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Can Bioluminescence drive photosynthesis?
I'm trying to construct an anaerobic kitchen-waste digester at home.
The major output from the digester is methane - with a significant component of carbon dioxide. To scrub/reduce the CO2 I was thinking of passing the methane through a freshwater container charged with algae ... then it occurred to me to also think of introducing some bioluminescent algae to drive the photosynthesis & absorb some of the oxygen released by the other algae. Understandably this would be an unbalanced system.
But ... can bioluminescence drive photosynthesis?

Sounds like an interesting project. But why not just expose the algae to sunlight?

Also, what are you going to do with the methane?

Don't laugh. I forgot why I didn't want to expose the algae to sunlight ... To answer the second question - burn it!

This mainly depends on three things: The emission wavelength of the bioluminescence, the intensity of the bioluminescence and the optimum wavelength of the photosynthesis. I don't have actual numbers, but my educated guess is that the bioluminescence, even if the wavelengths fit, is way to weak to show an effect.

this is like asking if opening a refrigerator in the kitchen can cool the kitchen.  it can, but only if you spend a lot of energy.

This would be a complex system to setup and would not run bet efficiently. Maintaining luciferin production would be problematic. Might be better to use a melatonin-producing microbe as a photon acceptor.

@shigeta - No, opening a refrigerator in the kitchen can only warm the kitchen.  The more energy you put in, the warmer it will get.  You can cool the kitchen if you put the refrigerator half in the kitchen and half in some other room (or outside).

@RexKerr that was more or less my point.  the open freezer is a freshman thermodynamics talking point.  For the same reasons, you could never create a closed  bioluminesence photosynthesis cycle.

@shigeta - Refrigerators are reasonably efficient air conditioners.  The key is not how much energy you expend, it's the configuration of the heat cycle (i.e. cooling coils and open door not in the same room if you want to reduce the mean temperature in one room).  It's really not analogous at all--here the issue is that you need the methane processed, and providing light input (and methane as the carbon source) is one way to accomplish it.

@shigeta: (+: I did expect it to be unbalanced. Off-topic, the depth of these inter/co-dependent networks in nature make one revere that nature developed so. Imagine the number of broken branches of evolution & mutation that must have occurred to develop to our present day ....

Yes and no. Yes as in the energetics do work out and you will be going down a small but non-trivial driving force as long as you continue to provide the luciferin to the algae.
However, the wavelengths of light by which photosynthesis absorbs its energy are well defined and narrow. As a result, light sources for photosynthetic organisms have to be fairly strong and bright to cover the whole spectrum to provide the necessary light. As a result, your bioluminescent algae will also have to emit light at the desired wavelength to achieve a high photochemical efficiency and provide light to both Photosystem II and Photosystem I which have different wavelength requirements.

(source: gsu.edu)

"Marine species tend to emit light of wavelength between 440 and 479 nm (bluish), which is the range of greatest optical transparency of seawater." - http://www.quantum-immortal.net/physics/biolum.php
So it's in the correct wavelength range, but I'm with shigeta - it's not going all that efficient (unless, of course, there's the possibility for breeding brighter algae).

Curiously enough, this was the subject of a paper in 2013. The authors claimed to have driven photosynthesis by submerging some dark-adapted leaves into a solution containing a mixture of luminol, hydrogen peroxide and horseradish peroxidase (HRP).
They measure the levels of starch on the leaves produced in three different solution concentrations and bioluminescence irradiance levels.
As the leaves were severed from the plant I do not see much of a future in submerging leaves or an entire plant in this solution but it would be interesting see how algae would react. Also, I am very curious the luminol could potentially be injected in the plant, although this might be far fetched.
The link to the paper below:
https://pubs.rsc.org/en/content/articlelanding/2013/cc/c3cc45264f#!divAbstract


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Can cancer grow forever if supplied with unlimited resources?
If somehow a human could give a tumor unlimited resources, would the cancer grow forever?  It seems like it would until it gets so large that it physically affects vital organs.  Is what would likely happen?

Yes. The very first cells used to study cancer are still around (HeLa Immortal Cells - Named for the subject Henrietta Lacks) and are basically immortal as long as they're fed.
As for tumors, whether cancerous or not they most definitely can continue to grow until they become a serious medical issue (WARNING: GRAPHIC - 3 Largest Tumors Recorded). One of the largest recorded tumors was 300lbs (~140kg) in a woman's abdomen that sprouted off of an ovary. They had to operate with her laying on her side, otherwise it would have crushed her abdomen and killed her.
Not all forms of cancer are immortal or produce large tumors (the 300lb tumor was benign), but it's definitely within the realm of plausibility.

Cancer will continue to grow as long as it is supplied with nutrients, as loss of growth inhibition is one hallmark of cancer. there are limitations in diffusion and access to blood supply that make some cancers better able to grow large tumors.

Well, there's evidence emerging that the bulk of tumors may operate aerobic metabolisms more than normal cell respiration because of the lack of blood. I'd never use the term 'Cancer' on its own because there's about a thousand different types, and while all have regulatory mechanisms gone awry - saying they all grow when fed is also wrong. A thyroid cancer I read about recently also couldn't elongate its telomeres - still potentially fatal, but definitely 'mortal.'

Fair points. I should have stated that any tissue, if it grows large enough, is limited by (passive) diffusion if no blood supply is developed. If it grows beyond the limit of diffusion, it will develop a necrotic core in the absence of a blood supply for richer nutrients.

not all cancer cell lines are immortal either.  But in some cases, in a liquid culture they appear to have unlimited growth potential.

@leonardo In my understanding most cancer cell lines are in fact not immortal. When they found that HeLa wasn’t dying they had in fact already been searching for an immortal cell line for quite some time without success, and finding HeLa was a big surprise.

source: Stack Exchange

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Does Dorsal Raphe Nuclei firing pattern change in response to voluntary breathing?
I'm reading this paper, which discusses how Serotonin may be involved in motor functions of mammals: 5-HT and motor control: a hypothesis .
The paper includes the following diagram of the Dorsal Raphe Nuclei (DRN) firing pattern in a walking cat, and cat on a tredmill. Each step is associated with a distinct firing pattern. I'm wandering if the DRN firing pattern, in humans, changes in a similar way in response to voluntary breathing?

After searching wikipedia, I found a line that says:

REM sleep is turned on by acetylcholine secretion and is inhibited by
  neurons that secrete serotonin. (Psysiology of sleep stages)

I'm interested in dreaming, and at times have practiced entering dreams consciously, from the waking state after laying in bed for a long time. One of the obstacles to entring a dream was seizing control of breathing and starting to breathe voluntarily. This prevented me from entering dreams on a number of occasions, and appears to support the idea that voluntary breathing would affect the DRN. But I'm looking for a more scientifically-validated answer.
Thank you for your input!

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What is the molecular basis of hangovers?
Well, most of us have experienced the wonderful feeling of the dreaded hangover. How does it work exactly? I imagine it has something to do with dehydration but what are the underlying mechanisms?
Extra points for explaining why mixing drinks makes it worse and why (or if) a hair of the dog (another drink) the next day can help. Someone once told me that hangovers are the first symptoms of withdrawal and if you drink (anecdotal evidence suggests that it should be the same drink as the night before, but I doubt this is true) a small amount of alcohol, the symptoms are alleviated. I don't really see how that can be true.

First, the hormonal and hemodynamic changes seen in hangover are distinct from those seen in alcohol withdrawal, so the advice to drink more is not good, even if some symptoms are in fact improved. See tables 2/3 in the cited review.
It appears the molecular mechanism of veisalgia (HA, a new word) is not well known.
1. acetaldehyde Part of it may be attributed to acetaldehyde but there is clearly more to it. The liver enzyme alcohol dehydrogenase 1 (ADH1) produces acetaldehyde from ethanol, and aldehyde dehydrogenase 2 (ALDH2) makes acetate from that, so the aldehyde does not exist for a long time, and is rather responsible for short-term illnesses.
2. ADH and diuresis

Hangover severity is proportional to antidiuretic hormone
  concentration (46). Alcohol inhibits the effect of antidiuretic
  hormone on the kidneys, thereby inducing  diuresis that is out of
  proportion to the volume of fluid ingested. As blood alcohol
  concentration decreases and dehydration persists, the serum level of
  antidiuretic hormone increases, maintaining water retention in
  dehydrated patients with hangover. In our clinical experience,
  hydration attenuates but does not completely relieve hangover
  symptoms.

3. cytokines

The constellation of hangover symptoms (nausea, headache, diarrhea)
  resembles that seen in conditions related to dysregulated cytokine
  pathways (for example, in viral infections and after administration of
  interferon-alpha). Alcohol alters cytokine production through a
  thromboxane pathway. Levels of thromboxane B2 are elevated during
  experimentally induced alcohol hangover (42), and the administration
  of tolfenamic acid, a prostaglandin inhibitor, at the time of alcohol
  consumption has a small prophylactic effect in reducing hangover
  severity (9).

4. further substances

Congeners, the byproducts of individual alcohol preparations (which
  are found primarily in brandy, wine, tequila, whiskey, and other dark
  liquors), increase the frequency and severity of hangover (24, 39,
  40). Clear liquors, such as rum, vodka, and gin, tend to cause
  hangover less frequently.

So there are factors that aren't even identified exactly, and these could fit the mixing of drinks observation.
There are several reviews out there, just search for hangover at Google Scholar.
Wiese, Jeffrey G., Michael G. Shlipak, and Warren S. Browner. "The alcohol hangover." Ann Intern Med 132.11 (2000): 897-902. Online at http://dionysus.psych.wisc.edu/lit/topics/Hangover/WieseJ2000a.pdf

Thanks for the comprehensive answer, I would have accepted it earlier but I was holding out in case anyone could explain the mixing drinks thang.


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How does sodium in one's diet affect blood pressure?
Due to high blood pressure, my doctor has recommended I go on a low-sodium diet.  So, that got me wondering what it is about sodium that drives this recommendation?
What does sodium do to a body that, by its presence or absence, affects blood pressure in humans?

Don't have the time to write a proper answer, but maybe you want to check out this review (and if someone wants to write an answer starting from it he/she is very welcome to do it!). Dietary Sodium and Blood Pressure

The basic reason is osmosis, the tendency of solutes to move from an area of high concentration to one of low concentration across a permeable barrier. So, ingesting large amounts of salt results in a high sodium concentration in the blood stream. This in turn causes water to enter the blood vessels by osmosis. More water in the blood means a greater volume of liquid and, therefore, higher blood pressure.
This process occurs primarily in the kidneys, specifically in the part of the nephron called the loop of henle (the image below was taken from wikipedia and is originally from Grey's Anatomy):

With low salt concentrations, water exits the loop and is retained by the body. When sodium concentration is high, the opposite occurs, water enters the blood stream by osmosis and increases blood pressure.

Great answer! I read that there may be variations in the blood pressure over the course of the day, and that the renal function itself has a circadian rhythm. Is there anything circadian in this loop that may alter how Sodium affects the blood pressure based on the time of day?

Blood pressure is far more attuned to maintain mean arterial pressure, and as a result, the level of activity and intensity someone is engaging. So during the day, when one is more likely to be active, blood pressure is overall greater, and then at night, when activity tends to decrease, so does blood pressure. This may be conflated with circadian rhythms (which likely do exist, but probably don't affect blood pressure all that much).

This is a nice answer. As blood sodium concentration increases, osmosis causes an increase in blood volume, which cause a greater degree of atrial and vessel stretching, leading to a secretion of atrial natriuretic peptide (ANP) which tries to regulate blood pressure. Read more about ANP at its wikipedia page (http://en.wikipedia.org/wiki/Atrial_natriuretic_peptide)

As salt accumulates in thebody, it also indirectly increases the extracellular fluid volume for two basic reasons:
1. When there is excess salt in the extracellular fluid,the osmolality of the fluid increases, and this in turn stimulates the thirst center in the brain, making the person drink extra amounts of water to return the extracellular salt concentration to normal. This increases the extracellular fluid volume.
2. The increase in osmolality caused by the excess salt in the extracellular fluid also stimulates the hypothalamic-posterior pituitary gland secretory mechanism to secrete increased quantities of antidiuretic hormone. The antidiuretic hormone then causes the
kidneys to reabsorb greatly increased quantities
of water from the renal tubular fluid, thereby diminishing the excreted volume of urine but
increasing the extracellular fluid volume.
Thus, for these important reasons, the amount of salt that accumulates in the body is the main determinant of the extracellular fluid volume. Because only small increases in extracellular fluid and blood volume can often increase the arterial pressure greatly, accumulation of even a small amount of extra salt in the body can lead to considerable elevation of arterial pressure.

Progressive changes in important circulatory system variables during the first few weeks of
volume-loading hypertension.

in addition to the increased thirst, and increased ADH mediated water reabsortion in the collecting duct, salt will also cause a shift of fluid from the intercellular space to extracellular space.

oops, thats supposed to say intracellular space, not intercellular space...

Salt will cause high blood pressure, but only under certain circumstance.
physiologic hormonal compensations for increased blood volume:

Atrial natriuretic peptide -- increases sodium excretion, hence this is INCREASED with high blood volume
Antidiuretic horomone -- ADH increases water reabsorption in the kidney, hence this will be DECREASED with high blood volume
Renin/Aldosterone -- increases sodium reabsorption from ultrafiltrate back into blood, hence it will be DECREASED

these explainations are a bit reverse (saying that these horomones have these effects and that is why they are released) for the sake of simplicity, and I'm not discussing the mechanism of release of these horomones (aka under what circumstances they are released in the place where they are released from)...
while these horomones help with the kidney regulation of sodium balance and blood volume, this still depends on the kidneys being given the circumstance where they can be effective.
Pathologic circumstances, when elimination of excess sodium fails:
Some people simply have a higher sodium sensitivity and there are a variety of factors that have been statistically correlated to sodium sensitivity, but often the mechanism is unknown. Here are various factors statistically correlated to affect salt sensitivity:
http://physrev.physiology.org/content/85/2/679
the above article shows that no organ systems need be compromised for excess sodium to raise blood pressure, but just for the sake of discussing more macroscopic things I want to discuss these organ systems based reasons for the kidney being unable to compensate for excess sodium in the diet=

The kidney:
A patient with renal disease may not be able to regulate the excretion of sodium. Even in normal humans, the kidney's capacity to excrete sodium declines with age, and smaller increases in salt intake induce a rise in arterial pressure, as GFR (the renal filtration of the blood sent to the kidney) falls by about 40%, though individual variations are wide and some people lose less.

Other than the kidney:
Other diseases can also interfere with renal excretion of sodium. A problem with maintaining blood volume will cause constriction of the renal artery. This would occur before a drop in blood pressure would occur, as this is a way of preventing a drop in blood pressure. This occurs in congestive heart failure and liver cirrhosis.

A patient with congestive heart failure may not have adequate renal
perfusion.  Hence, to maintain adequate blood pressure the renal artery is constricted.
Also, liver cirrhosis may decrease renal perfusion
because of the lack of blood proteins (proteins found inside the
blood vessels that keep water in the blood vessels via osmosis)
holding fluids in the intravascular space and having them escape into
the extra-vascular (outside the blood vessels but still outside the
cells of the body) space. Again, to maintain adequate blood pressure the renal artery is constricted.
burns, also because of loss of blood proteins--> leakage of intravascular fluid to extravascular space--> decreased blood volume and increased sympathetic nervous system output--> reduction of renal blood flow... same as for cirrhosis

In addition to reduction of salt in the diet, diuretics (ex. loop and thiazide) can help the body excrete even more sodium into the urine than what your body can do on it's own.
this article describes the renal handling of excess salt in the diet:
http://booksite.elsevier.com/brochures/thekidney/PDFs/TheKidneyCh36_P088488.pdf


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What marine animals exhibit deep hibernation/aestivation?
Do marine animals exhibit deep hibernation/aestivation as land-based creatures do?
If not, Why?

Turtles and frogs do, if you classify them as "marine" animals...

Fish are ectothermic, and so, by definition, cannot hibernate because they cannot actively down-regulate their body temperature or their metabolic rate. However, they can experience decreased metabolic rates associated with colder environments and/or low oxygen availability (hypoxia) and can experience dormancy. For example, epaulette sharks have been known to stay dormant for long periods without oxygen (reference) Turtles in freshwater lakes have been known to hibernate by burying themselves in mud (reference). The mechanism through which turtles can experience several months of hypoxia or anoxia is explained in this paper. The Antarctic fish (Notothenia coriiceps) has been found to be able to activate and deactivate their metabolic processes independent of body temperature and hence enter a state of dormancy similar to hibernation through metabolic suppression (reference).


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Do omnivore mammals vary food preferences based on dietary needs?
I'm wandering if mammals that can eat many different kinds of food (omnivores) vary their preference for food not only based on the availability, but also based on dietary needs?
I'm looking at this site Food nutritional content and see that "not all foods are created equal" - the vitamin/mineral and amino acid contents can vary dramatically. Is there some part of an omnivore brain/digestive system that "monitors" the micronutrient density of digested food and adjusts food preferences towards foods that make the diet more complete?

I want to say yes, as I've heard of cases that people starving afloat on the ocean and desperately in need of Vitamins will eat Vitamin-rich portions (eyes, liver, etc.) first, but I haven't the sources yet. There's also Geophagia, which can be common for pregnant women who are starving for the iron content of the dirt.

For what concerns amino acids, mice rapidly reject meals that are not balanced in essential amino acids and continue to look for other kind of foods. This behavior is called aversion response and it is an adaptive phenomena that can be observed already 20 minutes after exposure to the unbalanced food. The mechanism involves brain sensing of uncharged tRNAs. The significance of the aversion response is to minimize depletion of essential amino acids that can not be directly synthethized but are required for protein synthesis. You can find good reviews in PubMed, for instance Gietzen et al. 2007, Annual Review of Nutrition, and Gietzen and Aya 2012, Molecular Neurobiology.

Great answer! Reading the 2nd article, I see that there's "rapid
recognition of Indispensible Amino Acid(IAA) depletion in the rat brain's IAA chemosensor, the anterior piriform cortex (APC)".

Here's a paper that deals with pleasure in the brain, but also mentions that aversion response to salt can be decreased dramatically, and be replaced by "liking" response when brain experiences sodium deficiency: http://www.lsa.umich.edu/psych/research&labs/berridge/publications/Aldridge%20&%20Berridge%202010%20Neural%20coding%20of%20pleasure%20chapt%203%20in%20Pleasures%20of%20Brain.pdf

I found that there are seasonal rhythms in the nutrient intake:
Seasonal rhythms of human nutrient intake and meal pattern
The article's abstract mentions carbohydrates, while I'm more interested in the micronutrients, like amino acids and vitamins/minerals.

not sure amino acids can be considered micronutrients like vitamins.

That is a very good observation! I'll check the articles above to see if they mention vitamins as well


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mutant down but not out
I am interested in a gene which is null lethal but I need to temporary induce diminished capacity. If a cell is homozygous is it possible to induce heterozygous phenotypes or a partial knockout from WT with siRNA or other molecular methods without virus vectors? I'm not interested in a medillian solution but an inducible molecular way.
Thank you
I would like to generate a heterozygous Sod2+/- like they do in this paper in mice and possibly human:
http://physiolgenomics.physiology.org/content/16/1/29.full.pdf+html

It would help if you gave more information about the system that you are working with - what type of cells?

@AlanBoyd im interested in mice and humans and i added the gene of interest as well.

The tetracycline-regulated systems developed by Clontech would allow you to do something like this - the level of gene expression can be titrated by varying the concentration of tetracycline/doxycycline in the growth medium. See http://www.clontech.com/GB/Products/Inducible_Systems/Tetracycline-Inducible_Expression/Selection_Guide?sitex=10030:22372:US for links to more details - the early generation products might be a good place to start reading.

@AlanBoyd my growth\life medium would prohibit the use of tetracycline but thanks for using the key word titrated

what medium is this?

@AlanBoyd in vivo, live test subjects, not in vitro

You could use some tamoxifen sensitive promoter instead. They are commonly used in vivo (at least in mice)

@nico thanks but I'm looking for something a bit safer like Nimesulide...which induces changes to sod2 if I could inject it it might increase the ROS levels by mitigating sod2 in a way which isnt permanent yet sufficiently detrimental

@caseyr547: what makes you think injecting tamoxifen is unsafer than injecting nimesulide (I'm obviously talking about mice, not humans)?

@nico i'm sure they are both equally safe in mice :) i was thinking about humans the fda to my knowledge hasn't approved any gene therapy techniques yet but allows off label use all the time.

Antisense, promoter replacement and when possible tetracycline allows one to titrate of gene expression
http://www.springerprotocols.com/Abstract/doi/10.1007/978-1-59745-321-9_20#


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Is there some branch of biology that deals with the entire organism?
I'm reading about various parts of the human body and brain and started to wander if there's a branch of biology that deals with the entire human? I know that there are branches various -biologies, from neurobiology to something like heliobiology or chronobiology. All of them look at different organ systems or parts of an organism, but from different points of view.
Then there are sciences that deal with behavior and cognition of humans.
As I read about these, I notice that there's quite a lot of overlap, particularly when neurotransmitters and hormones are involved. For example Melatonin, a hormone has functions in both the brain and the gut.
I'm wandering if there's some form of biology or science that deals with the entire organism, its behavior , as well as its parts? Am I thinking about Biology or Medicine or something else?

Organismal biology?

I was thinking of Systems/Integrative/Predictive Biology reading your question. Studying the wikipedia entry it looks like a research approach with many problems trying to understand organisms from a biochemical perspective, identifying control circuits and macro-quantities like temperature and its relation to such biochemical control circuits. Basically you have to give up reductionism and use holistic/systemic perspectives and methods. While physics was successful with such research approaches (climate simulation, many particle systems,...), biology is lacking very accurate and proven mathematical theories to implement and test reasonable models of an organism, not surprising when biological systems have so many degrees of freedom compared to something like a ideal gas in physics. The wikipedia link doesn't show a lot of proven knowledge that this field/research approach has already created.

Medicine applies to healing illnesses of the body (with many subspecialties, including endocrinology which you may be interested in). Physiology is a branch of science which deals with the normal function of the body and its various parts.

This fits the question too, but I can only accept one answer

@AlexStone that's okay. It's hard to be more specific without a clear and specific motivation behind a holistic approach.


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Does pheomelanin have a useful biological function?
Melanin is a natural pigment that is categorized into two main forms, eumelanin and pheomelanin. It's well documented in the science literature that increased eumelanin levels reduces the risk of developing skin cancer, whereas it was recently reported in Nature that pheomelanin may itself be carcinogenic. So my question is:
Does pheomelanin have a useful biological function?

Can you point to some references that show the UK population has higher pheomelanin?

@leonardo not at the moment, so I've removed this statement from the question. But going by my observations, there's a greater variety of redheads and blondes here compared to regions near the equator such as Africa and Asia, so I'm assuming it's down to the higher levels of pheomelanin, lower levels of eumelanin. There is also the standard skin colour map: http://www.grida.no/graphicslib/detail/skin-colour-map-indigenous-people_8b88

You seem to have forgotten to cite the paper you mention.

How do you increase the amount of EUMELANIN but not PHEOMELANIN? Do we know if this is currently been looked at by scientists?

It is worth noting all cells that produce Eumelanin produce Pheomelanin first, so it could even be a bit of evolutionary baggage. The cell has to go through stages A-B-C even though B is no longer useful directly just because something in B triggers the change to C.

I don't think that the role of pheomelanin is known yet. To produce larger amounts of it, you need mainly two conditions: A weak (or absent) MC1R signalling and the availibility of the amino acid cysteine. If MC1R signalling is strong, the preferred way goes into the direction of eumelanin. Its known for quite a while that pheomelanin produces reactive oxygen species which either directly cause DNA damage or do it indirectly by using up the cells storage of antioxidants. You can find more details in this review as well as links to a number of original papers.

My understanding has been that it aids in sun absorption in the skin, specifically in low sunlight/overcast areas. I don't have source on hand, but that may steer you in the direction you are looking for.
Also, consider that that pheomelanin, red hair specifically, may encourage breeding success, depending on where you are.

That's my guess as well, but I can't find any references. Are you a redhead?

I'm not a red head, but if you need a source. I found an article with citations.   38 Red Hair and Redhead Facts    The article may lead you to some appropriate sources, and I'll post anything I come across.

I don't think that any use has been discovered yet for pheomelanin. I can't find sources about the claim that it increases UV absorption so I guess we can't say that yet.
I would simply guess that it's not harmful enough to warrant elimination via natural selection (in places where people are less exposed to UV, that is), and may, in certain societies, have increased sexual fitness. However even this is hard to tell, because historically red hair has been considered both an identitarian, desirable feature (as for Gauls during Roman times who would even bleach their hair with limewater to obtain reddish-blond hair) and abhorrent and cause for discrimination.
Vestiges and by-products of useful mutations may accumulate endlessly if their impact on overall fitness is marginal. In this case the useful effect would be the inhibition of eumelanin the skin, which is desirable in low lit/cold climates. This may in turn cause greater pheomelanin production and allows the normally concealed pheomelanic phenotype to show.

Pheomelanin has it normal function in transforming radiant heat to energy but can't protect its host from ultra violet rays from the sun as UV will destroy melanin cells.

ahh, interesting! Do you have a reference for this?


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PGC-1β Sod2 limiters/blockers
I'd like to block a percentage of PGC-1β or Sod2 expression. According to the following paper's figure beta-blockers inhibit some expression of PGC-1α. Are there any medicines/chemicals which safely and temporarily block 50%-60% expression of PGC-1β or Sod2 in fully developed mice or humans?
Thank you
http://jap.physiology.org/content/107/1/8.full
Fig. 1.
Interactions of β-blockers and mitochondrial biogenesis. Aerobic exercise activates β2-adrenergic receptors (β-AR) on skeletal muscle and induces peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) transcription, a regulator of mitochondrial biogenesis. Selective and nonselective β-blockers can blunt β2-AR signaling, which restricts the expected PGC-1α response following exercise and can impair adaptations to mitochondria and aerobic capacity. V̇O2max, maximum oxygen consumption.

Perhaps there is a transgenic mouse model available that uses a conditional knock-down approach?

@leonardo there is a transgenic mouse and there is a vector based method of depleting Sod2 and PGC-1β but it wont help me because the transition needs to be reversible

right, that's why I qualified the "conditional" knock-down. Not knowing these lines, vector based sounds like it could be reversible (eg, stop delivering the vector). The transgenic mouse might be a knock-out rather than a knock-down/conditional knock-out.

@leonardo yeah that is right the only thing is viral vectors cause leukemia in the long run; cell penetrating peptides are safe and fda aproved but they can only carry one cargo at a time as best i know

Maybe you can design a new transgenic model then. ;)

Dexamethasone can be used to regulate PGC-1β
http://www.ncbi.nlm.nih.gov/pubmed/20647557


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What selective factors drove the evolution of lactose in lactation?
As far as I can determine, lactose, and the monosaccharide galactose have few biological uses outside of mammalian lactation.  It not only required enzymes for its production, but enzymes in offspring for its digestion, suggesting that it serves some specific purpose.  Yet intuitively, it seems like it would have been significantly easier to just concentrate glucose from the blood or generate a disaccharide readily found in the diet like sucrose, for which digestive enzymes already existed.
What drove the evolution of lactose in mammalian lactation?

Galactose is also an important component of the oligosaccharides that are added to glycosylated proteins.

As it happens someone has just published a theory about this. To save you following the link, I reproduce the abstract below.
I must admit that I had never realised that lactose is synthesised within the organelles of the secretory pathway (β4-galactosyltransferase is a Golgi enzyme and α-lactalbumin is, of course, a whey protein, so is in transit through the pathway). This may go part of the way to answering your question: by having a disaccharide that is made within the Golgi, the cells of the mammary gland will effectively partition their glucose metabolism between the cytoplasm and that destined for secretion as lactose (transported into the Golgi lumen).

Mammalian milk or colostrum contains up to 10% of carbohydrate, of which free lactose usually constitutes more than 80%. Lactose is synthesized within lactating mammary glands from uridine diphosphate galactose (UDP-Gal) and glucose by a transgalactosylation catalysed by a complex of β4-galactosyltransferase and α-lactalbumin (α-LA). α-LA is believed to have evolved from C-type lysozyme. Mammalian milk or colostrum usually contains a variety of oligosaccharides in addition to free lactose. Each oligosaccharide has a lactose unit at its reducing end; this unit acts as a precursor that is essential for its biosynthesis. It is generally believed that milk oligosaccharides act as prebiotics and also as receptor analogues that act as anti-infection factors. We propose the following hypothesis. The proto-lacteal secretions of the primitive mammary glands of the common ancestor of mammals contained fat and protein including lysozyme, but no lactose or oligosaccharides because of the absence of α-LA. When α-LA first appeared as a result of its evolution from lysozyme, its content within the lactating mammary glands was low and lactose was therefore synthesized at a slow rate. Because of the presence of glycosyltransferases, almost all of the nascent lactose was utilized for the biosynthesis of oligosaccharides. The predominant saccharides in the proto-lacteal secretions or primitive milk produced by this common ancestor were therefore oligosaccharides rather than free lactose. Subsequent to this initial period, the oligosaccharides began to serve as anti-infection factors. They were then recruited as a significant energy source for the neonate, which was achieved by an increase in the synthesis of α-LA. This produced a concomitant increase in the concentration of lactose in the milk, and lactose therefore became an important energy source for most eutherians, whereas oligosaccharides continued to serve mainly as anti-microbial agents. Lactose, in addition, began to act as an osmoregulatory molecule, controlling the milk volume. Studies on the chemical structures of the milk oligosaccharides of a variety of mammalian species suggest that human milk or colostrum is unique in that oligosaccharides containing lacto-N-biose I (LNB) (Gal(β1 → 3)GlcNAc, type I) predominate over those containing N-acetyllactosamine (Gal(β1 → 4)GlcNAc, type II), whereas in other species only type II oligosaccharides are found or else they predominate over type I oligosaccharides. It can be hypothesized that this feature may have a selective advantage in that it may promote the growth of beneficial colonic bacteria, Bifidobacteria, in the human infant colon.


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Statement about Tropical Rainforests
I made a statement about tropical rainforests, and I want to know if it's somewhat true or not:
The soil in tropical rainforests is not exceptionally fertile, because it contains few minerals. The reason that a tropical rainforest has a huge amount of vegetation is because of the quick mineralisation. If a dead leaf falls onto the ground, it immediately gets turned into minerals, which the plants immediately use for sustaining theirselves

I don't quite follow your logic of why a dead leaf should be immediately turned into minerals.

that's what happens in a rain forest, it happens much more quickly than in a temperate forest for example

I think you need to clarify that point in your statement, then.  I would not buy that it happens immediately, nor would I buy that it is degraded into "minerals", likely there is some state where it is detritus and is then processed further by microorganisms.

I didn't mean immediately in the literal sense.. in the previous sentence I also said 'quick mineralisation' which shows that..

Well, to be honest, what you have is a statement laden with ambiguities, so to claim any truth in it, you'd have to be absolutely precise with the language.  If you made this statement to scientists, most if not all would assume you would have ballpark figures for "immediate", etc. with references to back them up.  I'm not sure what anyone can offer you in an answer beyond that.

@jonsca I don't know why I am coming back to this after a month and a half, but 'laden with ambiguities' is a hyperbole. I don't appreciate hyperboles on sites like these.

It was not meant as a personal attack, there are quite a few ambiguities in you statement "huge", "quick", "immediately".  If you attempted to publish that in a scientific setting, I'm sure you would get the same response.  I don't think there was any hyperbole in my statement at all, laden="weighted down".  I think they distracted from the message you were trying to put forth, that's all.

There are many websites which describe this phenomenon. They all seem to confirm the basic premise of the question: in tropical rain forests most of the minerals are held in the biomass and rapid decomposition contributes to the recycling of these nutrients for new growth. One example is here.

Tropical rainforests are noted for the rapid nutrient cycling that occurs on the ground.  In the tropics, leaves fall and decompose rapidly.  The roots of the trees are on the surface of the soil, and form a thick mat which absorbs the nutrients before they reach the soil (or before the rain can carry them away).  The presence of roots on the surface is a common phenomenon in all mature forests; trees that come along later in succession win out in competition for nutrients by placing their roots over top of the competitors, and this pattern is seen in the temperate rainforest as well.  What does not occur in the temperate rainforest, however, is a rapid cycling of nutrients.  Because of the cold conditions and the acidity released by decomposing coniferous needles on the forest floor, decomposition is much slower.  More of the nutrients are found in the soil here than would be the case in a tropical forest, although like the tropical forest most of the nutrients are held in the plants and animals themselves.

I looked for actual evidence of these differences in rates of decomposition and I found this:

Salinas, N. et al. (2011) The sensitivity of tropical leaf litter decomposition to temperature: results from a large-scale leaf translocation experiment along an elevation gradient in Peruvian forests. New Phytologist 189: 967-977

These authors reported a comparison of rates of decomposition at various elevations in Peruvian forest. The parameter k is the decay rate of dry mass, year-1. The following data are taken from Table 3.
site          elevation (m)   mean k (yr-1; 15 species)
Tambopata     210             1.753
Tono          1000            1.424
San Pedro     1500            0.968
Trocha Union  2720            0.546
Wayquecha     3025            0.424

and this:

Jacob, M. et al. (2010) Leaf litter decomposition in temperate deciduous forest stands with a decreasing fraction of beech (Fagus sylvatica) Oecologia 164:1083–1094

These authors studied leaf decomposition in a deciduous forest in Germany, with emphasis on the effect of proportion of beech trees upon overall rates of decomposition. Using data from Table 1 and Figure 2 (values converted from mg-1 g-1 day-1 to yr-1)
% beech yr-1
  96    0.2555
  67    0.657
  21    1.022

My Conclusion
Rates of decomposition can be much higher in tropical rainforest (k=1.753 yr-1 for the Tambopata site in Peru, k=0.256 yr-1 for a beech-rich forest in Germany). However, at higher elevations tropical rain forests are characterised by much lower rates of decomposition (Wayquecha k=0.424 yr-1), comparable to those in deciduous forests.
These are all measurements of loss of dry mass from leaf litter. This will be dominated by loss of carbon, and I would expect that minerals will leach from the decaying litter more rapidly than these values. Nevertheless it seems plausible that relative rates of mineral recycling will reflect these k values.

Fantastic answer


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Are the inverse problems of Systems Biology impossible to solve?
I have heard Sydney Brenner give a talk [0] on how the entire program of Systems Biology is suspect because, according to him, a chap named Hadamard showed that inverse problems are impossible to solve, or something to that effect.
I find it somewhat odd that no one seems to be paying any attention to this, and many are blithely carrying along trying to reverse-engineer biological organisms. I personally think that this reverse-engineering effort has its place, but Sydney Brenner doesn't seem to think so, and advocates tackling only the forward problem. Here's an excerpt from an abstract to a similar talk of his:

... This notion of computation is, in my opinion, the only valid approach to biological complexity and is opposed to many of the ideas underlying what has come to be called systems biology, which is very fashionable today. It will be shown that systems biology attempts to solve inverse problems — that is, obtain models of biological systems from observations of their behaviour — whereas, what I call computational biology, continues in the classical mode of discovering the machinery of the system and computing behaviour, solving a forward problem.

Is Brenner simply wrong on this or is there something to his objections?

[0] Sydney Brenner, Much ado about nothing: systems biology and inverse problems, 2009.

I've seen many a computational model that blatantly failed to consider very well known biological constraints and were, therefore, useless.

You might find this note useful - http://www.physics.ox.ac.uk/systems/agarwal/PhilSB.pdf
Also this blog post - http://www.pagev.net/2011/04/is-systems-biology-doomed-to-fail-no.html

Another Brenner quote: "Systems biology is low input, high throughput, no output science" and I fully agree.

First link in my comment is not working now - Updated link is http://web.iitd.ac.in/~sumeet/PhilSB.pdf

The answer is mostly no, and this is not as disruptive a statement as it seems to be.
I think Brenner has a point of course and he is not the only one who wonders whether the systems biology can create a holistic model of living things.  Still I wouldn't take this to mean we should stop doing systems biology research.
At 18:30 brenner illustrates the inverse problem with some examples 1) can you create a drum from only the sounds that come from the drum? (no he says). 2) can you solve the molecular structure of a molecule from a diffraction problem (no he says).
Of course we can do both of these, but the point is valid as we need to have an idea of what a drum looks like.  If we did have even a glance at a drum, this lets us build a model (cylinder of diameter d, height h and with a drum head of a tension t and material properties alpha beta, etc) from the sounds is a lot of work, but it could be done.
The problem of solving a molecular structure from diffraction intensities alone has also been solved for small molecules in the 60s I believe by so-called 'direct methods' which don't work well or proteins and larger molecules.  Still the point is that you had to have a good mathematical model of molecules and diffraction to get to direct methods, MIR, MAD and other diffraction only methods. Sorry I can't go into details here...it might bore you to death if you don't care about crystallography.
In both cases the statement is that you need to have that model - what does a molecule look like, what does an x-ray do when it encounters a crystal? In order to get there.  Which makes total sense and I agree with.
I wouldn't read too much into this though, because in practice this has never been done, yet Bragg started with just the diffraction pattern and drew in models from other fields of study.  Given the nature of the proof described, no scientific discovery has ever happened in a mathematical vacuum and systems biology will not either.
Rather I would read this talk as saying that the models we are using for action are not very good yet.  What is happening is that synthetic biology (engineering approaches), experimental observation, and intensive modeling (the 'inverse' and 'forward' approaches Brenner mentions) are all happening at once and are informing each other.
Its hard to imagine that data from inverse approaches can't be an important part of any solution to biology.  Its also looking likelier that a mathematical model alone of biology will be difficult or impossible to find also.  What is currently (IMHO) working is a framework that is both conceptual (and not entirely quantitative) as well as analytical (mathematical) and data driven.

The problem is that you need good data to do good sysbio, and you need lab work to produce good data. You can't simply rely on electronic annotation of genes and even manual curation introduces too many errors. Then where do you get your enzymatic constants from. It's all garbage in, garbage out.

@rwst v true - really the molecular mechanisms of biology are incomplete in every sense - models, mechanisms, data, observability... to some extent this is true for any major scientific system at first (atomic physics had no idea how large an atom was until early 20th century, and even the motion of the planets was difficult to discuss until adequate telescopes could be made).

The article is well known and discussed amongst systems biologists. It makes a good point - high throughput, observational biology cannot substitute for mechanistic studies that provide causal information.
But we know an awful lot about biological systems already. All systems biologists are using information from the forward approach implicitly when they formulate their models. More importantly however, most systems biologists combine the forward and inverse approach in their work. Models are tested and validated by perturbing the systems, and updated according to the results.
Discussions of these kind often devolve into a debate over the semantics of systems biology, in which it's detractors attempt to define "systems biology" in the most unflattering terms possible.

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Effect of extracellular molecules on membrane potential
I am reading about the effect of extracellular potassium and chloride on the membrane potential, and now a question has come to my mind about what would happen if we added some molecules that have no charge to the extracellular? (consider that only K+ and Cl− can cross the membrane.)
I think that membrane potential and volume does not change, but I'm not sure about that.

@MCM I cannot add comment after the great answer of MCM. Thank you alot. Then this means the volume also increase?

I'm wondering if you don't mean increase the volume of the cell - in which case, in extreme conditions where the cell cannot maintain water and salt concentrations, the cell would lose volume as water and salts move out. In a hypotonic solution (much more water than solutes), the cell would lyse as osmotic pressure favors water moving into the cell.

The absolute answer would depend on a lot of factors, but the basics of it would be that - Yes, the volume does change and Yes, it would have an affect on the membrane potential.
By adding mass to any liquid solution, you are changing the volume. Plain and simple. Liquids are not compressible, and the only way to maintain volume while adding mass would be to increase the density of the liquid. [Edit] I'm wondering if you don't mean increase the volume of the cell - in which case, in extreme conditions where the cell cannot maintain water and salt concentrations, the cell would lose volume as water and salts move out. In a hypotonic solution (much more water than solutes), the cell would lyse as osmotic pressure favors water moving into the cell
The membrane potential would change, but how much depends on a lot of factors. It would most likely change due to the movement of ionic solvents down their concentration gradients. Osmosis would move water out of the cell and into the extracellular environment, and ultimately reduce the membrane potential as more water outside the cell would essentially decrease the molarity of the solution. The cell would have to pump more ions out in order to regain the membrane potential.
The exception might be if you added so many hydrophobic molecules outside the cell that you basically saturate the environment, which could prevent exchange of all charged or partially charged atoms and molecules.

"The cell would have to pump more ions out in order to regain the membrane potential." So any change would be transient?

@AlanBoyd - Correct. The cell has the ability to open or close ion channels (free exchange down the gradient), and decrease or increase ion pumps (active transport). If the solution is hypertonic, the cell can open channels until the membrane potential is regained. If the solution is hypotonic, the cell can expend energy via ion pumps to move atoms into solution. This is particularly pronounced in neurons, where signal propagation relies on the membrane potential's existence (and is a little bit higher than your average cell). Barring extreme conditions, of course. Cells can't always cope.

A bit of an addendum: The cell almost never completely shuts down ion channels or pumps. The membrane potential is balanced between the two (and some other players).

I'm no electrophysiologist, but I do know that the membrane potential is determined by the distribution of ions across the membrane: mostly Na+, K+, Ca2+ and Cl-.
An uncharged molecule will only influence membrane potential if it has an effect upon the distribution of these ions. One example of such a molecule is valinomycin, a neutral ionophore which permeabilises membranes to K+ ions. Another example is ouabain which inhibits the Na+/K+ pump that is in part responsible for establishing resting membrane potential.
But in general the addition of uncharged molecules will have no direct effect upon membrane potential.
(I expect that there will be someone along shortly to explain why it is much more complicated than this.)
edit: It turns out that MCM got here before me!

Remember also that plenty of molecules have receptors on the membrane that can cause membrane potential to change, directly or indirectly.


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What hair do aquatic mammals have?
I'm reading an essay on the creating of the Mammalia zoological classification (Londa Schiebinger, The American Historical Review, Vol. 98, No. 2 (Apr., 1993), pp. 382-411).
It contains the statement (page 386)

All mammals (including the whale) have hair, and it is still today considered a distinguishing characteristic of mammals.

Is that statement correct? Do all known species of whale and dolphin have hair? If so, where is it? You can't see it on the surface of the animal, is it internal like we have nostril hair?

Well, technically yes, but most adult dolphins do not have hair:

Unlike most mammals, dolphins do not have hair, except for a few hairs around the tip of their rostrum (beak) which they lose shortly before or after birth. The only exception to this is the Boto river dolphin, which has persistent small hairs on the rostrum.

Whales do, and depending on your definition of "hair" - that includes Baleen - which is composed of fine keratin fibers, much like normal fur/hair, which is the distinguishing characteristic of "Baleen whales" (like the Blue Whale).

What about orca or other whales with teeth?

Yes and yes. A lot of marine mammals lose the hair before birth or shortly after, including orcas and many whales. However, because it is present during development, they can be classified as mammals if no other traits are present.

Orcas are dolphins by the way, not whales.

@terdon A lot of 'whales' are actually dolphins, which would be an interesting discussion on it's own.

I'll echo what others have said here. It is a characteristic of marine mammals as mammals. But not something you'd obviously see on adult whales. Humpback whales do have visible hair follicles. Another example where you can see hairs well are on gray whale calves. If you zoom in on this photo, you can actually see a few! This was taken in San Ignacio Lagoon, Baja, California Sur, Mexico.

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text:
How does hemoglobin-free blood transport oxygen?
Snails... We have some kind of huge garden snails appearing lately (read since the last 10 years or so). Try as one might, it's impossible to avoid them when driving. These snails do not appear to have red blood - I doubt they have blood at all. Wikipedia tells me blood's red colour is due to haemoglobin - which serves to transport oxygen.
How do snails (and any other animals that do not have red coloured blood) get oxygen? Or, do such animals need no oxygen at all?

Snails, like most molluscs, have a protein called hemocyanin dissolved directly in the hemolymph ("blood"). Hemocyanins are copper-containing metalloproteins: the binding site for a single O2 molecule contains two copper atoms. Unlike hemoglobin, where reversible oxygen binding is accomplished without a change in the oxidation state of the Fe(II) atoms in the heme prosthetic groups, in hemocyanin the copper undergoes a transition from colourless Cu(I) in the deoxygenated state to blue Cu(II) when oxygenated.
Incidentally, there are certain species of fish that manage with little or no hemoglobin - icefish.


text:
Diet of free-range herbivores
Giving minimal credence to estimates in popular media of the average biomass of  insects/arachnids, etc. in an acre of land, it seems that a "free-range" cow (I don't mean to pick on cows) might be something of an omnivore. Is there any evidence that herbivores derive essential parts of their diet from sources other than cellulose? Or that they do not?

Cellulose alone is just a sugar source. Plants do contain minerals and vitamins. They also contain protein, though the amount can be extremely low - thus the need for a lot of grassland to feed cattle. I'd expect the amount of protein intake from hapless bugs and spiders would be low, though, compared to the overall intake from plant sources.

As a fraction of diet it must be low, yes.

Deer have been known to eat bird eggs or young birds possibly to supplement calcium for antler growth.  I can't image it's a large part of their diet though.

@RioRaider: interesting, do you have a source for that?

@nico Here is an article in National Geographic.  Here is an interesting YouTube video of a deer eating a bird.  Here are two USGS webpages, 1st and 2nd, that discusses nest predation by ungulates.  Also, take a look at this Journal of Zoology article.

Animals lick salt deposits. It's an important part of there diet for plant eating animals.

One key nutrient worth thinking about in the context of this question is vitamin B12. Herbivores such as cows and sheep will derive this directly from the bacteria in their rumen. Rabbits produce two types of feces - soft and hard - and they eat the soft variety, rich in gut bacteria, as a source of nutrients like vitamin B12. Gorillas are primarily herbivores, but are thought to derive their vitamin B12 from insects, eaten purposefully or inadvertently.
So yes, herbivores derive this particular nutrient from non-plant sources.


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Does artificial heat (shower/tea) affect diurnal rhythms in humans?
I've been reading that over the course of the day, human body temperature follows diurnal rhythm with the lowest body temperature observed some time close to the middle of the sleep episode, while the peak body temperature is observed some time close to sunset.
Circadian rhythm on Wikipedia
I'm interested if humans have internal organ systems or brain "sensors" that "read" the body temperature as a part of synchronizing their own internal circadian clock to the master clock of the human body.
If there are indeed such sensors, then I'm interested if they can be thrown "off track" by artificial heat sources, like hot food, drinks or showers.

Well if temperature follows optical input, then it's not the other way round, is it? With warming up your body, you may get all sorts of psychological effects that obscure the rhythm but you can't simply exchange cause and effect of the diurnal cycle.

I've clarified the question to address your comment. Could temperature be a part of how circadian oscillators are synchronized?

Yes, the human body has thermoreceptors that "sense" the current temperature, but these merely help with regulation--you know, shivering to raise internal body temperature and sweating to cool via evaporation. The hypothalamus is primarily responsible for making sure that the circadian rhythm itinerary is adhered to reasonably well. So no, if the thermoreceptors detect that the body temperature is 97 deg F but it's 5 pm, the body will not "get confused" and decide that it is actually 4 am because a human body is about 97 deg F at 4 am.


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Are tuna fish present in the Baltic sea?
Yesterday my grandmother ate fresh tuna at a friend's party. She swears it was fresh and bought at a local fishmonger. The problem is, that we live in Gdańsk, by the south-eastern side of the Baltic sea and I have never heard of tuna in the Baltic. I told her that the fish couldn't have been local and therefore couldn't have been fresh but frozen and thawed. But the thought still bothers me, maybe tuna fish can reach the Baltic?
I did search a bit and found that tuna may be sometimes found in the Northern sea, so maybe it actually can travel so far east as to reach the Baltic? But the water in the Baltic is hardly saltwater (6-8‰), so would it be able to survive?

Indeed tuna are present in the Baltic sea, and they can also grow in the Pacific and Indian oceans. A lot of the tuna we see in tuna cans in supermarkets comes from the stocks in the Indian ocean, but it is possible to have fresh tuna from the Baltic.
Sorry, I only found a French answer from a famous French news paper: http://sante.lefigaro.fr/mieux-etre/nutrition-aliments/thon/dou-vient-thon

I know some french, so it's not a big problem. The problem is, that Le Figaro is quite far in the Science News Cycle (http://www.phdcomics.com/comics/archive.php?comicid=1174#), so if it's the only link you can find, is very weak. I searched on ncbi and found nothing on tuna living in the Baltic sea, but I don't know how broad is their database - generally I used it when I was a biotechnology student plus for some medical research for my family - not much of ichtiology.

@jkadlubowska there are no landings of tuna in the Baltic. Your research is correct.

There's a newly established Atlantic Bluefin Tuna fishery in Norway, and some bluefin landings as far North as off Greenland, so it's not completely beyond the pale to think there might be some very few that stumble into the Baltic Sea, especially with climate change-- but definitely not enough for a commercial fishery.

A good answer except for the fact that Fish that is shipped all over the world is frozen and never fresh, whatever your local fish shops tells you. Most fish is already frozen on board

I agree with you, @RHA , but I know you can get fish shipped on (dry) ice. I work in a lab that does research on tuna, and we have gotten fresh specimens before from off-shore Hawaii. (We're in MA). -- But it certainly costs more $$$$. I can't imagine getting bluefin fresh.

The big commercial fish trawlers are at sea for weeks at least. Then they return to the harbour and only then.the fish is shipped. This means that fresh fish is weeks old. I wouldn't call that fresh. The fish caught at the last few days is often kept and sold seperately to restaurants etc.

@RHA fair enough! I got rid of that part.


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What difference does it make in the organism's physiology/metabolism whether oxygen binds reversibly or not?
A follow-up to How does hemoglobin-free blood transport oxygen?
I'm unsure about the use of physiology/metabolism in the title there. The question in mind is whether this reversible binding makes an organism slower, or faster; perhaps more capable of surviving in rarefied atmosphere.
EDIT:
I apologize that my comment made it appear this question is only about the Icefish; it is not. There are still other species (for instance, molluscs, and arachnids) which acquire oxygen by means other than haemoglobin.

I'd love to answer this question, but I don't really understand it. If you are referring to oxygen binding by a carrier protein such as hemoglobin, then the binding has to be reversible otherwise the protein wouldn't be able to deliver oxygen to respiring tissues.

@AlanBoyd: The answer in the linked question indicates that species the binding is not reversible in Icefish; perhaps other species too. I'm curious about the nature of oxygen binding (reversible or otherwise) does it improve the ability of blood to deliver oxygen/nutrients and in turn what effect that has on the organism's physiology. Could it have evolved to enable the creature to survive adverse environment - as in the case of ice-fish?

The classic example of a hemoglobin adaptation to high altitude is found in the case of the bar-headed goose, Anser indicus.
This bird undertakes very high altitude migratory flight, crossing the Himalaya. It has a number of physiological adaptations that allow this, but it also has a novel form of hemoglobin with an unusually high affinity for O2. A single mutation changes the co-operative oxygen-binding behaviour of the haemoglobin molecule. In terms of the diagram in jello's answer, this shifts the binding curve to the left (i.e. toward that of fetal haemoglobin). This, in turn, means that the molecule binds more oxygen in the lungs, but it also means that it doesn't release the oxygen as readily in the peripheral tissues. On balance the former effect dominates and the efficiency of oxygen delivery is improved.

I think I see where you are coming from.  There is a misunderstanding here.
Ice-fish have relatively lost their hemoglobin gene over time because they have adapted such a slow metabolism in the cold water where the oxygen is richer (oxygen content in cold water is higher).  The don't need any binding of oxygen to a carrier protein like hemoglobin because enough oxygen diffuses in from the water for the needs of their tissue.
There is no binding - reversible or irreversible in their blood - that would imply that the oxygen is binding to a protein like hemoglobin or hemocyanin, which the fish does not have.   The oxygen is just diffusing into the fish from the water around it.  The circulatory system is helping by flushing the system out and keeping everything fresh as well.

Just to expand slightly on this answer, for clarity, the oxygen is diffusing into the blood at the gills, and diffusing out of the blood into the peripheral tissues where it is used for respiration. The blood and circulatory system of the icefish is performing the usual function, it just does it without an oxygen-binding protein.

@AlanBoyd thanks for this.  its possible there is diffusion through the gut and the skin too - remember salamanders and most reptiles have some oxygen from their skin too.

I don't understand your question either, but my response is to the question in the title. Oxygen has low saturation in blood plasma, so humans require hemoglobin to serve as a transport protein. Oxygen must bind reversibly, otherwise it gets stuck to hemoglobin.
Humans actually have two proteins, hemoglobin and myoglobin. Hemoglobin (HbA) circulates in the blood, whereas myoglobin is in the muscles. Myoglobin (Mb) has a higher affinity for oxygen than hemoglobin (see image). This makes sense, because the hemoglobin in the blood must unload oxygen at the muscles, and myoglobin must bind it. Hemoglobin's affinity for oxygen is regulated by 2,3-BPG, pH, and [CO₂] to ensure that it can unload oxygen at tissues.

(Curves to the left have higher affinity, meaning that they have a higher oxygen saturation for the same partial pressure of oxygen.)
Furthermore, humans have several types of hemoglobin. Fetal hemoglobin (HbF) has a higher affinity for oxygen than regular hemoglobin, ensuring that the fetus obtains the oxygen that it needs from the maternal blood.

Curious: If haemocyanin were to replace haemoglobin in a human body, would the person survive?

Ignoring the fact that hemocyanin is only in hemolymph and not red blood cells (as in humans), my guess would be no. Hemoglobin exhibits cooperativity, so that the binding of one oxygen molecule increases the affinity for other oxygen molecules. This leads to the sigmoidal oxygen saturation curve, allowing for more efficient dissociation of oxygen at target locations.


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How does one maintain balance sleepwalking?
Anectodal. Feel free to shoot it down.
Walking is an acquired skill; As far as I'm concerned exhaustion causes disorientation. Even after waking up it sometimes takes a second or so to get balanced.
How is it sleepwalkers don't stumble around when walking?

Balance is maintained by the cerebellum, not by any of the cortical areas that are less active during sleep. Thus, there's no reason sleep should affect your ability to balance.
Being asleep doesn't mean that you're fatigued. I wouldn't be surprised if a highly fatigued person who was sleepwalking did have poor balance.

In fact, repetitive actions like riding a bike or playing the piano (when experienced) are also stored in the cerebellum so should in theory be possible for sleepwalkers to do :D

An interesting question. When a person is asleep and dreaming, the person's brain is fairly active, similar to the waking state levels. The person is not exhausted, and sleepwalking is when muscle atonia is lost, and the dreamer is acting out actions in the dream. Maintaining balance in a dream might translate to maintaining it in a waking world (we all walk on floors after all, not mountain slopes :) )

@AlexStone: Agreed. But the floor is not a plain surface. There're various pieces of furniture on it. Perhaps even a step between one room, and another

Balance is mediated by 3 things: the cerebellum, vision and the ear via the semicircular canal + vestibular nerve (i.e. the ear).
Sleepwalkers lack the visual feedback, but they have a functional cerebellum and semicircular system which is sufficient.
As for waking up and feeling disorientated, if that's when you get up fast that's because your semicircular system hasn't yet reset (as well as your blood pressure has just dipped).

Mind all of you, even the cerebellum sleeps. The waves that are generated in the neocortex predict the same waves in the cerebellum. There probably is no active vision, but the activation patterns of the dreaming visual cortex may give the sleep walking person an idea of the world around him/her. This might, however imply that a great deal of luck is involved in getting somewhere in one piece (given that the patient even moves outside...). During normal REM sleep we speak of complete muscle atonia, the eyes not included. However, this does not work that well in all patients, meaning that they start living their dream. Mind you as well that keeping balance is partially programmed in the muscular innervation (connection patterns in the spinal cord that registers and partially controls muscle tone of agonists and antagonists), and in part by the cerebellum indeed. The cerebellum, however can be devided in a cortex and in cerebellar nuclei. The cortex is not involved in keeping balance as such, much of this is programmed by the cerebellar and pontine nuclei.

The part of the brain that maintains balance acts subconsciously, and so while you are sleeping in the behavioral sense, you part of your brain (the cerebellum) do not necessarily have to be asleep. And so it can still maintain balance.


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Do any birds beside the family Columbidae (or any reptile or mammal) feed their young "Crop Milk"
Birds from the family Columbidae (e.g., doves and pigeons) produce a fatty, milk-like substance in their crop.  The secretion is often referred to as "crop milk."  They feed crop milk to their young through regurgitation.  Does anyone know of another bird or reptile group (or even mammals) that has evolved such a mechanism; not regurgitation but secretion of a milk-like substance for feeding young?  Also, both male and female doves produce crop milk; are there cases where males of a mammal species produce milk?

Male galactorrhea exists in humans.

In mammals there are only two species (known, there may well be others) where males lactate. They are both species of bats and this paper discusses the evolutionary mechanisms that could underlie male lactation. I have ignored human cases because they are more of an unusual occurrence (often brought on by severe dietary stress) rather than an evolved mechanism.
Other non-mammals include Flamingo and Penguins. There is also a species of fish, called a discus fish, which produces a mucus from its skin which the offspring feed on (here). I would hypothesise that this evolved originally for different reasons (defence, scent communication, excretion...) but offspring "discovered" this was slightly nutritious so fed off it, those genetically predisposed to doing such things then had higher fitness and the trait spreads. Evolution of greater or more nutritious mucus production would be achieved because parents that produce more/better mucus would have more offspring that reach maturity.
The paper by Kunz & Hosken is a good discussion on current evidence and the potential for evolution of male lactation.
I hope that answers your question, happy reading!


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Preferred Aspect Ratio for Human Eyes
Our eyes are spherical, our retina is circular, but still our eyes can see more in the horizontal direction than in vertical direction. Why is it so, why is the preferred aspect ratio not square?

This is just a hypothesis: but there is probably not one "preferred" aspect ratio, even for one individual. It probably has to do with the following points: 1. the eyes are positioned on a horizontal line; 2. the width between the irises; 3. how far you are looking.
And let's not call it a "preferred" aspect ratio. It's more like an "effective" aspect ratio. My hypothesis is that the closer you look, the wider the effective aspect ratio is, and the further you look, the more circular it is. And if you cover one of your eyes, you'll probably get a circular FoV regardless of distance.

I have to agree with Kal, but mainly about #1. Essentially, the eyes are next to each other, and this allows for stereoscopic vision. If you cover one eye, your field of view is more or less circular (due to the retina and macula), but you'll lose depth perception. Plus, your eyelids slightly limit the amount you can see in the up-down directions.

@jello Surely the eyelids can't be having an effect as you describe because they don't normally cover any part of the pupils.

@AlanBoyd I think you're right. For some reason, I was probably thinking about ptosis, when a drooping eyelid does limit your visual field.

I will add that in other animals, having a wide horizontal angle helps in hunting and also in defending against hunters. The vertical angle is also important, for example for hunting birds, but not so much for terrestrial animals.

I found the explanation given below here (my emphasis). It may not be authoritative, but it makes sense to me.

You can determine the approximate shape of your visual field by looking straight ahead, and holding a hand out to each side and noticing where you can no longer see them. Do the same for above and below, and you'll see that your peripheral vision probably extends to about 180 degrees (or a little less) left and right, and about 100 degrees up and down. Your brow, nose, and cheeks narrow the vertical angle.
So your visual field has a ratio of about 1 to 1.8.
Interestingly, and not entirely coincidentally, ordinary films and wide-screen TVs have a ratio of 1.78 (16:9).

Another way to see this effect is to look at someone's head in profile and from directly above. In the former  case you have a clear view of their eyes, in the latter you don't. (Tested on a small sample - one 3 year old male, playing with an iPad).

The reasons your field of view is not circular are:

Even when looking directly forward your nose, brows, and cheeks obstruct your view.
You have two eyes which are aligned horizontally.

The field of view is measured by a method called perimetry, and looks approximately as depicted in this graphic. The guide here provides further comments on the graphic.
As you can see in the image I linked to, the field of view (were it to be approximated with a rectangle) spans 180° horizontally and 130° vertically. Yielding a width-to-height ratio of 0.72. Which is better approximated by the traditional 4:3 screen size and NOT by modern 16:9 displays. Having said that, 16:9 may not necessarily be a worse format, as researchers found that horizontal saccades are faster than vertical ones.


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What are the "stars" we see after a bump on the head?
Sorry  if this might appear funny. When I close my eyes for a longer time, and suddenly open  it, I see some twinkling white small circles, and when i concentrate on anyone of them it disappears, as if the image is falling on the blind spot.
This also happens when I am struck on my head sometimes accidentally. I would see thousands of tiny objects floating. What are these and why they appear shiny ?

i think they are randomly triggered neural impulses in the retina or optical nerve.

"Seeing stars", or as it formally is called, "phosphene", is caused by stimulation of the visual cortex or retina by causes other than light hitting the retina.
http://www.oubliette.org.uk/Three.html

Wikipedia on it's own is a poor reference, try following their sources back to find something less fluid :)

@RoryM Ok, I don't know what you mean with "something less fluid" but I've added the source that seems most complete on the subject, although that source is also based on other sources, IDK if that's ok? P.S: I tought that puting a wiki article would count as a good reference cause they are required to have "reliable" sources backing up their text...

Hi Jo,  Wikipedia can change every day, there's no guarantee that a reference to wikipedia will remain accurate if the source article is changed.  Of course, you can say that about virtually any online source but Wikipedia in particular is prone to this.  Ideally, you should look at peer-reviewed sources, however the source you now link seems a comprehensive review, therefore I will reverse my downvote.

@RoryM, I do not mean to imply that Wikipedia carries more weight as reference than proper sources, but I'd like to point out that it is possible to link to a specific revision of an article. Under Toolbox, you can find the article's Permanent link, which will always redirect to the revision you were viewing.


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How does fever physically work?
What is the physical mechanism that causes temperature to rise during a fever? I know that somehow the hypothalamus "orders" to increase the standard body temperature regulation, and this should stimulate mitochondria to produce more ATP. Is that right?
Is this the only heating physical mechanism (through increasing production of ATP) that acts during a fever?

From Wikipedia: "The [hypothalamus] ultimately orchestrates heat effector mechanisms via the autonomic nervous system. These may be: (1) Increased heat production by increased muscle tone, shivering and hormones like epinephrine; (2) Prevention of heat loss, such as vasoconstriction.
In infants, the autonomic nervous system may also activate brown adipose tissue to produce heat (non-exercise-associated thermogenesis, also known as non-shivering thermogenesis). Increased heart rate and vasoconstriction contribute to increased blood pressure in fever."

As John mentioned, pyrokines such as IL1 and TNF affect the hypothalamus. Your hypothalamus is a thermostat, similar to central heating for example. So when you set your core temperature higher, your body thinks it is cold. To warm up it does several things:

Vasoconstriction directs blood to the core body and prevents heat
loss
Brown fat break down in infants makes heat
Shivering which requires respiration which produces a lot of heat. Metabolism also
increases in other ways - this is why it is commonly advised to
increase food consumption during illness
We wrap up warm - an often overlooked mechanism that is incredibly important.
Limited piloerection: if we are hairy our hair will stand up attempting to
create a barrier for heat loss
We stop sweating (breaking of a fever or when the hypothalamus is reset to normal causes us to sweat)
Hormonal regulation via (nor)adrenaline/epinephrine, thyroxine - these are related to the increased metabolism.

Cytokine production in the body resets the thermoregulatory centre in the hypothalamus to a higher temperature. As a result, your muscles begin to contract violently (rigors) to generate more heat until you equilibrate to the new setpoint. Hope this helps.

Yes but just to mention the reset is to a higher temperature. From 37 to 38 for example.

@AndroidPenguin Thanks for pointing that out-its a higher temperature. I'll edit my answer.


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Fossils of intermediate stages?
If Humans are evolve from Monkeys, there must be stages in the evolution process, when it was 1% human and 99% monkey, 2% human and 98% monkey  and so on. This is because evolution was a very slow process that occurred in a span of thousands of years. So we expect there must be fossils of this intermediate stages under earth. These intermediate-stage fossils must be many times in no. as compared to 100% human or 100% monkey.
But why do we do not discover these intermediate fossils?

Humans did not evolve from monkeys, we are apes (along with chimps, gorillas, and others).  We apes evolved from earlier primates, as did the monkeys and prosimians (like lemurs).

you have to remember that we are also getting further from our ape cousins all the time, even if we do not change into a new species.  Just the passage of time accumulates mutational differences between us and other species we are related to like the apes.

in addition to the comments above and the answer provided, note that we created the labels "monkey" and "human" based on the characters of these organisms.  There is no absolute "human" or "monkey" to partition into fractions.

We do, all the time. Here's a nice graphic from Dr. Douglas Theobald. (Images copyright 2000 Smithsonian Institution.):

That's 14 Hominid species, ranging from about 4 M.Y. ago to a modern human skull ("N").
Here's a nice genealogy as well (although these change frequently as more evidence is gathered):


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How did giraffes develop their rete mirabile failsafe?
Giraffes, being one of the tallest mammals in the world, have a failsafe called rete mirabile to prevent them from dying from excessive blood pressure while lowering their head.[1]
Due to their long necks, a formidable amount of blood pressure is needed (quoted from animals.about.com):

A giraffe's heart has special adaptations to enable it to pump blood up the animal's long neck to its head.
  A giraffe's heart has the formidable task of pumping blood at high enough pressure so that it can flow up the giraffe's neck to the brain.
  To accomplish this, a giraffe's heart is specially adapted.
  It can weigh up to 10 kg (22 lb) and generates twice the blood pressure of other large mammals.
  Having enough blood pressure to pump blood to the brain when the giraffe's neck is extended upward is one challenge, but when the animal lowers its head it risks injury due to excessive blood pressure.
  To counter this, giraffes have a pressure-regulating system known as the rete mirabile which restricts the amount of blood that rushes towards the brain when the giraffe lowers its head.

How did this evolve? I believe in evolution but I can't wrap my head around this. If an "overload" of blood would reach the giraffe's brain while it is, for instance, drinking water and either instantly killing the animal or severely wounding the animals mental and physical capabilities by rupturing the brain, how could a failsafe like this evolve?

How could it not evolve? Taking the most laymanic interpretation of evolution by mutation, a proto-giraffe without the mutation of the heart would surely die. Those with it wouldn't and thus able to pass on the mutation to its descendants!

A giraffe's rete mirabile is located somewhere "behind" the brain, as a complex system of veins and tissue to form some sort of sack to store the excess blood, hence it's not the heart taking care of this matter. A proto-giraffe with this mutation would surely be the one to pass the genes on. But since this function, the rete mirabile, isn't really needed until the moment right before the sudden death/wound of the giraffe, how did it possibly evolve in the first place?

Where the thing is located is irrelevant. Mutation is purely random, and if that mutation gives you a step up on your neighbour, then your genes go on and his (possibly) don't. Again this is a huge oversimplification of Evolution.

According to Wikipedia, http://en.wikipedia.org/wiki/Rete_mirabile, these structures are widespread in vertebrates, and usually play a part in equilibrating two parts of the bloodstream (heat, ions). So this would simply require the adaptation of a prexisting structure to take on an additional role, with obvious selective advantage - if there is a selective advantage to having a long neck then there will also be one to changes that accommodate it.

Thank you for moving it to Biology. Im still navigating myself around StackExchange. Reading these comments they all make sense, but I feel my intention with asking this question is far too widespread and traces too far back in evolution, where it's more or less impossible to answer. Thanks for your time and input :). Question can be closed.

I think what leads to the confusion here is the assumption that the neck was evolved before the rete mirabile.  Giraffes evolved from creatures with shorter necks.  As evolution occurred nature was selecting for longer neck creatures (being able to eat more leaves) but at the same time creatures with longer necks had problems with blood pressure.
At this point this would also not be lethal because we are talking about animals with much shorter necks, just in some way disadvantageous to the animal.
So over time necks got bigger, blood pressure went up, and blood vessels developed that could better and better deal with the change of pressure. Rete mirabile also occur in other animals, so they are not a rare evolutionary phenomenon of giraffes.

its also true that since some reptiles and birds have Rete mirabile, that these short necked giraffes already had a mechanism to adjust the blood pressure rapidly.  Its not hard to imagine that theirs simply adapted to more extreme conditions as the necks got longer.  giraffes whose necks got longer without a well adapted compensation of blood pressure just didn't make it.

Thank you, this made a lot of sense! This'll make it easier to fall asleep tonight :)


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How is propagation of action potentials terminated once the "message" has been sent/received?
I'm thinking about neurons in the brain that are used for "thinking". As I read about action potentials, I see that an Axon is connected to a Dendrite of a neighboring cell and that there are neurotransmitters involved in the signal propagation from cell to cell.
I'm interested in learning how action potential propagation gets terminated. Let's say a message from the brain region A to brain region B has been delivered through action potentials.

How does the region B know not to "route" the action potential further down the chain of neurons?
How does the region A know that the message has been sent, to stop sending more messages?

Note that the same mechanism is valid for any neuronal type, not only those "used for thinking"

related question: http://biology.stackexchange.com/questions/3831/what-protocol-does-the-nervous-system-use

Action potentials do not travel from neuron to neuron. They travel from the body of the neuron to the end of the axon, and then stop because they've reached the physical end of the cell. To transmit a message from one neuron to another, we need to use neurotransmitters.

I'm not a Neurologist or Neuroscientist, so I can only share what I know about the subject!
TL:DR

Cease sensation
Neuronal recovery period prevents further signaling
Neurotransmitter inhibition prevents ligands from binding to receptors (usually Feedback mechanisms)
Neuronal hyperpolarization prevents signaling
Creation of signal (can be perceived as cessation of signal)

It's important to note, first and foremost, that a cessation of stimulation will result in a cessation of the propagation. This is one of the simplest ways that neurons can stop firing - you're no longer touching, tasting, hearing, seeing, smelling, or thinking of what you were previously.
Because of the way Neurons are constructed, and as far as I'm aware, signal propagation will persist as far down the line as possible. I don't believe there's a discrete point where an Axon will simply not send a signal once a dendrite on the same neuron has received the order.
What can happen is that a competing signal has exhausted the propagation potential for the next neuron in the chain (the neuron is still recovering), or a competing signal has released inhibitors that prevents the neurotransmitters from another Axon from affecting the target neuron. Competing signals is particularly common in the neurons of your eye, since the Amacrine cells fire depending on the competitive input of the Cones if I'm remembering everything correctly.

Then there are also substances like Benzodiazepines which block propagation by opening Cl- channels and hyperpolarizing a neuron's membrane, which prevents it from firing. Only a subset of GABA receptors have sites for benzodiazepines, but it's one more way that signals will cease.
Another way to cease a signal, or at least the perception of a signal, is to actually induce propagation. The Rods in your eyes only fire below a certain lumination threshold. What you perceive as light is them not firing, and darkness is what happens when Rods fire at full strength.
I'm not the last word on neurobiology, but I hope I've given you a good start!

You may want to add that GABAergic signalling is physiologically very important in the brain, without need to bring up benzodiazepines. GABAergic and glycinergic neurons in the brain (plenty of them) secrete GABA or glycine and will hyperpolarize their targets by acting on GABA receptors. The amacrine cells you talk about are a very good example of GABAergic or glycinergic neurons.

The neuron doesn't need to know "not to "route"" an AP because this is not necessarily it's default response.
Upon receiving an AP from another neuron (via either an a chemical synapse or a gap junction) the next neuron receives a signal. The nature of this signal depends on the nature of the connection between the two neurons - the proteins and neurotransmitters involved - and is therefore context specific. Also context specific is the sensitivity of the receiving cell. If the connection is strong and activating and the receiving neuron is sensitive, then it will fire and the AP would be "routed" as in your question.
However, there are other possibilities. For instance, the connection may too weak, such that it can only activate the receiving neuron given sustained activity, or in conjunction with another neuron (in effect forming an AND logic gate). The connection may also be inhibitory - meaning that it deactivates, rather than activates the neurons.
Analogies between neurons and electronic systems are useful, but it's important to remember just how drastic a simplification they are. Individual synapses are complex. Cells have thousands of them, and a good deal of other moving parts besides.

Nice answer! What is sustained activity, is it a pulse train(multiple spikes) on top of tonic activity, or tonic activity alone?

I just came across this answer when I was answering another related question. Although this is closed there is a strong claim from the accepted answer which needs to be toned down.
Cessation of stimulation does not always mean cessation of propagation. Once an action potential(AP) is fired it does not necessarily stop its propagation in the next cell. Also cells can make synapses onto themselves which can cause further AP firing without stimulation.


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How to Design an siRNA Experiment?
I'm going to undertake an siRNA experiment soon, but I have only read about them. I want to address the role an enzyme plays in processing a protein.
From what I understand, I will need to pick two specific siRNA's from  a screen of multiple siRNA candidates. As a negative control, I should also make a non-sense scramble siRNA. Of course the specific siRNA should show a significant knock-down of the enzyme; the control should not affect expression. As well, there should also be a validated positive control (such as GAPDH) and a mock treated control.
Is this experimental design sufficient? What are some common things to keep in mind, or pitfalls to avoid when doing siRNA studies?

In which system are you working, I'd guess cell culture? And I assume you know about the rules of designing siRNA, so that the correct strand will be picked?

@MadScientist I'm going to do this in mammalian cell culture (PC12 cells). Can you explain what you mean by correct strand?

The stability of the ends of the RNA duplex determines which of the two strands is chosen as guide strand. You have to take this strand bias into account when designing your siRNA.

First you should decide whether you want to design an shRNA or use siRNAs.
If you want to use shRNA you should look at the rules that "Mad Scientist" mentioned. You can insert mismatches but make sure not to disrupt the secondary structure. You can use RNAFold to verify.
shRNA always has issues and you have to optimize your design, test it by realtime PCR or Northern blot etc to confirm the production and the concentration.
You can design siRNAs and there are online algorithms to help you design one.
You have to choose a sequence which is specific to your gene. This step is important for both shRNA and siRNAs in order to minimize/avoid off-targeting.
A common practice is to use a pool of siRNAs for a single gene. Pooled siRNAs are commercially available for many genes.
For the experimental controls you would need to do two experiments:

mock siRNA treated; which wont affect any gene
Your siRNA treated

then test for a reference gene such as GAPDH and your gene. A good reference gene should be the one which is not expected to change expression. GAPDH may not be a good reference always (for example in cases where metabolism is affected). The choice of reference gene is intuitive and depends on your prior knowledge of the system. Instead of GAPDH you can also transfect GFP and quantitate that as a control (spike in).