text:
Physiological indicators of happiness and well being
If I understand it correctly, levels of serotonin in the brain can indicate if a person is happy. What other physiological measures indicate happiness or well being for a humans?
I am looking for indicators which can be measured quantitatively but don't be very strictly correlated with 'happiness'. And on the flip-side is there physiological  indicators that a person is/not depressed?

Check out Wikipedia Article on serotonin. There are multiple serotonin receptors in the human brain, and mutations of those receptors are related to depression and suicide. As such, serotonin levels aren't really a metric of happiness. I would look at long term behavior as an indicator of happiness or depression

There are beahvioral, physiological, and psychological indicators of happiness, and on the flipside of depression, all of which are quantitative.
Levels of the neurotransmitters serotonin and dopamine in the brain are a physiological indicator of depression. Higher levels of serotonin are correlated with increased happiness and decreased anxiety. Dopamine also contributes to good mood, and in addition causes an increase in activity and willpower. Both serotonin and dopamine show decreased levels in depression. However, it is important not just to look at general levels of the neurotransmitter, but to also consider which parts of the brain show decreased neurotransmitter levels. Depression correlates with decreased serotonin and dopamine levels in the amygdala, thalamus, and hyppocampus. (http://www.health.harvard.edu/newsweek/what-causes-depression.htm)
Behavioral tests of depression are used on laboratory animals. The most common tests are the forced swim test (in which scientists measure how long a mouse persists swimming in a water container before it gives up) and the tail suspension test (in which scientists measure how long a mouse struggles to free itself when suspended by its tail). (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3270071/)
In addition, self report questionnaires are designed to quantify depression in people. Some popular ones are the Beck Depression Inventory (BDI-II) (http://en.wikipedia.org/wiki/Beck_Depression_Inventory) and the Beck Hopelessness scale (BHS) (http://en.wikipedia.org/wiki/Beck_Hopelessness_Scale).

Hi, thanks this was a useful post. As a secondary question: do you know if any of these indicators (or others) could be tested for after a person has died? And even when the body has degraded to a skeleton?

I don't know of any indicators that can be used after death. Depressed people tend to have less gray matter in certain parts of the brain (http://www.ncbi.nlm.nih.gov/pubmed/18838632, http://www.ncbi.nlm.nih.gov/pubmed/18669941), but that could be a sign of many other mental diaseases, and wouldn't help in studying skeletons.

Facial Microexpressions can indicate happiness.  Not sure about depression, but sadness and other correlates might be useful there:

Microexpressions express the seven universal emotions: disgust, anger, fear, sadness, happiness, surprise, and contempt. Nevertheless, in the 1990s, Paul Ekman expanded his list of basic emotions, including a range of positive and negative emotions not all of which are encoded in facial muscles. These emotions are amusement, contempt, embarrassment, excitement, guilt, pride, relief, satisfaction, pleasure, and shame.

MRI seems to have some happiness metrics - though its not the easiest or cheapest method.


text:
Why can't you taste food when you have a cold?
It is a common observation that food is tasteless when we have a cold. Why is that so?
What is the cause of inability to taste when we have a cold? Are the nose and ability to taste connected?

This German review supports common wisdom that the sense of taste is predominantly informed by the sense of smell. For instance, common advice to children taking "nasty" tasting medicines is to plug one's nose. Any condition that blocks olfaction, such as sinusitis from flu or other sinus infections, or blocking nasal airflow, will decrease or block olfaction and as a result, the majority of taste.

Hüttenbrink KB. [Disorders of the sense of smell and taste]. Ther Umsch. 1995 Nov;52(11):732-7. [Article in German]

There are many factors that contribute to the flavor of food - the five "traditional" tastes (sweet, sour, bitter, salty, umami), smell, texture, spiciness, "coolness" (like peppermint), temperature, etc. Smell and taste are detected in similar ways, by chemoreceptors expressed in taste pores by specialized cells of the lingual epithelium (tongue), and in the nose by the olfactory epithelium. Both are affected by upper respiratory tract infections like colds and the flu, leading to diminished senses of taste and smell, and a corresponding reduction in the overall flavor of food.

This doesn't answer the "why" question.

@Kevin: yes it does... receptors are also on the olfactory epithelium.

When we eat something,the aroma of the food particles enters our nostrils and travel through nasal passage.While passing,through hair cells present in our nose,the information (flavor & taste) is sent to the brain.But during Common Cold,our nasal passage get clogged with mucus which don't allow the aroma to pass.Due to this, the brain becomes unable to determine the taste and flavor of the food.

Can you please [edit] your answer to add some references that would support your answer?

source: Stack Exchange

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

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

sort: votes


text:
Can frequent ultrasound diagnostics be harmful?
Are there any short or long term effects apparent in tissues if a zone (or the whole) of human body is scanned with ultrasonic waves often?

Medical advice questions are off-topic here, I think if you edit the last portion out and make the first question more general to the science behind it, it will be okay.

You might want to see this question though

@RoryM Thanks for editing and reopening my question. Your hat covers your eyes btw °<|)

Ultrasound is considered a safe procedure (reference) which is accepted by the WHO as well (reference). There have been studies however, that show the link of ultrasound treatment to some undesirable traits.
Ultrasound could be possibly linked to a decrease in body weight on birth of infants (reference).
Frequent use of ultrasound may influence babies scanned to grow up left handed (reference)
A significant migration of neurons (change of neurons from their rightful area) has been observed in mice on exposing them to ultrasound at the prenatal stage. (reference).
A study has found detrimental affects to the brains of mice on exposure to ultrasound in the fetal stage (reference).
So based on these papers, I wouldn't call them a 100% safe but these tests all relate to repeated usage of ultrasound imaging. Ultrasound usage sparingly and on valid medical indication should not be a matter of concern.

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


text:
Why Can't A Male Mule Have Offspring?
I've read that female mules can sometimes have offspring, but that male mules are incapable of doing so. Why is that the case? Is their sperm not capable of entering the egg or is their a genetic reason?

It's essentially genetic. The mule is a hybrid of a male donkey and female horse. A donkey has 62 chromosomes, a horse has 64 chromosomes, and a mule has 63 (mix of 62 and 64). There is a mismatch between both number and structure of the chromosomes and as a result, most mules are infertile.

You say "most mules are infertile". Are you implying that some mules are fertile?

Yes, there are rare documented cases where mules have birthed foals. https://en.wikipedia.org/wiki/Mule#Fertility

Bizarre and very interesting!


text:
In scuba diving, are nitrogen narcosis and high pressure nervous syndrome the same thing?
In training for scuba diving, they tell you that when you're bellow 100 ft or so you have to watch out for changes in mental state that resemble drunkenness. The cause of these mental disturbances is called nitrogen narcosis, and it has something to do with the increased pressure on the nitrogen component of the gas that you're breathing out of your tank. I just read this article from the what-if section of XKCD (halfway down the page, under the header about Michael Phelps) that mentioned a very similar sounding disorder called high pressure nervous syndrome. Are nitrogen narcosis and high pressure nervous syndrome related, or are the effects of high pressure nitrogen and high pressure by itself separable?

what does the linked paper (by Hunger Jr and Bennet 1974) say?

These are different things.
Nitrogen Narcosis or more commonly Gas Narcosis is the narcotic effect of gasses like Oxygen and Nitrogen under pressure. The effects are most prominent under 30m and commercial/technical dives doing dives to 40/50m on air tend to experience the effects most. (Narcosis is managed by adding an inert gas - in most gases Helium - to air to form a mixture referred to as Trimix (Helium/Oxygen/Nitrogen) this then produces an effect as if the diver is diving to a shallower depth and is referred to as Equivalent Narcotic Depth, in some cases Heliox (Helium & Oxygen) was also used)
High Pressure Nervous Syndrome is an interesting aspect of deep diving and used to be called Helium Jitters/Tremors as the accepted standard was that it was caused by breathing Helium mixtures under 150m. Some people hold this to be true and others claim that it has nothing to do with Helium but rather the pressure disrupting the flow of electric signals thru the nervous system.
What is interesting is that they found that if you used Trimix (Helium/Nitrogen/Oxygen) rather than Heliox (Helium/Oxygen) the onset happened later or not as severe. And the slower your descent is the slower the onset of the symptoms.
Some Docs to Read:
Narcosis - Relatively simple document on Narcosis
Narcosis - "Narcosis is not unique to nitrogen; however, it can occur with many of the so-called “noble” or inert gases, with the exception of helium. Add to this the fact that other inert gases each have their own brand of narcotic effects at depth, and you have a complicated picture for technical and commercial divers. One of these rare gases, argon, for example, has about twice the narcotic potency of nitrogen, but helium has very weak narcotic properties and is less soluble than nitrogen in body tissues."
HPNS - Relatively Simple doc on HPNS
HPNS - Very technical discussion on gasses, from a HPNS and Narcosis view point.
References:
Bennett, P.B. 1982b. The high pressure nervous syndrome in man. In: The Physiology and Medicine of Diving and Compressed Air Work. (P.B. Bennett and D.H. Elliot, eds), Balliere-Tindall, London. pp. 262-296.
Bennett, P.B. 1990. Inert gas narcosis and HPNS. In: Diving Medicine, Second Edition (A.A. Bove and J.C. Davis, eds.).W.B. Saunders Company, Philadelphia. pp. 69-81.
Bennett, P.B, R. Coggin, and J. Roby. 1981. Control of HPNS in humans during rapid compression with trimix to 650 m (2132 ft). Undersea Biomed. Res., 8(2): 85-100.


text:
Can gelatine digestion make blood more thick?
Can gelatine cause blood thickening if digested?

No, because gelatin is a mixture of collagen-derived peptides. When you eat them, they are first hydrolyzed by stomach acids into constituent amino acids. These amino acids are then absorbed from the small intestines as nutrients.


text:
If re-boiling does not curdle the milk, can that be taken as an indicator that the milk hasn't developed the bacteria (and their toxins)?
Usually when left in hot temperature, the milk curdles (which I know when I boil it and it starts separating).
If the re boiling does not curdle the milk, can that be taken as an indicator that the milk hasn't developed the bacteria (and their toxins)?
This is the milk that I use.
http://www.amul.com/products/amul-taaza-info.php

Just to clarify: when you say reboiling, you mean boiling pasteurized milk right?

@Jay Yes, I get milk in packets which IS pasteurized. Thanks.

Interesting question. I know that heated milk will separate when it is acidified. Another take on this question would be "Do all harmful bacteria acidify milk?"

@Sobachatina: Even if all bacteria did acidify (which, to a layman in microbiology, sounds like a difficult claim to prove), wouldn't absence of curdling potentially just mean that whatever bacteria are there have not acidified it enough to curdle? So in order to answer "yes" to this question we'd need to not only prove that (a) all harmful bacteria acidify milk, but also (b) that acidification to the point of curdling will take place before growth to a harmful degree, and not some time after. Without a mountain of evidence I think it's easier to just say "no".

Doesn't separation refer to the fat separating from the water component? When protein is removed, I've heard it referred to as denatured or "burnt" or curdled. I would think you can re-pasturize the milk to sterilize it, but if it was previously contaminated, you would not be able to remove bacterial toxins. One toxin that may remain would be endotoxin which causes illness in humans and is only denatured at temperatures in excess of 300ºC.

the fact that there are bacteria in the milk (and unless you get sterile milk you WILL have bacteria in it) does not mean there are toxins in it (note that sterile is not the same as pasteurized) 2) yes, bacteria will acidify the medium they grow in, as a result of their metabolism (like any other cell would). 3) the milk should not really separate when you boil it, unless you acidify it at the same time (like when making cheese).

Fresh milk does not separate when boiled. I use it in sauces and pan gravies and it always boils and never separates.
My suspicion is that you are separating it on purpose, for example to make cheese. In that case you have to add acid or rennet to separate it. If you then re-boil it to separate it again, you get very little solids. I have made cheese at home then tried to 'ricotta' the left over whey and all I get is a tiny bit of solids.

"My suspicion is that you are separating it on purpose," No need to suspect anything. Please read the question again.


text:
Why do people feel extreme cold at different temperatures compared to other people of same body structure?
I have seen some people shivering in the room temperature of 18°C while others of similar body structure do not feel that much amount of cold.
Of course the clothing of both people is similar if not same.
What can be the cause of such different body reactions?

Do you mean why does the same temperature feel different for different people?

@TAbraham exactly

First of all, this observation is the norm across human perception. While humans react in roughly the same way to similar stimuli (e.g. both a cranberry and a tomato are seen as red, the destruction of tissue is felt as painful), the intensity tends to be different. Also, many stimuli elicit not just a knowledge of the state of the world or one's body, but also a reaction (e.g. shivering when cold, or emotions like fear when physical pain is felt), and these reactions differ between humans too. So, on a very general level, it can be answered with "Because that's how human perception works".
I know that this is a very unsatisfactory answer, so here are some factors off the top of my head. For any given case, one or more of them will cause the difference, and you cannot tell which ones from casual observation.

Your observation of "similar clothing" could have been incorrect. For example, an acrylic sweater can look exactly like a sheep wool sweater, but warms much less. Or, slightly shorter sleeves can cause much cooling if they leave the wrist exposed. Layering is also very important, and we generally only notice the uppermost clothing layer.
Your observation of "similar body structure" could have been not precise enough. People who have the same appearance can have different amounts and distributions of body fat. Maybe one person is simply better insulated than another one.
The state of their circulatory system was different. Vasoconstriction and vasodilation will change the skin temperature, which is sensed by peripheral thermoreceptors.
Estrogen is involved in thermal perception. The gender of the person and the current point in the menstrual cycle (or pregnancy) in women will make a difference.
The circadian cycle of the two people is probably not perfectly synchronised. Core body temperature varies during the cycle, and thermoperception depends on core body temperature too, not just skin temperature.
A different metabolism will cause one person to create more body heat than another
Other hormones (beyond estrogen and the ones ruling the circadian cycle and metabolism) probably have an effect on thermoperception, but I can't tell you details here. Temperature is regulated in the hypothalamic-pituitary-adrenal axis, so the hormones from it are likely to have an influence.
Normal variations in the two people's neural networks will change the intensity of signal perception. People are born with very unconnected neurons, and build unique connections depending on the environment they encounter while growing up. As a result, each person's brain functions slightly differently when given the same input.
Differences in neurotransmitter sensitivity can account for the difference in intensity of perception. People sometimes react differently to the same level of neurotransmitter, or also their brains secrete different amounts of neurotransmitter as a response to the same stimulus. These differences exist on an average level (e.g. glutamate can potentially "do" more for me than for you) but are also affected by drugs and illness.
Attention is a major part of perception. The CNS can suppress information from sensory organs at a very low level if the brain is focusing elsewhere.
Habit: people can intentionally or unintentionally learn to disregard or misinterpret their body sensations.
Psychological stress increases the core body temperature
The above reasons all assumed differences between a pair of healthy individuals. Some conditions, for example running a fever, but also neurological disorders anywhere along the complex pathways from sensors to cortex (and the other way round!) or diseases which for some reason alter thermoregulation, will all change the feeling of hot or cold.

This list is probably incomplete. Also, some of the factors I listed will overlap to some extent (e.g. vasodilation is frequently mediated through hormones, and ingrained habits are reflected in neural network connections). But the take away point is: Human perception is an active process, very far removed from simple "reporting" of the state of the environment. It is unrealistic to expect two individuals to have the same perception when exposed to the same stimuli.
For an in-depth description of how thermoperception and thermoregulation work physiologically, see this summarizing paper.

Human body temperature is a measure of the body's ability to keep, generate, or get rid of heat as the need arises. The body is very adept at maintaining temperature within a narrow and safe range, despite occasional huge variations in the room temperature.
But some bodies are more efficient than others. Even bodies of the same height and weight may differ dramatically in the ability to maintain body temperature.
Humans also differ in their preferred room temperature. Some like it warmer, some cooler. This is called thermal comfort. Thermal comfort is not merely physical, but psychological too. In one's choice of preferred temperature, besides psychology, other personal factors come into the equation.
Also the feeling of cold or hot depends upon the DIFFERENCE between one's normal body temperature and outside temperature. And contrary to popular belief, different people have different normal body temperatures. It also depends upon the amount of muscle mass and fat, as fat stores heat (decreasing the normal temperature) while muscles dissipate it (increasing the normal temperature.
Following links might help:
http://www.mnn.com/health/fitness-well-being/stories/why-are-some-people-colder-than-others
http://www.medicalnewstoday.com/releases/5711.php


text:
Are there people cured of HIV by means of HAART?
I wonder if there people who were cured of HIV only by means of highly active anti retro-viral therapy (HAART) or other drugs rather than by bone marrow transplant?
I know that HAART can suppress HIV below detectable level but are there people who stopped HAART and did not experience the HIV levels rising?

This very recent (and freely available) review pretty much sums the problem up in the introduction:
http://dx.doi.org/10.1038/clpt.2012.202 (Barton et al., 2013: Prospects for Treatment of Latent HIV)
And here's an update more specifically on the problems with actually curing an individual of HIV infection, if you have access: http://dx.doi.org/10.1016/S0140-6736(13)60104-X (Katlama et al., 2013: Barriers to a cure for HIV: new ways to target and eradicate HIV-1 reservoirs)
Essentially, current antiretroviral therapy (ART) is able to nearly fully suppress active HIV, practically restoring the individual to a healthy status, including the prevention of transmission from them. However, the therapy needs full adherence (missing a dose can already cause viral loads to rise) and is lifelong. The reason for this is because HIV integrates into the genome of host CD4+ T cells, of which there are latent populations in places difficult to reach with therapeutics such as peripheral lymph nodes.
Apparently, some rare individuals actually achieve a "functional cure", i.e. the body is able to suppress viral replication for a given period of time (5 years) without ART. But these patients "are characterised by a favourable HLA profile and potent HIV-specific CD8 T-cell responses that are associated with a low viral DNA reservoir" (Katlama et al). They also mention another group of five patients who did not seem to have a favourable genetic profile and were still able to control HIV following cessation of ART for several years (http://dx.doi.org/10.1097/QAD.0b013e32833b61ba Hocqueloux, 2010: Long-term immunovirologic control following antiretroviral therapy interruption in patients treated at the time of primary HIV-1 infection). So it seems there are plenty reports of people who are able to remain free of detectable viral loads and maintain CD4+ T cell counts for a long time after treatment, but it doesn't seem like any of them stay permanently virus-free.

Since early March we know, that there is the first patient which has been cured by HAART. According to the paper it has been proven that the infant was infected with HIV. This was done by detecting the virus even after the first 48 hours, this rules out that the virus transmitted by the mother without infection.
The infant was first treated when it was 30 hours of age with a triple therapy (zidovudin, lamivudin and nevirapin). On the seventh day the therapy was changed to zidovudin, lamivudin and lopinavir/ritonavir. After one month of therapy no replicable virus particle could be found. The therapy was continued until the age of 18 months. The infant is now 26 months without a sign of a rebound of the HIV infection.
The approach was atypical, since they used a therapy scheme with not established high dosing of the antiretroviral drugs. They ruled out a innate HIV-immunity by certain HLA variants, since Mother and child had matching HLA-Haplotypes. But other genetic mutations are still possbile.
This is scientific progress, the answer to your questions changes in only 2 months.
[1] http://www.retroconference.org/2013b/Abstracts/47897.htm

Is not it the same as post-exposure prophylactic, which is used if a surgeon or a dentist get wounded when performing operation on a HIV patient? I know that one can be cured if the treatment is started within 48 hours after infection.

It seems what is important is whether the latent reservoirs were established.

It's not the same, since the infant was already infected, which was proven by detecting the HIV Virus on the 20th day after birth (the virus wouldn't persist so long otherwise). The treatment was started so early to give the infant the highest chance to be cured. PEP(post-exposure prophylactis) can prevent infection with HIV. But this was not a prevention, it was a therapeutic approach. This is also a big question in the paper, since a successfully PEP would be no big deal.

The authors of the paper claim that there are no latent reservoirs with high probability (by droplet digital PCR and undetectable HIV-specific antibodies). But you can never be 100% assured. Time will tell. But it sounds promising.

While it's difficult to prove a negative, I know of no cases where a patient has been treated with HAART to the extent that their viral load never rises again. Keep in mind that, if nothing else, such a study would be extremely hard to do, as proving you've "cured" someone would require extremely long term followup.
HAART is however quite good at suppressing HIV, and there's currently no known upper bound on the lifespan of an HIV+ individual undergoing treatment. Compared to a 10 year post-infection life expectancy a decade or two ago, that's pretty darn good.

I would add to this that any reported case of this happening, however spurious a publication it appeared in, I'm sure would attract great media attention.  When the reports came in of the bone marrow transplant cure, I remember it being reported by the BBC as the 'first cure'.

@RoryM Indeed - a drug-based 'cure' for HIV is hardly a finding that would go under the radar.


text:
Why Is Most Life Symmetrical Externally But Not Internally?
Mammals, reptiles, arachnids, insects, etc are all as far as I am aware symmetrical in appearance.
Take a human for instance, make a line from the top of our head right down the middle. However, internally it is not the same. Our organs excluding the kidneys, lungs, reproductive organs, etc are not symmetrically placed in our body.

Why do we not have an even number of each organ so it can be placed symmetrically?
If we have a single organ why is it not placed in the middle like the brain or bladder is for instance?
Is there some evolutionary advantage that led to this setup?

I am not sure I completely agree with your conclusion that we are not symmetrical internally.  There are exceptions but I would say we are more symmetrical than not.

@DQdlM, yes, there are exceptions to organ symmetry. However, externally there are no exceptions to symmetry. Why are not all organs symmetrically placed? That is what I am trying to understand. Why full symmetry is not internal as well?

The question of why there are no major exceptions to external symmetry is subtly but interesting different from why are we not symmetrical internally.  I am interested to see the answers you get.

Flounder fish aren't the most symmetrical guys. Just thought I should point out that external symmetry is not essential. http://www.google.co.uk/imgres?imgurl=http://www.dnr.state.md.us/fisheries/juvindex/flounder.jpg&imgrefurl=http://www.dnr.state.md.us/fisheries/news/story.asp?story_id%3D130&h=480&w=640&sz=28&tbnid=_PWh1T3gGBB50M:&tbnh=92&tbnw=122&zoom=1&usg=__lSMRjlJzASOX2hcwsLpOoXtKSjY=&docid=Qy-9gfEvf_FxcM&sa=X&ei=ReScUcOdJYmp0AXwuoGwAQ&ved=0CD8Q9QEwAg&dur=1064

This question was first asked by Sir Isaac Newton: "Can it be by accident that all birds beasts & men have their right side & left side alike shaped (except in their bowells) & just two eyes & no more on either side the face & just two ears on either side the head & a nose with two holes & no more between the eyes & one mouth under the nose & either two fore leggs or two wings or two arms on the sholders & two leggs on the hipps one on either side & no more?"

It is worth noting most animals ARE symmetrical internally, One which are not tend to be highly derived and very different from their ancestral body plan, animals like tetrapods or mollusks

First, I think it worthwhile considering 'Why would internal symmetry be beneficial?' Developmental simplicity jumps to mind immediately. You can also consider relationship to external organs; the stomach and esophagus are lined up with the mouth which is symmetrical about the sagittal plane. Or maybe even balance; the lungs are large organs and if put to one side would likely cause locomotive issues. (Perhaps this is even an interesting topic for another question.)
That said, I feel, at it's core the evolutionary advantage which led to the lack of ubiquitous internal symmetry is space. Simply put, there is only so much room inside an organism and every little counts. Thus, if there isn't a need for a particular organ to be mirrored about a plane then there is a benefit in putting elsewhere: utilization of space.
I think a fantastic example of this is the human digestive tract. The key factor in the shape of the intestines is utilization of space, which directly affects the point at which is connects to the stomach, itself contributing to the asymmetrical shape of the stomach. One could envision other configurations, sure, and nature has. However, this configuration works quite well and the extraordinary use of limited space seems to outweigh all benefits of symmetry.
To directly respond to your questions above:

Question: Why do we not have an even number of each organ so it can be placed symmetrically?
Response: Each organ addresses (or addressed) a need of the organism. Addressing that need with multiple organs working in concert has benefits and consequences, as does addressing the need with a single organ alone. These benefits and consequences are balanced throughout the evolution of an organism.
Question: If we have a single organ why is it not placed in the middle like the brain or bladder is for instance?
Response: I feel space. Again, there are benefits to symmetry but there are many other factors at play. Some of which, it seems, are more important than symmetry at times.
Question: Is there some evolutionary advantage that led to this setup?
Response: I hope this has been addressed - I don't claim to have 'answered' anything, this is a question for discussion.

Other fuel for discussion:
In thinking through this question I found myself able to rationalize why internal symmetry isn't necessary. However, I'd be interested in seeing opinions on why, then, external symmetry is so prevalent.

External Bilateral symmetry permits streamlining, favors the formation of a central nerve center, contributes to cephalization, and promotes actively moving organisms.

@Mew: Why and how?

So our body is a iPhone 7plus

This works just as well on external symmetry, locomotion is a lot easier if you are symmetrical.  you will not most asymmetrical animals are asymmetric in something not involved in locomotion.

Building on the answer given by Sean Connolly above, it would be very easy to imagine evolutionary scenarios where organs are more likely to develop asymmetrically than symmetrically.
For instance, imagine an organism that has a simple digestive system that consists only of a single undifferentiated intestine that runs directly from mouth to anus in a straight line, as in primitive annelids. Let's say that there is also only one enzyme present to break down the food particles, and that this is present throughout the intestine.
Now, perhaps for space issues, or for reasons that are entirely unrelated to internal organs, the intestine itself becomes asymmetrical. This could be because a longer intestine is needed to dissolve and take up more of the food, but the organism cannot become longer (for instance, it might live in dead coral reefs, and the size of the hollows cannot be controlled by the organism itself, so there is an external limitation to how long the organism can become). One way to solve this would be to fold the intestine, which can make it asymmetrical.
Now, because food particles that enter the mouth are exposed to the single enzyme throughout the intestine, the gut fluid will be less and less nutritious the farther posterior it gets along the gut. Possibly, more anterior parts of the intestine will become specialized in breaking down and absorbing more frequent kinds of food, while more posterior parts will become specialized in less common foodstuffs. This could lead to differentiation of secretory organs along the intestine, and if this is already bent because of external selection pressures, it is not impossible that a given secretory organ will develop asymmetrically simply because the intestine at the point where the enzymes secreted by this organ are to be used is not near the mid-line of the body.
For instance, if we needed to absorb substance X from our food, but substance X only became abundant in the gut fluid at a distance from the mouth that corresponds to a place when our intestine is located on the left side of the body, it is not unreasonable that development of this excretory organ would develop on the left side of the body. This could then be self-reinforcing, as a more ready access to substance X may mean that this substance becomes more important for us, and the secretory organ may become larger and more dominant, and eventually we have a large organ that exists only on the left side of the body, without ever having existed in a symmetrical form.
This is, of course, pure speculation, and I know of no example of this, but it is one that is not at odds with evolution in general, and could certainly be plausible. The same could occur if differentiation of enzyme secretion organs occur in a symmetrical gut, which later becomes asymmetrical and the whole secretory organ becomes displaced to one side. Retaining a symmetrical pair of secretory organs on each side of the body, but having the enzymes work on food only asymmetrically would imply that one of the secretory organs had a very long duct and the other had a very short one. It is reasonable to assume that over evolutionary time, the one with the long duct would become less important and may disappear.
A similar reasoning could be applied to the blood circulation system and any organs relevant to that.

There are many examples of external asymmetry throughout the animal kingdom. Many decapods, for instance, have asymmetrical claws that are used for different purposes (feeding in lobsters, for instance). Several genera of bird lice (e.g. Struthiolipeurus, Bizarrifrons) have asymmetrical heads, which probably have something to do with how they attach to their hosts' feathers. I believe that many groups of sessile invertebrates have anal openings displaced to one side, but that may be caused by internal asymmetry or because it is less efficient to have our anus situated so that feces is filtered into your mouth again.

Thanks for the response. It was very difficult choosing who to accept, so opted to just choose the highest voted one. If I could choose multiple answer I  would have chosen yours as well. I did upvote!

You change one thing and you have to change everything else to compensate.
Lets look at what organs are not symmetric in tetrapods, the heart and the digestive system, everything else is symmetric. Note these are symmetric in more basal vertebrates like fish.
the heart starts symmetrical in vertebrates but that changes when animals evolve independent circulatory systems, that is flow of blood to the lungs that is separated from the flow to the body, allowing for differential blood pressure. that evolved by having one side of the heart supply the lungs and the other supply the body, since they have vastly different blood pressures it would make sense the sides of the heart creating that blood pressure would also be different. this change in shape forces some asymmetry on the lungs that have to share space with the heart.

The digestive system is even easier, again it starts as a straight tube, but two major changes occur. first a longer digestive track allows you to extract more nutrients, and making a human (or nearly any animal) long enough to hold a straight digestive track of the same length would be incredibly wasteful. For scale the human digestive tract is about 10 meters long.
The other change is the development of the stomach (which not all vertebrates have). having a portion of the digestive system dedicated to storage and soaking is useful by allowing animals to eat larger quantities when situations allow without having to hurry it through the digestive system and lose most of the benefits. And again the only good way to enlarge a section of a straight tube without elongating the body is to have it turn and be offset, this forces many other organs out of place (liver and spleen) which attach along the digestive tract's length. Note in many fish this is all still symmetrical, but this changes when they evolve away from a tall thin cross section into a more rounded cross section which is favored in shallow water and eventually life on land. Once that happens you can't simply stack everything up along the mid-line without wasting a lot of space.

you can see how changes to the digestive track might evolve in many different lineages that change the shape of the body like crabs or molluscs. which are the other groups with asymmetric internal organs. Note these other two groups are often externally asymmetric as well. Snails in particular because they changed a  long straight shell into a compact coiled shell, which forces asymmetry on many systems.

I would like to add an answer here to explain how the internal asymmetry of animal organs might be consistent with their external symmetry.
Here's my argument:
1) In the case of vertebrates the important internal organs are protected by the animal's skeleton.
2) The internal organs are soft matter and so their physics is very different from how they would behave if they were nearly rigid bodies.
3) Internal asymmetry isn't a big issue because the mass distribution is approximately symmetrical in a bilateral sense.
To make this concrete I mean:
a) If you should try slicing a vertebrate down the middle you will notice that the left and right sides of a vertebrate have approximately the same weight
b) The left and right sides of the vertebrate's head have approximately the same weight...etc.

Imagine that the intestine is a long, symmetric, flexible tube, about 20 feet long.  Now imagine what the tube would look like if it were packed into a 5-gallon bucket.  It would be literally, mathematically, impossible to pack it in symmetrically.  In physics we call that "spontaneously broken symmetry".  It would take a lot of genetic instruction to pack a long intestine into a small volume even approximately symmetrically.  Of course this doesn't explain all the asymmetry you're wondering about, but does explain some of it.


text:
Difference In Telomeres Between A Thale Cress Plant And A Methuselah Tree
From what I have read and understood telomeres cap off how many times a cell can divide before it can no longer divide and that is what causes aging.
A thale cress plant apparently has a life cycle of 6 weeks before it dies, while the Methuselah tree has set the record at over 4,800+ years.

What is the difference between these two plants regarding their telomeres?
Is the cell division rate different between both plants instead of a telomeres difference?
If given ideal conditions what could the potential life-span of a Methuselah tree be?

Btw you don't have to answer all these. Just curious and looking for some insight into why the stark difference between both plants' aging.

Telomeres do not "cause" ageing as such - although you are right that they limit the number of times a somatic cell can divide.
Each time a cell divides the chromosomes are replicated in an imperfect way, and as such a small amount of DNA is lost from the end of the chromosome during each round of cell division. Telomeres are just extensions to the chromosomes, so that the DNA that is lost is not important. When a cell runs out of telomeres it ceases to divide.
However it is a big generalization to say that telomere length is therefore correlated with lifespan. For instance a recent study has shown that mice have telomeres 5-10x the length of humans, but live 30x shorter (1).
Inter-species differences in lifespan
Whilst I am no expert on these 2 plants, it is quite an obvious thing to say that organisms age at different rates. Mice, for instance, live 3 years in a protective environment, whereas humans can live 30x that. The difference is down to the life strategies acquired by natural selection: it is more advantageous for a mouse to develop very fast to reproductive maturity and have as many offspring as possible, because there is a very high mortality rate for mice. Conversely for humans, in takes more than a decade for us to reach reproductive maturity! Our "rate" of development/ageing is lower, which is completely related to our reproductive strategies.
I imagine that a very similar story is true for plants - for some it will be advantageous for them to "live fast, die young", whereas for others the best strategy might be to take a long time creating less, but more robust, offspring.
At the molecular level
I have answered a related question previously (Do trees age on a microscopic level?) which might be of interest to you.
In short, the phenotype of ageing is associated with irreparable damage at the molecular level - be it to DNA, organelles, protein aggregations... you name it! Organisms that have a higher metabolic rate, such as mice, accumulate this damage faster. This gives them the benefit of being able to reproduce much earlier, at the cost of reduced overall lifespan.
Plants age slightly differently, but at the genetic level much the same repair pathways are conserved throughout the kingdoms of life, with some alterations of course - for instance plants seem almost completely immune to cancer (2)!
As I argue in the linked to question above, plants have a potentially indefinite replicative potential, as every cell has the capability of regenerating its telomeres, because plants do not have a conserved germ line as animals do - any cutting from a plant has the potential to create an entirely new plant. This varies from plant to plant of course, and plants are still susceptible to damage, they just have modified/adapted repair pathways to cope with their specific lifestyle.
You ask whether it is the telomeres or the "rate" that differs between the plants - the answer is almost certainly a combination of both, amongst the other myriad of factors that influence lifespan!
Refs

Colado, et al, 2013. Telomere dynamics in mice and humans. Seminars in hematology [PubMed]
Doonan & Sablowski, 2010. Walls around tumours - why plants do not develop cancer. Nature reviews cancer [DOI]


text:
Are there records of monozygotic twins in which one experiences androgen insensitivity syndrome
I have given my high school biology students the thought experiment of "What would happen if a researcher induced twinning of a female zygote and then replaced one of the X Chromosomes with a copy of the father's Y chromosome". In theory you should get what would be about as close as possible to male/female identical (monozygotic twins). However, I don't believe it would be possible for this to occur in nature (feel free to correct this if I am wrong). The closest I am familiar with is "Semi-identical twins in which the egg is fertilized by two sperm and then twinning occurs. However this isn't really the same.
However, I realized that Androgen Insensitivity Syndrome, in which a mutation leads to the body not responding to masculinizing hormones, leads to a male developing as female. Is anyone aware of this ever happening? I realize it would need to occur after the zyote/morula split.
Similarly if the SRY gene (essentially the master control switch for masculinizing an embryo) has ever been transferred on to an early embryo of a pair of female monozygotic twins, essentially inducing one twin to develop male.
In essence I'm asking for evidence of physical manifestations of (near)identical monozygotic twins. Has any of this ever been done in research on other species?

This is an important question to geneticists because monozygotic twins are the only ethically acceptable way to research genetically identical humans.
I'm sure the sort of non-symmetrical fission where specific DNA coding for genes are not present or are modified to completely different phenotype in the formation of the twins probably has happened, but it incredibly rare.  In stem cells, asymmetric division has been observed frequently (warning: google doesn't like PlosOne right now).  In development, unless its actively been activated as an asymmetric division, this would be incredibly rare- this would be akin to a birth defect in a single fetus - how many cases of mixed male and female cells in a single baby. I can't even find a reference for such a thing.  Much more common are semi-identical twins, where two different sperm fertilize a single egg which may have split.  Semi-twins are still vanishingly rare - the first report was in 2007).

Such twins are probably very rare. Their existence and discovery relies on three unusual, and possibly unlinked, events: first, that an egg fertilized by two sperm develops into a viable embryo; second, that this embryo splits to form twins; and third, that the children come to the attention of science.

This might be the case you are thinking of?  In one case reported there was a gender difference.

Souter and her colleagues investigated the twins' genetic makeup because one was born with ambiguous genitalia. This twin turned out to be a 'true hermaphrodite', with both ovarian and testicular tissue. The other twin is anatomically male.

They weren't monozygotic though.  Just others from the same mother ;)
Monozygotic twins are not completely identical, epigenetic fingerprinting - including DNA methylation and chromatin DNA binding patterns (pnas - paywall) change while the fetus develops and as the child and adult age.  This can cause quite significant differences as the twins age. Epigenetic markers change the dynamics of brain development and can make a difference in the occurance of leukemia.
There are also modifications to the DNA sequences of cells, copy number variations (CNVs) are multiple (sometimes hundreds or thousands of times over) repeats of short (2+ base pairs) DNA sequences.  These also occur as the cells differentiate and divide to form tissues and organs.  Twins show significant differences there too as this is not a deterministic mechanism in development.
I can't find any references to twins showing asymmetric AIS. but the number of variants requiring this makes it sounds like its possible.  If you have a reference post it and I can have a look?
note added: this paper shows that methylation profiles appear identical at least in utero.

I am aware of the semi-identical twins (which to me is a bit of a misnomer). Also, while I share your sentiment that monozygotic twins vary (quite significantly over time) in their epigenomes, let's remember that, by definition, this is not genetic variation. My students got me to thinking a bit more about it simply because of the fascinating idea of being able to see what one would look like if they had developed as the other gender. I'm sure that it would be vanishingly rare, if it's happened, but that doesn't mean it hasn't happened...:)

@single_digit just doing my best to be comprehensive.  (The CNVs are genetic variations tho.)  It probably has happened - with 8 billion people on earth, the odds are not bad.  The article notes that such oddities are usually not reported, esp if they don't result in some defect of some kind..  cheers.


text:
Can viral proteins cause infection?

Possible Duplicate:
HIV Rapid Tests

Can proteins found on the surface of RNA viruses cause infection without the presence of the actual RNA and other components used in the virus?


text:
Have any genetically altered organisms actually become abundant in a natural environment?
Most of the things that come up in Google and Google Scholar for this question have a mostly/completely speculative tone, or at best use models instead of measurements. This report describes some actual measurements in pollen transfer to neighboring fields from GM fields, though they all seem to have been one-off measurements at some unknown time after the GM plants appeared, rather than investigations on if the genes are becoming more common over time, which might imply the ability to become unavoidably common in some environments or even a weed/pest/parasite. This doesn't seem like an obvious problem to me, because the traits associated with those genes are always meant for the context of being farmed or raised by humans and therefore probably wouldn't contribute more to fitness in wild populations relative to the wild alternatives of those genes, but a few counterexamples would smash that belief to bits.

Many organisms including plants, bacteria, insects, fishes and even mammals have been GMed. Most of them have experimental purposes, but GM crops have been released for commercial purposes. Maybe the most amazing between them is triticale, which is a hybrid of wheat (Triticum) and rye (Secale). Triticale, BT Potato, BT Tomato, BT Maize (I am not sure), BT and Golden Rice and lots of other GM crops have been released in almost all lands in world. Almost all these GM crops suppose to have higher yield and higher resistance to pathogens and physiological problems and as a result they have higher chance of surviving (specially in natural environment).
A study published in Nature in 2001 reported that Bt-containing maize genes were found in maize in its center of origin, Oaxaca, Mexico. In 2002 Nature concluded that the evidence available is not sufficient to justify the publication of the original paper.  A significant controversy happened over the paper and Nature's unprecedented notice. Also there are safety concerns about modified gene transfer during pollination in GM Rice(s). Even some scientists think that that this would not be a problem because rice is a self-pollinating plant. Any way GM crops can become abundant and release their genes by themselves or through gene transfer to other organisms.

Notice: Some of non crop GMOs also have commercial purposes but they didnt't release to environment and are restricted to laboratories.

Increased yield and higher resistance to pathogens and physiological problems don't seem like they must necessarily increase fitness in the wild. The mechanism of action behind those effects seems vitally important--for example, increased yield could be due to increased nutrient uptake from the soil, or just due to diverting nutrients from growth elsewhere. The sickle cell trait comes to mind as an analogous situation in humans; "grants malaria resistance" sounds like it wouldn't be harmful, right?
The Nature paper is what I was looking for. Are there any less controversial examples?

In India, rice is modified, resulting in the loss of almost all local varieties. It was cause of excessive cultivation of Modified rices. Then this rices can easily transfer thair genes to environment (Even local pest and deasises some times had bad attacks).

I encountered this article discussing transgenic salmon, and it says that the modified genes don't find their way into nature because transgenic salmon are bad at the salmon mating ritual. It wasn't on purpose from what I can tell, but that's still a neat way to ensure modified organisms don't spread their genes into nature.
It's a relevant counterexample to what the question sought, but not a general argument against the possibility.


text:
Why does the apex of the human heart usually point to the left?
In the majority of human beings, the apex of the heart (left ventricle) points towards the left side of the body.  Sometimes however (approx. 1/12000 births), a person is born with a condition known as "Dextrocardia", in which the apex of the heart points to the right side of the body instead.
Is there an evolutionary reason as to why the human heart usually points to the left side as opposed to the right side of the body?
(Note:  Please don't answer with, "because there is a notch in the left lung", because I will simply reply with, "is there an evolutionary reason for the apex of the heart AND the cardiac notch being on the left as opposed to the right side of the body").

Also note there is a condition known as Situs Inversus with Dextrocardia, which is where the placement of all the organs in a person with this condition is a mirror of that of a normal person.

So I am asking that since people can live normal lives with Situs Inversus Dextrocardia, why is the placement of the heart on the left so much more common than placement of the heart on the right?  What's the evolutionary advantage?  Thanks

Is the orientation of the heart in humans different from other mammals? If not, then there would appear to be nothing special about humans. Heart orientation is just inherited from ancestral mammals.

Good point Kevin.  I'm not sure if mammals hearts also are directed to the left or not.

https://www.sciencemag.org/content/306/5697/828.abstract seems to have the answers you seek. You'll need a subscription to Science though.

From a quick look at the paper @ChinmayKanchi links to (Palmer, 2004) it seems that:

All living vertebrates possess a heart that is conspicuously asymmetrical and normally displaced toward the left (Fishman & Chien, 1997).

So the heart orientation seems to be evolutionary conserved in vertebrates (as are many fundamental traits), and no specific explanation is needed for humans.
This is said with the reservation that human anatomy is not my subject field, and the refered paper also digs deeper into the molecular basis for the orientation/symmetry of organisms. For instance, it also says that:

Second, the molecular pathway directing hearts leftward—the nodal cascade—varies considerably among vertebrates (homology of form does not require homology of development) and was possibly co-opted from a preexisting asymmetrical chordate organ system.

so the molecular mechanisms governing this seems to differ between species. This could indicate that there is a selective pressure molding species into the same heart orientation. This is pure speculation on my part though.
I also want to mention that evolutionary outcomes doesn't have to have a "reason" (i.e. a selective advantage). Much depends on chance events and evolution can only act on what is present at the moment (i.e. is restricted by earlier evolutionary history).

I think this deals with the steps of Heart development during organogenesis, together with the influence of external factors (such as the lung development and the hemodynamics), which by nature would lead heart to occupy the optimal positions for it and for those interrelated organs. Basically, the organs tend to develop on the midline, or symmetrically to the midline, but due to cardiac tube contortion during the development, it changes the position.
You can check the details on wiki (https://en.wikipedia.org/wiki/Heart_development)

I think it is because of the reason that the left ventricle pumps blood throughout body, thus is bigger than the right ventricle. So, actually, the human heart is along the center septum, but seems just a bit to the right. 1.5 cm to be precise.


text:
Temperature Tolerance In Relationship To Body Temperature
A humans body temperature averages at around 98.6°F
A dog's body temperature averages at around 101.5°F

If the temperature outside is 45°F who would feel colder?

The dog's temperature is higher than the human. So you would assume since its temperature is higher it would feel warmer than the human.
However, the temperature difference between the body and the external temperature is the following:
Difference in humans internal and ambient temperate: 52.6°F
Difference in dog's internal and ambient temperate: 56.5°F
I'd like to know as I keep telling my mom that the dogs feel hot when she puts on doggy sweaters for them when its slightly cold for us humans.

Things other than the temperature that could affect whether or not the coat is necessary: Is it raining? a wet dog will get cold quicker. How long/thick is the fur? thin coats of fur will be less efficient at keeping the dog warm than thick. Is it windy? Wind blows warm air out of the fur. How big is the dog? Size & body fat will affect the rate of heat loss. How active is the dog? A dog doing lots of fetching will keep warmer than a dog ambling along the pavement

Clues as to whether the coats are necessary: Is the dog shivering? if yes, give it a coat. Is the dog panting? yes, take the coat off before you bake the thing!

@rg255 would you like to post your comments as an answer?

done (and here's some extra characters to let me post this comment)

Things other than the temperature that could affect whether or not the coat is necessary: Is it raining? a wet dog will get cold quicker. How long/thick is the fur? thin coats of fur will be less efficient at keeping the dog warm than thick. Is it windy? Wind blows warm air out of the fur. How big is the dog? Size & body fat will affect the rate of heat loss. How active is the dog? A dog doing lots of fetching will keep warmer than a dog ambling along the pavement.
Clues as to whether the coats are necessary: Is the dog shivering? if yes, give it a coat. Is the dog panting? yes, take the coat off before you bake the thing!
this probably does not fully answer the question "If the temperature outside is 45°F who would feel colder?" but as requested by the OP I have posted my comments as an answer. I would expect a dog without a "doggy sweater" to be better able to cope with the cold than a human not wearing a "people sweater" or any clothes, just like the dog, if you want to make it a fair test!


text:
Does body temperature affect human lifespan?
If a human body were somehow to be kept at a cold temperature (say 30C) for the entire life of the given individual. And somehow the brain could be fooled into thinking that this 30C feels nice and warm.
Would that given individual live longer as a consequence?
What effect does a tempreature have on lifespan?

A core temperature of 30°C?  That's right on the edge of severe hypothermia, I wouldn't expect it to be a survivable condition for too long.  Especially for neonates if you wanted to maintain the temperature from birth.

okey then, 32. Could even keep them a bit warmer in the beginning.

As a flypushing biologist I know that if I want my flies to live longer I keep them at 18 degrees C, rather than the normal 25. Not sure if any work has been done to understand the mechanisms and whether or not these mechanisms would apply to larger organisms.

Epic, so u just put them in the fridge like food u want to last longer? How much longer do they live at 18c compared to 25c?

This phenomena is observed in simple organisms (flies, E. coli, yeast, etc) but I suspect would be acutely fatal in humans and large animals because of the need to maintain chemical reaction rates and proper temperature for protein folding.

A boat sank close to Icelandic shores in march 1984, all died but one who managed to swim to land, took him five hours and the ocean was around 4C. So there are people who can tolerate unbelievable drops in body temperature and suffer no long term harm.

And frogs are relatively advanced animals, there are those who can just freeze in the autumn and thaw back in the spring: http://www.youtube.com/watch?v=Fjr3A_kfspM

So advanced animals seem to be really capable of cooling.

Could you please define what an "advanced animal" is? A vertebrate? A mammal?

I don't have an exact definition at hand but humans and frogs are what I would call advanced. I might as well rephrase and say 'humans and frogs and such animals' instead of 'advanced'. The point would remain the same.

@Hermann Ingjaldsson: no, it is extremely important to define it. For instance, a frog is cold-blooded, a human is not.

Okey I changed it.

@HermannIngjaldsson re the boat thing, whilst a pretty spectacular feat his core temperature couldn't have dropped anywhere near that low, indeed not beyond the temperatures earlier mentioned in comments.  Even if the temperature did not kill him then the muscle co-ordination apparent before the condition becomes lethal would have surely resulted in his drowning.  The discussion in comments on this question is really interesting however perhaps we should all move to chat to keep things clear.

As you probably know, hibernating mammals can lower their core temperature dramatically. There are even cases with mammals recovering from core temperatures below zero., e.g. arctic ground squirrels and bats. This is clearly not the same as being functional with drastically lowered core temps, but could be interesting/relevant.

I am assuming that you are referring to a baseline human cooled to a core body temperature of 30C from birth. I am also assuming that you are ignoring the fact that the environmental temperature (and thus the temperature of the extremities) has to be much lower than 30C to cause a core temperature of 30C. Thus, I am ignoring hypothermia-based gangrene, necrosis, and extremity loss.
If you had a normal human with a 30C core temperature starting at birth, I have doubts that it would live any longer than a human at 36.8C. Unlike flies, which are ectotherms, humans need to have a more or less constant temperature to successfully complete most of their metabolic processes efficiently. Since humans are not built to withstand extremely low temperatures, it is likely that lowering the core body temperature to 30C will cause it to have organ impairment, causing organ failure, followed by death. Though you might be able to "fool" the brain on thinking that 30C is normal, it is unlikely that the organ functions can follow. It could be possible to breed successive generations of humans in ever-lower temperatures, but it is unlikely for a baseline human to withstand such a large temperature drop. Sensory neuron adaptation =/= bodily adaption. However, lowering the core human body temperature by 1-2 degrees (typical of sleep) may have a chance of altering a human's lifespan in a more meaningful way. Though cooling may prolong the lifespan of temperature-conformers and single-celled animals, it is unlikely that the same can be said for endotherms. Endotherms have had biological processes that run on a fixed temperature for a long time already.  One more thing: @Hermann: Their core body temperature may not have been much lower than the baseline.

Nice (up-voting that answer!), I was thinking more about this on my run this morning, and I agree with you - flies do not regulate their temperature internally and are adapted to survival within normal temperature fluctuations. Humans on the other hand use homeostasis to maintain a core temp of 37(ish) degrees, and when that drops the body actively tries to warm it self up. I think this could actually decrease lifespan because it would increase metabolic stress (more calories are required to survive).

Another argument for cold-induced longevity is that I know a person who's been working at the ER for decades, and she says people who die in extreme circumstances, such as drowning in sub zero water, can be brought back after unbelievably long amounts of time with far less damage than when in normal temperatures. Indicating the temperature is slowing things down.

I agree though that if the body is constantly trying to raise the temperature then that should increase metabolic processes and thus probably shorten lifespan. But if the brain could be fooled into thinking this lower temperature is the nice new norm..

"Since humans are not built to withstand extremely low temperatures, it is likely that lowering the core body temperature to 30C will cause it to have organ impairment, causing organ failure, followed by death." Are you sure about that? The Icelander who swam for 6 hours in the 5c ocean, surely had a core temperature below 30c, and he was fine.

@ Hermann Ingjaldsson. Core body temperature is maintained at all cost. Including shutting down circulation to the skin, and  limbs. The moment core temperature is affected, the brain slows down, heart beat diminishes, breathing slows, even stops.  And organs start shutting down.

In humans the optimal temperature for enzymatic action is 37 C. See the image below:

Our body temperature is set at 37 C (~ 97 F) because all our metabolic processes are most efficient at this point. Any decrease in the core temperature will cause a drop in all the metabolic processes imitating hypothyroidism. Hypothyroidism is a very unpleasant condition to live with - extreme fatigue, inability to utilize the energy stores, very poor appetite with increasing fat stores are few of its symptoms.
For humans to efficiently operate at lower temperature the DNA has to be remade to code for enzymes that would not loose their efficacy at a lower temperature - maintaining a good reaction rate. This is impossible as of now where even a single gene modification or single nucleotide correction is extremely difficult and is under experimentation.

Source:
https://sachabiochem0001.wordpress.com/2013/04/09/factors-affecting-enzyme-activity/

Movement is life. If the human body where to undergo this kind of temperature that would be below the normal temperature for the human body, we would in fact either have to move more and or do more as in eat, exercise, communicate etc. If your body did not have this mental capacity basic survival skill you would be in the process of slowing the function of your body down leading to death.
Also the person who had swam in freezing water had a better tolerance to the cold than normal, but this does not mean that if a person had the capacity to tolerate cold temperatures that this kind of treatment of the body whould be good for you.
Over a short period of time your body can undergo extream circumstamces so it was a basic survival skill that had kicked in from the metal material of that persons being telling their physicsal as in nervous system that if they were going to survive they would have to move in order to regulate their body temperature.


text:
Is there an entry-level circadian model of serotonin, ghrelin, dopamine and the sense of well being?
I've long been interested in circadian rhythms and recently came across a variety of articles that appear to indicate that the following neurotransmitters, transferases and hormones are connected. There are mentions of some circadian rhythmicity and maintaining homeostasis for these compounds(Are serotonin levels in humans affected by light?):

Serotonin
Dopamine
Melatonin
HIOMT, NAT
Ghrelin
Leptin

Additionally, their expression is related to Suprachiasmatic Nucleus and light exposure.
I'm interested if there's a good article or a talk that discusses the homeostatic system that those compounds are a part of. I'm particularly interested in their effect on the feeling of well being.
It seems to me that all these compounds are in some way related to moving and feeding. However, I cannot wrap my mind around multiple separate articles that describe how, and am looking for a single paper that may shed light on the connection between these compounds.

Most hormones have some circadian/ultradian/infradian component. These questions are somehow related to what you're asking: http://biology.stackexchange.com/questions/2732/do-men-have-significant-hormonal-cycles http://biology.stackexchange.com/questions/1982/what-can-the-timing-of-human-urination-tell-about-the-humans-physical-condition/ http://biology.stackexchange.com/questions/3590/how-are-long-time-periods-measured-in-biological-systems/


text:
Interlocus Contest Evolution means suicide?
I was reading Matt Ridley's "Genome" book. I am trying to understand the Interlocus Contest Evolution in his X-Y chapter. I do not understand why the X and Y chromosome would want to kill each other. Wouldn't that cause the death of the species (actually, have any species died that way?).
Can someone shed light on the issue?

X and Y chromosomes don't "want" anything-they are not conscious. I know that sounds obnoxious, but it's very important in evolutionary biology to understand that there is no agency and no intended final product for natural selection. I think the best way to think about it is like this: let's say there's a mutation on the X chromosome that happens to make females more fit at the expense of making males less fit. It seems possible that the evolutionary arms race that this establishes (i.e., males bearing a mutation that compensates or overcompensates for the new expense of the mutation that, say, their successful mom gave them, would then start to sweep to fixation in the population, and so on and so on) could result in population collapse. Apparently, there's theory out there that confirms this: http://www.els.net/WileyCDA/ElsArticle/refId-a0003669.html. Also, I vaguely remember a paper about toxic sperm (vs. female mating behavior) in Drosophila melanogaster suggesting that populations could collapse. As Bonduriansky mentions in the link, though, one resolution to the arms race would be the evolution of genes that get expressed very differently between the sexes (i.e., a gene that is good for a female but terrible for a male would evolve to only be turned on when it's found in a female). I hope that helps?

Did this answer your question?


text:
Can a new Y-chromosome be created?
The major gene of the Y-chromosome is SRY. Would it be possible to get the X-chromosome and add SRY to create a "fuller" Y-chromosome?
What advantage does the skinny Y-chromosome give an individual anyway? Females only use one X-chromosome (via the Barr body) so they don't seem to gain as much from having the pair.

Females do not always use only one X chromosome - eg Drosophila. And why would an X with SRY be better than the current Y? It is not junk - it is now being found to affect many genes through epigenetics.

SRY translocation to the X chromosome clinically exists and characterizes the De La Chapelle Syndrome. The phenotype associated to this syndrome demonstrates the necessity of other components on the Y chromosome to develop full masculine characteristics.

Would it be possible to get the X-chromosome and add SRY to create a "fuller" Y-chromosome?

Possible? Sure. You could sequence both chromosomes and then create some artificial DNA that included the combined sequences.
Would it be viable? Probably not.

What advantage does the skinny Y-chromosome give an individual anyway?

If there is a genetic condition in the father's X-chromosome, the male child is spared from it.
If there is a genetic condition in the mother's X-chromosome, the male child has a 50/50 shot at being spared from it.
If the genetic condition requires two homogenous X-chromosomes, the male child is spared.
If the genetic condition requires two heterozygous X-chromosomes, the male child is spared.
These are all advantages of simply requiring a Y-Chromosome, and there are certainly disadvantages to having a Y-Chromosome as well; X-linked genetic disorders will definitely affect any male heirs, unlike...

Females only use one X-chromosome (via the Barr body) so they don't seem to gain as much from having the pair.

...Female offspring. Because women have two X-chromosomes they have redundancy. If there is a bad gene on the extra X-chromosome that is deactivated, then it doesn't matter - where for a man with the same X-chromosome it would definitely affect them.
Also, because of the redundancy, what X-linked conditions do exist usually affect women less-so. If both X-chromosomes are utilized for a specific gene, then one bad protein product is partially made-up for with the one good protein product.

If the genetic condition requires two homogenous X-chromosomes, the male child is spared..... hmmm can you point to an example of that? If the condition is recessive the male child is definitely not spared.

Nope, as I'm not sure if one exists. I was being hypothetical.

Further points> Y chromosomes, contrary to popular belief, are not junk - they contain very few genes but these can have epigenetic effects (for example via regulation of other genes). This gives a huge benefit to even "skinny" Y chromosomes because it offers the opportunity to resolve intralocus sexual conflict as it is male limited. Another point is that females do not always use just one of the X chromosomes (X inactivation). Some species use other methods of dosage compensation - drosophila males double the transcription of their X to match the output of both in the females.

Would it be possible to get the X-chromosome and add SRY to create a
  "fuller" Y-chromosome?

Yes. Nature has done that. https://en.wikipedia.org/wiki/XX_male_syndrome
However there are more there is more than just the SRY gene on the Y chromosomes. As such XX males with SRY translocations are sterile.

What advantage does the skinny Y-chromosome give an individual anyway?

To an individual nothing much (as far as we know). However Y bearing sperms swim faster as they have smaller heads than X bearing sperm. So much so that for every 100 girls conceived, there are 140-160 boys conceived.

Females only use one X-chromosome (via the Barr body) so they don't seem to gain as much from having the pair.

Actually there is a lot to gain. X inactivation is random. So female tissue is composed of a mosaic of cells expressing one or the other X chromosome. So if there is deficiency in one allele, the other allele can compensate at the tissue level. This is why despite so many boys being conceived, only 106 boys for every 100 girls are born.
Also why women have smaller standard deviation in intelligence than men (as many of the genes regulating intelligence are on the X)...So while there are fewer women with super high IQ, there are also fewer women with super low IQ.


text:
Cine-MRI versus MRI
Could someone explain the difference between Cine-MRI and MRI?  I am reading conflicting things online, such as Cine-MRI uses ECG-gating, or that Cine-MRI takes many images of the same position of the heart before stitching together the final result, and it is confusing me.

I'm not familiar with the technique, it is as I'm sure you already know very specialised and I've found it fairly difficult to find resources specific to cine-MRI.  At a glance at the wikipedia entry, however, there are a few differences that I can point out to you.
A normal MRI will take a snapshot image of a section of the body in time, therefore can not be used to show motion of internal structures.  By contrast, cine-mri takes several snapshots at different times and stitches them together into an animation, allowing the physician to see movement.  For example, the technique is useful for imaging the beating heart and has also been used to examine the flow of cerebro-spinal fluid.
ECG gating refers to how the images are collected when the scan is of the heart.  The timing of the scans matches up with the electrical activity in the heart measured with a surface ECG.  As a undoubtedly hugely oversimplified example, the scanner might take an image at P,Q,R,S and T on the ECG waveform before then stitching them together into an animation:


text:
Why does not the host produce any immune response to antiserum antibodies?
When an antiserum is injected to a person to protect oneself from a certain disease, the antibodies in the antiserum come from another organism. The question is:
Why don't the injected antibodies cause an immune response in the individual?

If an antiserum derived from another animal was used then it would be active immediately, whereas the patient would take 10-14 days (this figure from memory) to mount an immune response against the foreign antibodies. So the antiserum would have plenty of time to 'cure' the patient.

That's a good question - because its certainly possible to get antisera against antibodies.
Sometimes antisera is actually human antisera, so there would be no rejection at all.  But that is for extreme cases, e.g. serum transfusions from convalescent Ebola survivors to current Ebola patients.
One would expect that you could only give an antiserum once and then it would be less effective each time you get it.  Since antisera to snakebites is the most common application, where its quite possible to be exposed to multiple bites over one's lifetime.
I found one reference to a horse antiserum treatment that's being used. It makes reference to a source of antiserum which sounds like its been designed to reduce the antibody antibody immune reaction:

Horse-serum antivenin has been available since 1956; a purer antivenin with improved properties was released in 2000 (see Medication). With the reduced side-effect profile of antigen-binding fragment antivenom (FabAV) and the improvement in tissue injury with antivenin administration, the threshold for dosing is lower.

Even before the availability of these new treatments, its probable that most patients can endure multiple anti serum treatments from the same source animal.  Even goat, horse and rabbit antibodies are pretty similar to ours and the reaction will not be as strong, in addition to which, the immune system will tend to clear out the antigen-xenoantibody complexes from the blood.
I can't find references, but my guess is there must have been some cases of rejection and reaction otherwise they would not have bothered to improve the serum treatment.
Update: just read this little blurb in scientific american, that describes how venom antisera will occasionally cause deadly reactions, while most of the time simply disarming the venom.  The new generations of antivenoms described have the Fc portion of the antibodies removed.  This eliminates the adverse immune reaction but I also think also eliminates any immune resistance the patient might get out of the antisera.  The Fc portion of the antibody is the part which our immune cells bind to.  In this case the new antivenoms aren't anti sera exactly, but they do use the antibodies to deactivate the venom toxins and crosslink them to make them less effective.


text:
Would ovoviparous to viviparous mutation have been gradual? How would that work?
It seems unlikely that an ovoviparous ancestor of mammals long ago could have had a viviparous offspring in a sharp one-generation dividing line, but what would be the gradual steps between egg birth and live birth? Are there any examples of answers to the first question today? It seems that marsupials are a different thing altogether, not something in between egg laying and live birth (no modern mammal's ancestors aren't believed to have marsupial-style birth in their evolutionary history, right?)?

I happen to have seen a talk by an anthropologist who was working on this (i can't reference them here i'm sorry to say - forgotten her name).  I can only give an example from their work...
If you look at old world and new world primates, there is a large difference between the gestation time.  If you look at the table in the link, lemurs have half the gestation time that humans and gorillas have.
What I can recall is that the lemurs placenta lacks many of the structures that primates have (see section 5).  The lemur placenta is supposed to be primitive and a lot more like an egg sac which was internalized as opposed to a more articulated womb that primates have.  So her thesis was that eggs would start out being internalized and subsisting only on their own internal structures, still isolated from the mother, then later placental structures would come about that nourish the fetus and enable it to enjoy longer gestation and better development pre-partum.
The stage I'm describing is only the divergence between primitive wombs and 'more advanced' wombs in the sense that they were capable of supporting the fetus for 9 months rather than just 4.  That development happened over about 30 million years.  The divergence of mammals is thought to have happened about 270 million years ago.
So the rough answer would be hundreds of millions of years for the whole shebang, but internalized eggs and live birth would be a relatively smaller amount of time.


text:
Do T-cells express MHC molecules?
T-cells recognize the MHC molecules and body's own peptides. When it doesn't, it alarms the immune system. But do T-cells express MHC molecules ? If so, how are they using it? If not, what happens when a virus infects T-cells? (Yes, I am confused about HIV infection mechanism too. They escape from immune response by altering their genes and disrupting the MHC-peptide bonding. I can see that this can work in macrophages. But what is the situation in T-cells ?)

They express MHC1.

They do not express MHC II molecules.

It is incorrect to say that T-cells do not express MHC class II molecules. Please see: https://www.ncbi.nlm.nih.gov/pubmed/15120183

There are two types of MHC molecules:
All nucleated cells express MHC class 1 proteins.  A sample of all proteins produced within the cell are 'sliced' into their constituents which are then presented by MHC-I receptors.  This means that if a virus infects a cell, the foreign proteins the cell is induced to make are expressed on the cell membrane by MHC-I.  This is important as antibodies can not cross cell membranes, therefore this is the method by which a cell signals that it is infected by a virus.
MHC II are the special molecules that are only expressed in antigen-presenting cells, which I think is what you are referring to.  As neither CD4 or CD8 T-cells present antigens, they do not express MHC-II themselves.  Instead CD4 have receptors for MHCII  (while CD8 have receptors for MHCI), allowing them to interact with antigens presented by other immune cells.
If a virus infects T-cells, the viral proteins are sampled by the MHC-I pathway and presented via MHC-I on the surface of the infected T-Cell.  The immune response then progresses as for any other virally infected cell, destruction by CD8 T-Killers that destroy the cell by non-phagocytic means.

Are you positive CD4 cells don't present antigens? I could have sworn they had the capability to.

@MCM that was off the top of my head, I'll have a read of my notes tomorrow.  Happy New Year!

Are antigen-presenting cells a specific type of cells? I've always been confused about this because the label seems so general.

@shigeta I would say they're a class of cell, defined by their expression of MHC-II.

I would expect that they do something else besides only presenting antigen - is that their only function?

Antigen-presenting cells include dendritic cells, and B-cells, but there are more: http://en.wikipedia.org/wiki/Antigen_presenting_cells

"All nucleated cells express MHC class 1 proteins." - This is a pretty bold statement... :D At least I would add "human cells"...

I believe this is the better answer, though I recall this being a debated issue. Some MHC class II molecules are found on at least some subtypes of T cells, though it is (at least was) unclear whether they acquire them through expression or from other cells.
http://www.jleukbio.org/content/63/6/707,
http://www.bloodjournal.org/content/101/7/2704,
http://www.ncbi.nlm.nih.gov/pubmed/7522009,
http://www.sciencedirect.com/science/article/pii/S1074761305003006


text:
How do multiple replication forks function without 'colliding', and what is the benefit of this method?
I'm currently reading a little about DNA replication, and have come accross the following statement;

Replication starts from a fixed point and is bi-directional ... In Eukaryotes, there are multiple replication forks, each progressing in a bi-directional fashion.

If there is a single, long strand of DNA in a Eukaryotic cell, I see potential problems with this:
These forks involve opening up a section of double-stranded DNA, and each strand becoming a double strand in a newly synthesised piece of DNA. At some point, before any single fork has become two new double-stranded molecules, another fork could 'collide' with this, causing it to attempt to replicate the non-finished section.
Simply, how can one replication fork meet another without either exponentially increasing the number of strands being replicated?
Also, on a more general level, I would be quite interested to know the actual benefit of this, when, typically, only a single copy of the double-stranded molecule needs making.

To get to the exponentially increasing number of strands, the replication would have to be started on the already replicated strand, and not on the original strand. Replication in eukaryotes is tighly controlled and such an event is prevented by the regulation.
How can the cell prevent re-replication of the strand that is currently synthesized? By timing the steps of the replication in strict order and preventing any replication outside of that order.
Replication starts at defined origins of replication. In the G1 phase, pre replication complexes (pre-RCs) are assembled at the origins of replications. At these pre-RCs the replication can be initiated, but pre-RCs itself cannot be assembled in the later phases of the cell cycle. When the replication starts, the pre-RC is converted to a post-RC which can't initiate the replication anymore, preventing re-replication.
The benefit of multiple origins of replication is replication speed. Eukaryotic genomes can be much, much larger than those of simple bacteria. Replicating them using a single origin of replication would take a very long time.
Some further reading material:

Genomes, 2nd edition, chapter 13
Cell Cycle Regulation of DNA Replication


text:
Does coloring affect the perception of depth?
I have a question about the mechanics of human vision which may be as much of a physics question as it is a biology/physiology question. I noticed that if I try to imagine a clear blue daytime sky contrasted with a clear night sky and ask myself which of the two appears closer, my intuition says the daytime sky appears closer. My next thought was, given that a night sky is mostly black, visually the only difference between the two skies is their color. So why is that I want to "blue" is closer than "black"? And if the difference in color is truly what produces the difference in perceived depth, can similar effects be noticed with other color pairs at more familiar distance scales?
But then again, there are a couple of alternative explanations that seem more plausible to me on second thought. A black night sky could just as easily be called a dark sky, and the difference in perceived depth is really more a matter of shading. Then I remembered a night sky has stars of course, and it might be that my mind just wants to place the stars at normal "sky depth", forcing the black backdrop to appear even further away.
(Another related question I've been somewhat curious about: what precisely is the perceived "distance to the sky" as far as our intuitions are concerned?)

see Wikipedia http://en.wikipedia.org/wiki/User:Karam91/Chromostereopsis for a starting point

That was very helpful. Good to be able to a name to the effect. Thanks!

Yes, color and shading can certainly affect depth perception, as explained by wikipedia:

Aerial perspective – Due to light scattering by the atmosphere, objects that are a great distance away have lower luminance contrast and lower color saturation. Due to this, images seem blurry the farther they are away from a person's point of view. In computer graphics, this is often called "distance fog." The foreground has high contrast; the background has low contrast. Objects differing only in their contrast with a background appear to be at different depths. The color of distant objects are also shifted toward the blue end of the spectrum (e.g., distant mountains). Some painters, notably Cézanne, employ "warm" pigments (red, yellow and orange) to bring features forward towards the viewer, and "cool" ones (blue, violet, and blue-green) to indicate the part of a form that curves away from the picture plane.

Here are a few examples:

The above is Manet's "Luncheon on the Grass" - and if you look at it briefly it seems the bathing woman is sort of hovering amidst the trio instead of rinsing herself off in the background. This is because the warmer colors flanked by more saturated greens in the grass around her "pull" her forward into the same space as the rest of the painting. Here, scale is one of the major cues that she should be in the background.

Above is Cezanne's "The Bay" and is an excellent example of how warmer colors (reds, yellows, oranges) are used to add depth when contrasted with cool colors (blues, greens, violets). The image works very well, and that's partially because of the colors chosen. You can almost draw a diagonal line between the warm and cool portions of the painting.

I noticed that if I try to imagine a clear blue daytime sky contrasted with a clear night sky and ask myself which of the two appears closer, my intuition says the daytime sky appears closer. My next thought was, given that a night sky is mostly black, visually the only difference between the two skies is their color. So why is that I want to "blue" is closer than "black"?

Well, there are many differences between the two! The daytime sky has numerous reference points - the horizon, mountains, clouds, airplanes, nearby buildings, etc. I would bet the reference points are the number one reason you perceive the daytime sky to be closer, as our brain is constantly taking them into account without us thinking about it. There are other cues, too: The daytime sky has a gradient to it - that is, the blue of the sky differs due to the curve of the atmosphere, and gradients increase depth perception with more saturated colors being perceived as closer (as opposed to the edges of the daytime sky, which are often less saturated).
The night sky, on the other hand, is pretty much solid black (if you live in suburban or urban areas). The lack of a gradient or other colors immediately robs the observer of some depth perception, and because of the inky blackness of night the other reference points - the horizon, nearby structures, airplanes, clouds, etc. - can practically disappear, robbing the observer of additional depth perception.

Thank you MCM. Your response was very helpful, and I feel like it gives me a lot to go on for learning more. Cheers!

I had this same question.  I believe the answer is this is a known effect caused by aberrations between your eyes and the way they perceive color.  This effect is called Chromostereopsis.  I know this is an old topic but hopefully this information will be useful to people like me who were also trying to learn more.
http://en.wikipedia.org/wiki/Chromostereopsis

More information (as opposed to a link, which could rot) would be appreciated.


text:
Historical recovery from mass extinction events
Is there a way to generally characterize how species "regrew" after the various mass extinction events happening periodically from 450 Ma to 65 Ma.  Would the surviving species just start back where they had left off and evolve willy-nilly as if the destroyed 50% or 70% of biodiverse species had never existed?  Or would the biome in some way have the capacity to regrow something resembling the former order based just on the remaining species.  This is probably a whopper of a dumb question, my apologies in advance.

I think the concept of adaptive radiation is what you may be thinking about, since adaptive radiations have been observed following historic mass extinctions.
When organisms are placed in environments with low diversity (either due to mass extinction or the recent creation of the environment) they can undergo adaptive radiation.  This generally occurs when there are lots of unoccupied niches in the environment - essentially there are lots of potential ways to make a living that are not being exploited by an existing organism.
In this situation, any organism with a heritable trait that was able to utilize a niche better than other organisms would have a selective advantage and would increase in frequency.  Over time this process can result in new species of organisms.
There is nothing really different about adaptive radiation and the normal process of evolution and speciation except that in an environment with lots of unoccupied niches, the probability of having a trait that gives you a selective advantage is greater so speciation occurs at a faster rate.
It is the normal processes of evolution and speciation that give the biome the capacity to increase diversity based on the remaining species.


text:
How does prolonged exposure to high frequency noise affect hearing?
Is there any research showing how prolonged exposure to background noises, particularly high frequency noises, affect hearing abilities? Does constant high pitched noise cause damage even a low volumes? E.g an alarm sounding, noise of an air plane, or noise from road works and building sites.
If so, what is the effect? and why does it happen?

You're asking about high-pitched noises even at low volumes, but your examples are high in volume, not (necessarily) pitch. Which are you actually interested in?

Rodent protection modules for car engines give off high-pitched but quiet noises :) In any case, I don't think a high-pitched sound has any different effects of prolonged exposure compared to a low-pitched sound.

What about that from an industrial vacuum system for moving plastic pellets? The noise is in a high frequency not heard immediately by many (say 10,000 hz) but only after exposure of time. The more exposure, the more extreme and potential for hearing damage. Any comments pertaining to this?

It turns you into a bat.

The ear uses a series of hairs to parse out sound frequency in the cochlea.  When the cochlear hairs die, we lose some frequency response.
As we get older, even without exposure to loud noises, the higher frequency responses tend to lose their response first.  But loud noises have been linked to hearing loss and high tones are often lost first.
Hot off the presses: there's been some success in regenerating the cells which respond to sound in our ears.
I want to add @Armatus has a good point.  Ultrasonic sounds - above hearing range - seem to not adversely affect hearing at all.  Will humans and animals be harmed by frequencies outside their hearing range?

In regards to your "hot off the press" link... Ear Rogaine? ;-)

Lol - that would be one tricky q-tip!


text:
Why Do Ruminants Require A Multi-Compartment Stomach To Digest Food?
Cows, camels, sheep, goats, etc being ruminants must chew their food repeatedly by regurgitating their food from their first stomach compartment and chewing their 'cud'. This then finer chewed material makes its way to the various stomach compartments to be digested.
These animals are eating plant material, the same plant material animals such as elephants, horses and hippos eat as well. However, these animals only have one stomach compartment.

Why does one need a multi-compartment stomach and one does not if they are all eating the same/similar food?

There is more difference than just the parts of plants that are eaten.
Two of their stomachs - rumen and reticulum are not used for digesting food at all. Multiple rounds of chewing and mixing with saliva, wich result in very small particles of undigested food help the bacteria in those stomachs reach, digest and use that cellulose-rich plant material. Cows "eat" the bacteria from their stomachs and the grass is just food for these bacteria. You could say that cows are not herbivores but secondary consumers.
Look at this picture (from Wikipedia article on ruminants, a good place to check all this in more detail but still simpler than most professional books):

See that the ruminants have the same second and third part of their digestive system (though the bacteria use up most of carbohydrates, so some difference in absorbed material), but have an additional part in the front - where the microbes digest and ferment the food, that the ruminant has provived them. The reticulorumen needs to be large in order to provide space for all that plant material and bacteria.

It is not a biology question but simply a logistic problem. The digestion of cellulose just because of the presence of celluase producing microbes. Rumination itself, by the action of chewing, can enhance the cellulose digestion efficiency by incresing the surface area. Still nothing related to the multiple compartments of the ruminant stomach.
Actually, the multiple compartments allowed the anti-directional peristalysis and multi-tasking of the stomach. That is Ruminants need A Multi-Compartment Stomach to perform rumination for the reason of logistic.

If you ever look at a huge pile of elephant/horse dung you will see it is full of poorly digested vegetation. I had an (unfortunate) 4 day project on a field trip in south africa which involved handling a lot of elephant s***, more than once I found whole amarula fruits!
Think about this in comparison to ruminants which have a much better digested pile of dung, e.g. a cow-pat. The ruminant digestive system allows them to digest cellulose (found in plant material) much more efficiently than other vertebrates thanks to a specialized gut flora. You may want to look at this and this for more details.

They are not all eating the same/similar food.
Elephants, horses and hippos are herbivores that have different diet to ruminants. Elephants, for example, have trunk to access fruits that is less difficult to digest.

100 kg for a 5000 kg elephant is 2% of body mass.

ok, i have edited.