closer to this - most of the disease causing germs continue to be around us all the time.  When conditions are healthy, the immune system and competition with other more benign organisms keep them from becoming a full blown disease.  Soap helps them from reaching critical numbers and does not affect the immune response much, helping to keep them in check.  Antibiotic chemicals do not because they create the conditions where antibiotic resistant strains appear.

Wouldn't soap create the conditions in which soap resistant strains appear?

There is a Wikipedia page  which gives some typical values for infectious doses of bacteria. I suspect that lot of these have been taken from this slideshow which confirms the values on the Wikipedia page, gives more interesting details of how they have been arrived at, and also mentions a few viruses.
It seems from the slideshow that infectious dose isn't estimated in the way that the OP envisages - "What is the probability of infection if I ingest one cell?".
What is clear is that the infectious doses for some bacteria can be less than 10 cells (e.g. Shigella flexneri, E. coli O157:H7). Conversely for many other pathogens such as other strains of E. coli the estimate is >106 cells, so standard hygiene precautions will always offer some protection.

I think that aside from the probability of illness if you ingest a few cells of bacteria XYZ, one important factor to consider is the probability of finding bacteria XYZ on your hands. While the first may probably be fairly high for, say, Yersinia pestis, usually the second should be very very low for that bacterium.

Washing your hands is an exercise in probability rather than absolute values. An important thing to keep in mind is that not only is it very hard to kill all the bacteria on your hands, it's also not something you actually want to do.  Most of the bacteria we encounter day to day are either benign or beneficial to personal health. We know that gnotobiotic mice (sterile mice) exhibit impaired development, especially in the immune system.  We want to come into moderate contact with bacteria.
Because it is a balancing act, I think hygiene needs to be reframed. For one things anti-septic soap should be reserved only for situations when it is absolutely necessary.  Anti-septic soap has a tendency to apply a selective pressure that encourages propagation of resistant strains.  Situations where it is worth using would include visiting an international transit center (airport), working in an Operating Room ward at a hospital, or going to a cafeteria during an epidemic.  In other situations, regular plain soap and water should be good enough to rub the majority of cells off your hands so that passive immunity has a good chance of eliminating any threats before they get to vulnerable parts of the body.  If you have the opportunity, paper towels are better for getting cells off your hands then blowers.


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Why does the cold make us sick?
From the moment we learn to communicate, we always get told, whether by our parents, or our teachers, or by anyone else, to avoid the cold, or to put a jacket on to avoid catching a cold, to dry our hair before we go outside, because we'll get sick otherwise, so on and so forth. I also was diagnosed with a pneumonia last year, while in Switzerland under chilly conditions ($-20^◦\text{C}$). This made me wonder, why does the cold make us sick? It doesn't seem logical to me that a viral infection like the common cold, or a viral/bacterial infection such as a pneumonia is more prevalent when it's colder outside. I always figured it was because our bodies are less 'effective' under cold temperatures, but this seems lacking to me. Can anyone explain?

Generally, I presume it is caused by a decrease the enzymes in the body's rate of activity, causing slowing of vital bodily functions like the immune system. There are probably a plethora of specifics to add to this.

I agree with Alyosha above, I don't think that coldness is a cause of disease as much as a contributing factor. And cold air is also more dry, causing your tracheae to dry out, becoming more susceptible to any potential virus and bacteria...

When the body gets cold, the body diverts energy away from the immune system to the effort to stay warm.

I'd prefer answers to this questions under 'answers', not under comments.

I've looked around a bit and this is a hard one - its clear there is a corelation but its hard to find an explanation.

This is a comment based on anecdote, so I don't feel comfortable listing it as an answer. But one explanation I have heard is that much of the sickness we see during the colder season(s) is not the result of our bodies actually being in the cold, but the result of spending more time indoors sharing each other's germs rather than being outdoors in the fresh air.

@DanielStandage I doubt that's the main reason. I'm sure it has some truth to it, especially with the common cold, however, I find it hard to believe that it's the main reason.

it does not, really. unless we're talking about things like frostbite or severe hypothermia.
it's a myth that it does.
the virus is more stable in colder air, however.
see more here:
Study Shows Why the Flu Likes Winter
Influenza Virus Transmission Is Dependent on Relative Humidity and Temperature

Innate responses proved to be comparable between animals housed at 5 °C and 20 °C, suggesting that cold temperature (5 °C) does not impair the innate immune response in this system.

But a virus must be considerably more stable in colder air, since 'catching a cold' from the cold is very easy, and I have never caught a cold in the summer. Is it that considerable a difference?

The virus may also come from prolonged exposure to rain. I would argue (unfortunately without substantiation) that it is the core body temperature, or the temperature differential that is the factor.

"a virus must be considerably more stable in colder air" -- yes, it is. see the links above. low humidity also plays a role.

Cold weather makes your body use more energy for keeping warm and less energy for other activities. This is made at various levels: 1) modifications of the diameter of arteries changes the blood supply in specific regions
2) In the electron transport chain, that is a metabolic pathway involved in producing energy after glycolis and Krebs cycle there is a disjunction between the electron transport chain and the oxidative phosphorylation caused by the production of thermogenin. This causes a minor production of ATP (energy available for metabolic processes) and dissipation of energy as heat.
Moreover enzymes need a specific environment to work (ph and temperature). A cold weather can decrease the temperature of the body and reduce enzyme activity. When you are sick your body can use fever to stimulate enzymes and power immunitary system activity.
Moreover cold weather causes a reduction of the movements of the cilia of the trachea, so dust and bacteria can enter into the respiratory system more easily. These are just a few examples. There may be others. I'm available for further discussion.

This is what I thought but how can for instance wet shoes/cold feet increase the risk of getting the common cold virus? Feet are so far from the respiratory system..

It is still a shock for the whole system.

From what I understand, the current top answer states that it is a myth that us being cold or warm has little to do with the likelihood to get sick.
This cannot possibly be the compete answer, without even needing any additional science. Simply go outside, at times of equal temperature and humidity, with or without adequate clothing.
Are you getting sick more easily being warm or freezing your butt off?
That's an experiment anyone can do and has inadvertently done at some time. I have VERY strong data that your own body temperature has a HUGE effect on your likelihood to get sick, so the virus alone cannot be the complete answer.
Constricted blood flow during times of cold might be a factor in this. There is data on this.
https://www.ncbi.nlm.nih.gov/pubmed/6131011
But there are also studies that do confirm that the virus itself is adapted to cold.
http://www.pnas.org/content/112/3/827.full
The evolution of this virus might have been reciprocal actually. Other cells seem to divide better at higher temperatures. The interaction between animals, being more susceptible, due to their bodies conserving heat in winter, might have caused these particular pathogens to also adapt in reverse and to do better in colder weather.
The complete answer whether it is our bodies or the cold temperature is probably "both".

Still, being cold may support being sick, but the cause are viruses/bacteria. Additionally: How does your reference support your claim? It says that vlood flow is constricted in cold tissues, but no connection is made by it to the cold. This is your claim which is not backed by references.

It might have been the wrong link. I should have quoted the passage. Let me go over it.

I think this site best answers the question:
Cold Weather Can Make You Sick
Here is a part:
"Professor Eccles explained this effect by saying that our bodies restrict blood flow to the extremities when we get cold to help conserve body heat for the torso and brain, which really need to be warm. Cutting off the blood flow reduces the supply of white blood cells which are the immune system’s primary weapon against germs.
While his explanation makes sense, there may be a more general effect at work. The human body is a machine that accepts fuel in the form of food, and uses that fuel’s energy to keep us warm and to power our immune systems, muscles and brains. However, in frigid conditions our bodies have probably evolved to say “who cares if I might get sick a week later when I’m going to die of hypothermia in half an hour?”"

Most likely the energy to stay warm is not being used to fight infection. Also the virus is likely designed to operate with your respiratory system at a colder temperature more effective that the immune system is at that cooler temperature.

It would be a stronger answer if you included some references to back up your statements.

"O" as in observation or "O" as in opinion?


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Why does getting certain chemicals in cuts hurt?
More specifically, shampoo. What are the mechanics of detecting a noxious chemical stimulus in terms of which receptors recognise what, how do they do it, and how is this information relayed to the nerve cells?
Why is the pain (and so signal, I presume) larger if one is having a hot shower at the time?

I edited the question a bit, as I don't think the sensation is specific to shampoo, but this is interesting.

I guess the second part has to do with hot water dilating blood vessels, facilitating extravasation

Shampoo is a detergent. Detergents emulsify lipids, including those in membranes. Skin cells are probably a bit more resistant to detergent than other cells. When it gets in cuts, the shampoo is probably causing rapid cell injury and/or death. I think pain is a perfectly proportional response to that.

@ChinmayKanchi I'd be happy to accept that if you post that as an answer I (perhaps with an extra link).

@Alyosha There you go...

I don't have a definitive answer, but most of the surfactants in shampoo are sodium salts like sodium lauryl sulfate. Perhaps it's the sodium ion from the shampoo causing the same pain effect that sodium chloride does when it gets into a wound and not damage caused by the detergent.

Shampoo contains surfactants, chemicals which cause lipids to emulsify. The cell membrane is composed primarily of phospholipids, which are vulnerable to action by surfactants. In fact, sodium dodecyl sulphate (SDS, often labelled SLS on shampoo bottles), an integral component of many shampoos is also used in the lab (albeit at substantially higher concentration) to achieve cell lysis.
The outer layer of skin is composed largely of a very tough type of cells called keratinocytes, which form an impenetrable barrier to potentially harmful chemicals like surfactants. Once the skin is ruptured, the surfactant can act on cells that don't have the protection of keratin, causing damage to cell membranes, and perhaps even cell death. This will obviously lead to an immune response and inflammation, which is likely to be the source of the burning sensation/pain that one feels.
The inflammatory process involves various immune system-related mediators such as bradykinin and prostaglandins, which act to increase the sensitivity of neurons to pain.
With other chemicals that cause a burning sensation, the mechanism of cell injury might be different, but ultimately, the immune mechanisms kick in, causing inflammation and pain.
Kid & Urban (2001) reviews the processes that cause inflammatory pain in great detail (full text is available for free).