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What are the minimal chemical requirements for a food which we all can eat?
I've been puzzled by the following though experiment for the past few days:
I want to make my own food from scratch, but I do not know where to start from.
I want to be 100% sure that what I eat will never contains something that can damage my body. For example: If you buy something from the local market you can not be 100% sure that it's safe to eat. (99.9 % maybe... but that's not 100%)
I want to ask you to tell me, how can I make a food that I can eat, or should I say - live on it, for the rest of my life, that's 100% safe, I can control every aspect of it's creation and has many combinations of taste because I love diversity.
Thank you for your time : )
Edit:
Because I realized my question is very broad and indeed is a little... too much scientific I want to close it. But before I do so, here's what I had in mind:
I wanted to take some chemical elements, put them in a jar, run some electricity, heat, whatever through it, filter it, do some additional processing and eat it.
 I wanted to know if the stomach can take it, because I was going to eat food that's not hard to digest.

Can you please work on your question? You want to know which food is sufficient to live from only?

Does it sound better now?

"I want to be 100% sure that what I eat will never contains something that can damage my body" Our current knowledge in nutrition in order to know such thing.

Your question seems to be mixing marketing and cultural references and from this asking for an objective response. It sounds like you want to know how to eat healthy. This isn't really a question of how biology works. Is your base question: What sources of chemical fuel do humans metabolize?

This question is very broad and can not be answered without a very high degree of opinion and assumptions.

Considering the three basic biomolecules used by the body are carbohydrates, lipids, and proteins, you would need to consume these three molecules only. Now we can choose three substances.

Glucose, one of the most basic carbohydrates, is needed for ATP production, so that would be a food choice there.
Any oil or butter will provide lipids.
Protein comes from a variety of sources. Meat is typically though of as the best, but nuts are a pretty good source too.

Since nuts satisfy proteins and lipids, I'd say honey roasted peanuts are the most basic food you could live off of, if you replace pure glucose for the honey.

This seems to the closest to my expectations regarding the answer, thank you : )


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What is the evolutionary purpose of white spots in nails and how can they be characterised due to Leukonychia?
Suppose you haven't hit your nails so the white spots are due to Leukonychia.
Are the discoloration i.e. the white spots due to lower porosity (less minerals absorbing) or some other factor? I cannot understand their physiobiological chareterisation and why are they created due to evolutionary terms? To show a person that he is lacking minerals? Or why do some people have them?

Do you have any reason to believe there is an evolutionary purpose? Having nail spots don't seem like a fitness increasing feature.

You just stated the person develops the white spots because he hit his nail. Does he get them because he struck his finger, or because he's missing something? Why do some people have them? Or, does everybody have them but don't injure their nails at the same time? Please think about what you're asking. One of the most important principles in science is to ask, and answer (by collecting evidence) one question at a time.

@MarchHo There are different kinds of white shapes: lines, gathered things, surfaces -- what they tell to each person I have no clue. Absorbing not perfect yes due to multiple reasons: diseases affecting absorption rate directly, allergen reactions in which body does not absorb things -- body is all the time in certain mode. Are they really just stochastic noise or is there some real purpose for them like signalling bad nutrition? Has nature developed some mechanism to nails that we should look at to help us somehow?

This is a common misunderstanding from newcomers in evolutionary biology. Not every trait is the result of an adaptation. Evolution is way more than just natural selection and is not as deterministic as you may think. There is stochasticity inherent to mutational processes and there is stochasticity in reproductive success (called genetic drift). This seemingly totally unrelated post may help you getting a quick grasp of what are the stochastic processes in evolution.
The white spots you observe very likely do not result from an adaptive process but it just happen to be the way it is. For the physiology part (but this would be the subject of another question) I have no idea what drives these white spots.

Good point +1! I totally missed the stochastic nature, it would be super cool to understand this process better.

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Difficulty in developing certain vaccines
I have a college level background in Biology, say at the level of Campbell. I am very curious to know why it's extremely difficult to develop vaccines for certain diseases. Two cases which I am really interested in are Malaria and AIDS. It would be great if someone can give a brief sketch of the major issues being faced without getting into extreme technicalities. Thanks in advance.

Not an easy question, especially since the reasons for both pathogens are different.
For HIV the problems are manyfold:

Insufficient knowledge about required immunity

Its not known, which parameters are really important to raise an adequate immunity.

Variation in HIV strains

HIV has a very high mutation rate, which results in many different subtypes. This makes the virus extremely successful, but also causes problems for making vaccines. We have a similiar problem with vaccines for the flu, but there the number of subtypes is known and not very high. Still we need a new vaccine for each season based on the current viruses. For HIV there are no knwon proteins against which immunity can directed like in the case of the flu.
HIV also recombines very fast, so new variants can come up pretty fast.

HIV targets the immune system

The HI virus targets cells of the human immune system (namely CD4 T-cells) which are important for developing a proper response to a vaccination. These cells need to be stimulated, but on the other hand are destroyed and specially targeted by the virus.

Lack of an effective animal model

To develop and test good vaccines, scientists need good animal models to test the pathogen and see the effect of a treatment.
Chimpanzees show some response to HIV infections, but they are expensive to keep as laboratory animals and also rare to get. The problem is, that HIV is pretty good adapted to its human host.

Human subjects trials

This is more an ethic problem, but still needs to be adressed. To test the efficiency of new drugs, double-blinded placebo controlled test are done. Afterwards you can compare the placebo group to the treatment group and analyze the outcome. How do you do this with a deadly disease?
More information can be found on this webpage from the NIH.
For malaria some of the problems are similiar, others are different. he greatest problem was for years, that not enough money was available for research, which has been overcome only quite recently:

Plasmodium goes through different stages

The parasite causing malaria goes through three different stages in its development in the human body. With each step it hides again from the immune system. The different stages are also present in different cell types, see this image from JCI ("Advances and challenges in malaria vaccine development"):

antigen

Its not clear, against which antigens such a vaccine shoud be directed. This is due to the problem with the different stages and hasn't been found yet.

different pathogens

There are four forms of plasmodium which definitely cause malaria - : Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale and Plasmodium malariae. Newer results suggest, that Plasmodium knowlesi is also a pathogen for humans.

lack of animal models

More information can be found here.

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Can (any) human cells learn?
I'm not talking about single celled organisms, but actual cells in your body. Is there any evidence that they can learn to, say, navigate an environment or avoid an aversive stimulus like an animal could? Is their behaviour understood well enough to say that it's entirely mechanistic, or are there things we still don't know?

I'm not entirely sure what you're asking. What do you mean by "learn", and are you proposing a situation where the cells have somehow become removed from the body?

you can start by reading on acquired immunity. http://en.wikipedia.org/wiki/Adaptive_immune_system

yes they do.. what do you think the epigenetic mechanisms are for.. 8-)

@MCM yes - I'm thinking along the lines of classical conditioning.

Memory B cells learn the molecules of the pathogen?

For this specific question, let's divide the cells into two categories:
Cells that rarely "navigate" are the cells that are connected to give the tissue its mechanical properties. How do these avoid an "adverse stimulus"? Well, they don't avoid it. But if that stimulus "harms" cells they react in some way:

if the cell is destructed by the pathogen, it will release chemical compounds that have chemotactic properties and attract specialized cells.
if the pathogen has intracellular tropism, the cell may release some chemical compounds (see interferon) to "alert" other cells that something is wrong. Most cells can also present antigens on their surface.
there are also some stimuli which change cellular life cycle turning cells into cancerous cells. These cells can gain excretory properties and produce substances that destroy intercellular jonctions. This is how metastases occur.

Cells that "navigate" are the blood cells. White blood cells respond to different kind of stimuli (chemical) in two ways: either they are attracted (by inflammatory cytokines for example) either they are repelled. Macrophages are attracted by cytokines released when a pathogen agent triggers inflammatory response. They "ingest" that pathogen through phagocytosis and expose some parts of it (the antigens) on their surface receptors. This stimulates lymphocytes which process that antigen and decide if it is self or non-self. If it is non-self, they stimulate proliferation of specialized cells against that antigen. Another type of blood cells, the platelets, although they have no nucleus, have interesting properties: they can adhere to the broken endothelium where they change shape and start to produce different chemical mediators.

Read more on:

Wikipedia contributors, "Chemotaxis," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Chemotaxis&oldid=600637322 (accessed June 28, 2014).
Wikipedia contributors, "Interferon," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Interferon&oldid=608718450 (accessed June 28, 2014).
Wikipedia contributors, "Adaptive immune system," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Adaptive_immune_system&oldid=612379171 (accessed June 28, 2014).
Wikipedia contributors, "Platelet," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Platelet&oldid=614627651 (accessed June 28, 2014).

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Healing rate of cut while suffering from a cold
I recently cut my finger fairly deeply with a box cutter and had to have it stitched. During the healing process I contracted a strong cold/mild flu (a sore throat and runny nose with a high fever, aches and shivering). I doubt the two have anything to do with one another apart from happening to occur at the same time.
But they did occur at the same time. So I'm wondering: what is my body going to do?
If I recall my junior high biology, a cut is healed by platelets and [other stuff I can't recall], whereas a virus is fought with antibodies. Presumably in both cases it's a bit more complicated than just that. I'm also not sure if there is any crossover - are antibodies, for example, needed to protect the open wound from bacterial infection? Regardless, my question is:
Since the resources in the human body are finite, would having to fight off the cold have a detrimental effect on the healing of the cut?
If certain resources are needed for both tasks, would the body divide its resources or give one precedence over the other?
I'm guessing this is not something that is easy to measure, since it would be difficult to conduct a control experiment given the insane amount of variables. But presumably there is a consensus in the biological community on whether there would be an effect, even if it is not possible to determine the degree of said effect.
I should mention in closing that I am not remotely worried about any of this; it just piqued my curiosity.

First of all: No, there is no connection between these two incidents, correlation does not imply a causation. Cold and flu viruses affect the respiratory system and the infection route goes via it. A cut is a local wound, which does not affect the respiratory tract.
Then: Recovering from an infection is a task for the immune system (its both, the innate and the adaptive immune system, the last involves the antibodies), which is not doing much for wound healing. The wound attracts neutrophils and macrophages which are attracted by factors released by the wound and they react to bacterial infections (when they occur). See this Wikipedia article.
The ressources of a normally healthy person are quite big. This is demonstrated by the fact that many secondary infections only occur in a opportunistic fashion (for example viruses like Herpes or certain fungi) when the body is weakened by other infections. So there is a limit, but this will certainly not be reached with a severe cold.


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How do you express and detect GLP-1 receptors?
I am currently working with a peptide which is an analogue for glp-1, but during invitro studies am not able to detect for the presence of GLP1- receptors.
The cell line used is Min-6. How do I detect it?

If you have an antibody against the GLP-1 receptor, you could make a whole cell lysate and do a western. How old are your cells? According to this they alter their behaviour over time and alter the expression of genes.

Try polyclonal antibodies. It might just be that your antibody isn't picking up the epitope.

does the cell line express GLP-1 mRNA? You could easily and cheaply use PCR to amplify the GLP-1 mRNA. That technique would be exquisitely sensitive and specific for what you want - and you don't need to worry about expensive antibodies.

The question is slightly unclear since it fails to clarify whether the GPL-1 receptor is endogenous or is over-expressed. Also does the GLP-1 belong the same species that Min-6 originates from or it belongs to a different species? Those are important points since if the receptor is endogenous then the main problem is sensitivity of the detection method, which can be difficult sometimes to detect an endogenous protein relative to an over-expressed one. Also if the GPL-1 belongs to a different species, which you are trying to over express in Min-6 it might not work since the cellular machinery might not support its production (tho unlikely) or its transport to the cell surface, which I have had this problem before. It could be that for the particular expression levels you have in those cells, if the GLP-1 is over expressed or if its non-endogenous, it causes toxicity and kills the cells that are expressing it hence why you do not see any GLP-1 expression (e.g due to excessive receptor activation). Also could you clarify what you mean by "analogue for glp-1"? does this mean it is not exactly GPL-1 or its a homologue or orthologue, which you are trying to detect using a GLP-1 specific antibody? that might again be a problem if the GLP-1 Ab you are using detects a region of the receptor, which is not conserved in its homologues.
In terms of solutions as pointed in the comments, the best way to go about this is to use a polyclonal Ab, which is raised against a large section of the peptide in question, allowing you a better chance of its detection. If that did not work, you might have to resort to GLP-1 mRNA detection using RT-PCR or qPCR, which you would need to design primers for based on you GPL-1 sequence which you can get help with here.


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Monochromator in fluorescence microscopy
I'd like to ask why are there no fluorescence microscopes that use a monochromator instead of filters?
If there are any, then I should change my question as, which ones use it and why are they so rare?

Add Little bit of more data.

Well, according to Cold Spring Harbor Protocols, xenon arc lamp/monochromator-based fluorescence microscopes are economical, performant, and rather common.

It is a very clear question about use of a specific piece in a laboratory equipment. It doesn't mean that a question is unclear, whenever you don't have the necessary background to answer it.
I don't think each question should be asked by providing background information in such a way that, anybody related to biology should understand what is going on. Biology is a wide field and it is very unpractical, if this is what you are suggesting. And if not, I really can't see the point of putting this question on hold.

Zeiss LSM780 uses essentially monochromator to spread all fluorescence across 34 detectors for multi-spectral acquisition. It is used to detect autofluorescence, unmix closely positioned emission spectra (unmix GFP and YFP for example) and to measure precise spectral peaks with ~1nm resolution.
Monochromator is useful when you need to transform frequency domain information into spatial domain. In fluorescence microscopy we usually collect light from wide bands of well-separated GFP-like proteins, so that filters make more sense. We usually don't detect 1-nm wide lines or plot spectra. LSM780 does allow all that, if you need to.
You can use spectral imaging, but for that you will have to either scan for very long time, or spread signal onto array of detectors.

I'll add that signal is usually limiting in biological fluorescence microscopy, so it can be impractical or impossible to get good data in narrow wavelength bands. As a result most people use filters. And in turn this creates strong market pressure to design new fluorescent probes to match the spectra of existing probes and filters.

@TSwayne I think it is funnier: GFP and other proteins and dyes are/were designed to match laser lines (e.g. 488nm argon line).


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Do Asian women have more difficult births than Europeans?
I recently heard a claim that Asians in general have more difficult births than Europeans. Is this true?
I have found a few studies(1,2) on the effect of ethnicity on birth outcomes but they seem to be limited to a small geographic area or focus on aspects such as risk of premature birth, neonatal and/or maternal mortality, etc. Those are of course important facts, but I am more interested in whether an otherwise normal birth is likely to be longer and/or be perceived as more difficult by this specific ethnic group, on basis of their ethnicity alone.
I found a few articles dealing with possible effects of specific genes on duration of labor. Debiec et al. (3) write that

Asian women had slower active labor than other ethnicities (P < 0.01). Asian women also reported less pain during their labor compared to all other patients (P < 0.001). Slower labor progress was associated with less rapid progression of pain, but this did not obviate the effect of Asian ethnicity on pain.

According to Reitman et al.(4,5) the genotype CC at the SNP Rs1042714(9), which is more prevalent in ethnic Asians, is associated with longer duration of first-stage labor. Polymorphisms in the oxytocin receptor (OXTR) gene have also been tied to variations in labor progress (6,8), but I haven't found data on the prevalence of these polymorphisms in Asian populations.
Greenberg et al. (7) write that "Nulliparous Asian women had a significantly longer second stage and higher rates of prolonged second stage". However, after controlling for confounding variables the actual increase in mean second-stage duration compared to white women was only  5.2 and 5.9 minutes for nulliparous Asian women with and without epidural analgesia, respectively. They also write that

When the rates of second stage of >3 hours were analyzed by epidural subgroups in the multivariate analysis, black women with epidural analgesia had lower rates than white women, and Asian women with epidural analgesia had higher rates than white women, regardless of parity, although no differences were demonstrated among women without epidural analgesia.

Considering the above sources and any other that may exist, is it reasonable to state that Asian women in general have more difficult births than white/European women?

Pure speculation: could this be related to the fact that Asian women tend to be smaller than Caucasians and would therefore have thinner hips which might make giving birth harder? Also, you might want to define "difficult labor", the first study you cite claims that Asian women had less pain, despite longer labor.

I think that was mentioned in one of the articles. How to define "difficult labor" is definitely an issue. I'd think that maybe there's some official objective or self-reported measure that's used in research?

There probably is but I have no idea. Still, less pain seems like easier labor to me. But then, I am neither an MD nor a woman, let alone a mother, so what do I know.


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What is the main challenge in creating a chemical male contraceptive?
More than 50 years after hormonal contraception for women was invented, a contraceptive pill for males is still not available. With the obvious major biological differences in mind, why does it appear more difficult to create a chemical contraceptive for males? What are the main challenges that must be overcome to create a viable, reliable and marketable contraceptive pill for men?

You could try to target the production of semen. The problem here is that this needs to be reversible, otherwise you couldn't reproduce afterwards any more. In that way it is easier with women since you can trick the body into "believing" that it is already pregnant. This is something that obviously doesn't work in men :-)

see: http://www.newmalecontraception.org/nonhormonal-pills/  As a market, I think men have a tendency not to want to take chemicals contraceptives...

I'm not so sure about that. A study in Australia found that 75 % of the men asked would consider trying a hormonal contraceptive. https://www.mja.com.au/journal/2002/176/5/will-australian-men-use-male-hormonal-contraception-survey-postpartum-population

See also http://www.medscape.com/viewarticle/775627_7

@shigeta neither men nor women have any desire to take chemical contraceptives. I don't see why that would be truer for men than for women. The only difference is that women are expected to while men aren't.

While you may be right after some period of adjustment that male contraception may be adopted, there is the fact that men are not left carrying the baby, a fact of which some biology does take note of.  Men often complain about condoms for instance. If you look at the link I sent above there are reversable (nonchemical) male contraception available. If you ask 20 of your male friends how many of them have adopted?  Attitude reports like the ones you all link are not absolutely proof of your point, btw.

@chris some antipsychotic medications have shown significant attenuation of seamen volume

Well a nice hot bath really reduces sperm count... A couple of reasons you don't see male chemical contraceptives is that the female ones are very effective and fairly safe. Condoms are effective and protect against disease. Because of all this the drug companies probably think there would not be much demand. No demand, no recuperation of the high cost of R&D, clinical trials, licensing, marketing and production.

I recall some touring academics claiming that injected testosterone works as a male contraceptive. That has a few drawbacks, the major one being: are you seriously expecting men to do something? Also, related to your question, one can't take yet testosterone by mouth.

I am going to summarize a few reasons for both why contraception is "easier" for women, and for why it is "harder" for men. They are both biological and sociological.
Easier for women
The female cycle is more complicated
The female cycle leading to ovulation is regulated by several hormones that interact. As such, it is easier to disturb.

The system is so sensitive that even the slightest alteration in any of these factors can disrupt its fluidity and lead to anovulation

(Anovulation = a cycle where no ovulation occurs) Source: Anovulation: Background, Pathophysiology, Epidemiology
Even in young women, this occurs naturally.

Estimates of chronic anovulation rates range from 6-15% of women during the reproductive years

Female bodies l already have a "built-in mechanism for contraception
As ovulation needs to be suppressed during pregnancy, there is already a mechanism in place by which this can happen.
Women are more affected by pregnancy
Since women are more affected by pregnancy and childbirth, the risk they feel they have when they don't use contraception or use it incorrectly is larger.
Contraceptives for women have more than one use

More than half of pill users, 58%, rely on the method at least in part for purposes other than pregnancy prevention. Thirty-one percent use it for cramps or menstrual pain, 28% for menstrual regulation, 14% for acne, 4% for endometriosis, and 11% for other unspecified reasons.

Beyond Birth Control: The Overlooked Benefits of Oral Contraceptive Pills
Harder in men
It only takes one
While the saying "it only takes one sperm"  is probably an exaggeration, it carries a certain truth - you really need to shut down the production of sperm or the risk of a pregnancy is too high. Both the pill and the various IUD options have set a high bar for what's considered an acceptable risk.
Side effects and effectiveness
While hormonal contraception for women already has a multitude of side effects, often unrelated to the reproductive system, this is certainly not easier in men. The most prohibiting side effect encountered so far is impotence - not much use in taking birth control to have sex without risk of pregnancy when doing so leads to no sex at all.

Progestins have been used in multiple small studies of men for suppression of spermatogenesis and testosterone production. Progestins used alone result in significant side effects such as loss of libido and erectile dysfunction.

Update on Male Hormonal Contraception: Is the Vasectomy in Jeopardy?
(Decreased libido is also a side effect in female hormonal contraception, though. The reasons why it's seen as more acceptable there are probably sociological)
That review is a good overview on what has been tried until 2010. Many solutions failed because of side effects or because they didn't work well enough.
On testosterone:

Of note, this international study revealed that 91% of Asian and 60% of Caucasian patients became azoospermic, suggesting an ethnic difference in endocrine response

Testosterone proved to be rather good in other doses and combinations, but is not that easy to handle because it requires injections and can't be taken orally.

Testosterone alone has side effects, including acne and oily skin, mood changes, increased hemoglobin and hematocrit, weight gain, decrease in testicular volume, sleep apnea, gynecomastia and possible effects on cholesterol. There are no long-term data with testosterone use and normal men regarding prostate symptoms, growth or cancer. In an era of fear of using medications on relatively healthy individuals, acceptability of routine use may be a major concern, given recent data on medical treatment of menopause with estrogen/progestin therapy. In addition, anabolic steroids are a controlled substance and regulation of this industry is very strict at this time. Abuse of these drugs could easily become prevalent with its widespread use and availability for contraception.

On cryproterone acetate:

Doses ranging from 25 to 100 mg per day have suppressed spermatogenesis, but side effects have precluded subsequent studies.

And so on...
The market factor
A side effect of the contraceptive options for women being so well-accepted, women often feeling responsible for contraception and also using hormonal contraception anyway, for reasons unrelated to pregnancy, is that the market for male contraception is not that easy and pharmaceutical companies have been pulling away from it. Especially in light of the research difficulties.

Although Bayer, Wyeth and Organon were once active in research and development of a male method, all three discontinued their programs between 2005 and 2008 although the industry continues to actively pursue programs for hormonal contraception and hormonal-replacement therapy for women. In withdrawing support, company representatives cited corporate changes in direction and the perception that safety standards demanded by regulatory bodies would require such extensive evidence as to make further research financially infeasible

Current challenges in male contraceptive research
This is not to say that there really is no market. As you mentioned in the comments, at least in questionnaires, many men say they would use male hormonal contraception and many women say they would like their partners to use it. See, for example, Market size for male contraception (plus the following pages of that paper)
But you asked about the challenges ;-)
I think it's also interesting to note that the search for hormonal contraception started for both men and women. It's just that the "solution" was found for women first and then got popular really fast.


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What are typical values for bone mass in humans?
I wonder what are typical bone mass values for adult males and females? And do they change significantly with workout and diet?

I wonder what are typical bone mass values for adult males and females?

This seems hard to find. The only value I could find is on Bionumbers at it says that vertebrates compact bones have a mean density of 2 mg/cm$^3$ [1]. However in medical practice two scores are used to indicate the ratio between tested bone density and ideal bone density [2, 3] and absolute values are uncommon.

And do they change significantly with workout and diet?

Bone mass is mainly influenced by genetic factors. Only up to 25 % may be influenced by environmental factors such as diet and exercise [4].
Among the medical conditions that influence bone mass, osteoporosis is the most frequent especially in women. Other conditions are: hyperparathyroidism, glucocorticoid therapy, other bone abnormalities and fractures [2].

References:

Brian Cotterell, Fracture and Life, Imperial College Press, 2010 p.77 bottom paragraph via http://bionumbers.hms.harvard.edu//bionumber.aspx?id=108642&ver=2
Bone density. (2014, September 15). In Wikipedia, The Free Encyclopedia. Retrieved 17:08, September 29, 2014, from http://en.wikipedia.org/w/index.php?title=Bone_density&oldid=625737182
http://www.niams.nih.gov/Health_Info/Bone/Bone_Health/bone_mass_measure.asp
http://www.niams.nih.gov/Health_Info/Bone/Osteoporosis/bone_mass.asp

it is really hard to find absolute values. maybe because it is hard to estimate, or maybe just because total mass is irrelevant for medical interest. my motivation was actually a bit off-topic, I wanted to know if my body composition estimator scale gives reasonable values.


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Physiology of benign eye twitching?
About four times in my life I have experienced the feeling of my eyelid fluttering for a few minutes by itself, and then it stops.
I have talked to other people who have had the same experience so I presume there is no pathology.
Could someone please explain the physiology behind these random eye twiching experiences that I and many others have had?

Could the down-voter please comment on how the question can be improved?


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How does chromosome cross-over occur?
I have heard that during meiosis, homologous chromosomes from each parent "cross-over", which enables the off-spring to inherit some alleles from the mother and some alleles from the father.  The picture below illustrates this "cross-over", but of course this must occur at multiple sites, rather than just the one shown in the picture.

Now my question is what causes the chromosomes to align perfectly during cross-over so that the loci of a particular gene will substitute for the corresponding loci on the homologous chromosome, as opposed to being substituted with a completely random locus?  Does each gene have a unique non coding sequence before it specifying what gene it is to enable this process to occur?

You might enjoy reading  the section on crossing over from Bruce Alberts' The Cell. I love that book as it has answers to many beautiful questions that may arise regarding cell biology.

Quite simply, because chromosome pairing is sequence specific. Holliday Junctions, which are the functional structures of a cross-over, occur through a process called "strand invasion," during which a region of one chromosome physically base-pairs with that of another.  Thus one locus cannot pair with a random locus, as there is generally insufficient sequence complimentarity between two random regions to form a functional Holliday Junction.  One interesting consequence of this mechanism is gene duplication and deletion in repetitious regions of the chromosome.  For example, genes with large repeated regions, such as the gene responsible for Huntington's disease, can expand and contract during homologous recombination due to strand invasion occurring at non-equivalent, but still homologous, sites.  Wikipedia does a nice job going over homologous recombination.  I also recommend looking over the relevant sections in Molecular Biology of the Cell, available on the PubMed Bookshelf.

Most of the time sequence differences between alleles are quite small.  Two genes with large changes between them are not alleles, they're homologs.  Alleles tend to have one or a few Single Nucleotide Polymorphisms (SNPs) that distinguish them.  For example, the gene that causes sickle cell anemia, differs from the wild type allele by only a single base change. http://www.nature.com/scitable/topicpage/genetic-mutation-441.  These very small changes are irrelevant in the context of a 10 Kb cross over.


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How does anxiety cause chest pain?
An acute instance of anxiety can cause a sudden sharp chest pain for a very brief period of time.  What is the mechanism behind anxiety leading to chest pain?
Is the pain coming from the heart itself, or surrounding muscles?  What structure is in pain and what is the physiology behind it?

you mean pain similar to a heart attack?

I would also notice that I think that this pain you're talking about is related to the more well-known feeling of heaviness in the chest in the period of depression. Maybe this is the same thing. Or maybe not.. however, I would like to know.


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Do adjacent axons in a nerve influence each other?
Suppose I have a nerve fiber consisting of several axons all running in parallel to each other.  When an action potential is generated in a certain axon, this will alter the concentration of sodium and potassium ions inside the axon, and in the extracellular fluid around that axon.
The question is, will this change in ion concentration in the extracellular fluid, alter the threshold potential of an adjacent axon, which shares the same extracellular fluid?

Yes, activity in other cells can affect the surrounding electric field and thereby influence the behavior of nearby neurons. This phenomenon, known as ephatic coupling, can be important but is usually small.
For many cases, it is likely too small to be of physiological importance. Note that individual action potentials are quite transient and, especially in myelinated axons, the resulting currents are local and small. Therefore it's unlikely that a single neuron's activity will have a noticeable effect on nearby neurons.
However, in unmyelinated axon tracts and/or when a larger group of neurons is active, ephatic coupling is more likely. In particular, it seems to play a role in synchronizing cell populations during oscillations. For example, Anastassiou et al (2011) found that firing of cortical neurons could be entrained by the extracellular field and affected the intracellular membrane potential by about 0.5 mV.
Anastassiou, C.A., Perin, R., Markram, H., Koch, C., 2011. Ephaptic coupling of cortical neurons. Nature Neuroscience 14, 217–223.
Also, for reference:
Jefferys, J.G., 1995. Nonsynaptic modulation of neuronal activity in the brain: electric currents and extracellular ions. Physiol Rev 75, 689–723.
Buzsáki, G., Anastassiou, C.A., Koch, C., 2012. The origin of extracellular fields and currents — EEG, ECoG, LFP and spikes. Nature Reviews Neuroscience 13, 407–420. (see pages 411-412)

Edit:
For your particular case, action potential propagation in one axon is very unlikely to affect the other axons in any relevant way in a tract of myelinated axons. This is especially true because the initiation of action potentials does not occur along the axon itself, but where the axon is just branching from the cell body (the axon initial segment). Threshold is important at the initiation site, but is not really relevant in the tract itself, where the axon is just conducting the signal it receives from the initiation site.


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Why does weight loss lower blood pressure?
I have read that weight loss is an effective lifestyle modification for people with hypertension, and systolic pressure may be reduced by up to 1-2 mmHg for every 1kg of weight lost.
What is the physiological reason for weight loss reducing blood pressure or weight gain increasing it?  Please provide a physiologically detailed response rather than simply saying that more weight means the body must work harder to pump blood.  I understand this but I want to know the mechanisms of how the body detects the increased weight and adjusts the blood pressure accordingly.  Thanks!

As someone in the health-care field, it's great to see someone who wants to know more than the surface of things. I would like to answer this question, but I don't want to repeat stuff that you already know. What did you find out when you researched this? Thanks.

Weight gain increases blood pressure, the reason for this process is due to the effect of hormone called Leptin.

Leptin is made by fat and circulates in the bloodstream to reach the brain, where it acts as a signal for energy reserves, adjusting both energy expenditure and the sensation of hunger – hence it is sometimes referred to as the ‘satiety hormone’.
The group showed that some obese people who were lacking the hormone leptin because of a genetic disorder had low blood pressure despite being very heavy. This was also the case for people lacking the gene for the leptin receptor in the brain, meaning that the brain was unable to respond to the hormone.
Reference

The team lead by Professor Michael Cowley, Monash University, Australia, in collaboration with Professor Sadaf Farooqi, from the University of Cambridge, UK suggests that the leptin signalling is necessary for obesity-induced increased blood pressure. The clinical studies in severely obese humans showed that these observations are relevant to humans.

Professor Cowley said: “High blood pressure is a well-known consequence of obesity. Our study explains the mechanism behind this link, showing that leptin, a hormone secreted by fat, increases blood pressure.”
Professor Farooqi, from the Wellcome Trust-Medical Research Council Institute of Metabolic Science added: “We now know that leptin regulates both our weight and our blood pressure through its action on the brain. Targeting this action could offer a useful way of helping people fight obesity and associated problems such as high blood pressure and heart disease.”
Reference

It is thought that Leptin's only task is to activate the sympathetic nervous system connected to the brown fat and there by directly burns energy. But it is also behind the activation of sympathetic nervous system of heart and kidney, thereby increase the blood pressure.

Genetic and drug experiments in mice, they have pinpointed an area in the mouse brain that increases blood pressure when it is exposed to high leptin levels.
This region is called the dorsomedial hypothalamus, and is thought to be involved in controlling energy consumption. Their findings show that high levels in leptin do indeed boost blood pressure, via this brain region.

Reference
http://ndt.oxfordjournals.org/content/15/8/1115.full.pdf+html


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Which organism is this?
Place: Bangalore, India
Month: September, 2015
Current weather: Cloudy and rainy
Google images search was just giving me dragonfly photos. That organism is on grass blade.

Image is captured by me.

Certainly not a dragonfly. This looks like a grasshopper but I can't tell the species.

I doubt it is grasshopper. Few of my friends suggested it is some kind of grass insect which uses it's wing to camouflage.

This is an insect in the order Neuroptera, definitely neither a dragonfly (order Odonata) nor a grasshopper (Order Orthoptera).  The name of that order means "nerve-wing", which referes to the intricate network of veins throughout the wings, which have a very different appearance and pattern than the wings of either dragonflies or grasshoppers.  I'm not familiar with Indian fauna per se, but the long antennae with slightly curved/hooked tips make it look more like an antlion (family Myrmeleontidae within the Neuroptera) than an owlfly (family Ascalaphidae within the Neuroptera; their antennae have small clubs at the ends), though it's a bit hard to tell from the photo.

I also think that an antlion is likely. Either way, the front legs and antenna seems to be directed forward along the leaf/overlaid, which makes the antenna look a bit weird.


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When is an ant colony at its loudest?
I want to make a sound recording of an ant colony located in a wood pile in a German forest (I don’t know the exact species).
To optimise this, I would like to select a time for this when the ant colony is at the height of its activity, i.e., loudest.
My naïve guess would be that noon in summer with some time after the last rainfall is best, but I could find anything to confirm or go beyond this.
Thus I am asking: When is an ant colony loudest, more specifically:

What time of the year?
What time of the day?
What weather conditions?

I believe you speak of some species of Formica spp., such as Formica polyctena (nest example)
You should mind that (i) ants are not particularly noisy insects; (ii) ant nests are 3-dimensional structures within which ants are heterogeneously distributed. So considering a microphone somewhere on the nest where you happened to see more ants, mostly you will be picking up noises from foragers stumbling into debris while moving around. And that only when that region of the nest happens to be most active, which was your original concern. In case I am wrong and you're interested in some smaller ant species (e.g. Solenopsis fugax or Lasius flavus) then you will probably record few if any significant sounds resulting from ants' activities.
Thus my first advice if you're focusing on foragers moving around the nest surface is that you record them in the afternoon of your hottest days, particularly if they're refurbishing their nest or upon disturbance. If you leave the microphone for extended periods try to find out where most foragers are coming out from (and pray they'll not damage the equipment) and leave it there in the afternoon of a dry, hot day.
Now, I am not sure about your ultimate goal, but in case you want to actually hear the ants instead of their stumbling around, then you should focus on having a tiny (protected) microphone inserted into a nest chamber. It is hard to say when the insides of a nest of unknown species will be particularly active, but usually during a fair day, under the sunlight exposure following a wet night. Finding the best region to record ants stridulating inside their nest will depend on finding the best nest location(s) and equipment.
Good luck!

Thank you for your answer. The ant colony in question is actually surprisingly loud, probably due to being above the ground, its size, and its domicile acting like a sounding box. I can still hear it from eight metres distance. This is what inspired me to attempt this in the first place.

Still this is probably their bodies moving about the vegetation, dried leaves, etc, right? If that's the sound you want (i.e. not their true sound communication) and it is so loud, then leave nearby the most busy exit at these times suggested. But I do not know too much about Germany, all the more without knowing species.

Yes, I want to capture the general sounds produced through moving, etc., not communication sounds.

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


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What type of mutation causes Progeria?
I'm doing my High School biology final on Progeria, and am wondering what type of mutation causes this disease.
I know that the LMNA gene codes for the "prelamin A" protein, and that protein contains a farnesyl group that is then not able to be removed (in the case of Progeria). The abnormal form (with the farnesyl still attached) of prelamin A is then called progerin, and attaches to the nuclear rim resulting in an abnormally formed cell nucleus, making mitosis impossible.
Is this a structural mutation? What sort of mutation is this?
Thanks in advance.

Hutchinson–Gilford progeria syndrome is almost always due to to a de novo mutation (i.e. not an inherited mutation) in the lamin A gene (LMNA). The mutation responsible is a C-to-T substitution at position 1824. Remarkably this doesn't change the encoded amino acid but rather creates a new splice donor site in the RNA transcript. When this splice site is used it results in the deletion of information corresponding to about 50 amino acids internal to the protein and near to the C terminus.
During biogenesis of normal lamin A a C-terminal -CAAX motif is recognised as a signal for isoprenylation, in this case farnesylation. The added lipid group acts as a C-terminal membrane anchor. However this anchor is subsequently removed when the protein is proteolytically cleaved near the C-terminus, removing 15 amino acids including the C-terminal cysteine (by this point the three C-terminal residues have been trimmed away). The cleavage site for this final modification is missing in HGPS lamin A so the farnesyl group cannot be removed. The accumulation of unprocessed lamin A causes the observed defects in the nuclear membrane.
Eriksson et al. (2003) Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome. Nature 423: 293-298
Capell et al. (2005) Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome. Proc. Natl. Acad. Sci. USA 102: 12879-12884


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Why does DNA mutate?
I just read that pregnancy in space would be super dangerous because - among other reasons - of a higher risk of mutations due to radiation. This made me wonder: why does the DNA in organisms mutate? What are the main natural reasons? Is this due to the construction of DNA and would happen even in "perfect" conditions or is it due to something that is in the environment, like radiation?
So far I got two answers on reddit and also asked this question to a doctor and what I heard is along the lines of "this is how it is". I heard about "cells being worn out". But what makes the process non-deterministic, probabilistic? I guess I don't know enough about biochemistry to formulate the question, but I guess it's related to "given certain conditions, what determines at which point (and what kind of) a mutation occurs?"

I got something that is probably at least a partial answer: "peroxides, wrong pH, nanoparticles that can go through cell membranes".

If I am not mistaken, the vast majority of mutations happen during DNA replication.
DNA must replicate itself so that cells can replicate itself. The DNA polymerase is one very important protein that replicates DNA. The human genome (to consider this example) is 3.5 billions nucleotides long. Just to realize how long is 3.5 billions letters, let's make a book analogy.
Book analogy

In the Harry Potter series, there are about one million words (ref).
In the LOTR series, there are about one 400 thousands words (ref).
In the Chronicles of Narnia series, there are about 230 thousands words (ref)
In the King James Bible, there are about 788 thousands words (ref)

This sums to about 2.4 millions words. As, in english, there are 5.1 letters on average per word (ref), this lead to a total of about 12.3 millions letters. Imagine you have to rewrite all of these books almost 300 times (12.3 millions * 300 ≈ 3.5 billions)! How many typos would you make?
There are several cell divisions between a zygote and the ovule/spermatozoid produced by this individual but as most mutations happen during meiosis, I will just ignore mitotic mutations. The DNA polymerase makes about one typo every 100 millions nucleotides (Kong et al. 2012; Rahbari et al. 2016)! So really, the DNA polymerase is doing a pretty good job!
What is causing mutations?
Shit happens
I am hoping that form the above analogy, you may have a sense that mutations are just small mistakes. They happen because the replicating machinery is not perfect. Sometimes a molecule comes sideway, does not bind very well and another molecular passing by sticks to the DNA, etc.. Errors happen just like you would be making a lot of typos, rewriting books.
Mutagens
There are of course factors that can affect this mutation rate. Physical, chemical and biological agents increasing the mutation rate are called mutagens and they include radiation decay, ultraviolet radiation, ROS, benzene as well as some viruses and some parasitic bacteria.
Variation along the genome
Note also that the mutation vary along the genome too. Regions with high repeats (e.g. AATAATAATAATAATAATAATAAT) such as microsatellites for example tend to have a much higher mutation rate.
Variation among species and Drake's rule
Mutation rate also vary among species. There is a general tendency that the per nucleotide mutation rate negatively covary with the genome size, a phenomenon called Drake's rule (see for example Bradwell et al. 2013 or one of the early Drake's paper).

Short answer, Chemistry runs off probability, and life and DNA replication are in the end chemical reactions.
DNA is a chemical, and the bonds between different nucleotides sequences are all extremely similar, if there was not an opposing strand, mutations would be extremely common becasue any sequence is essentially equally energetically favorable,(AKA equally likely probabilistically/chemically). Having two joined strands means you cant just swap nucleotides becasue they can't bond across strands equally well, there is a heavy chemical bias for only bonding with the opposing partner. A=T C=GT. Any other bond is less energetically favorable ( AKA less likely, which is not the same thing as impossible). The dual strand nature of DNA makes errors less likely but we are still talking chemistry and no chemical process is absolutely perfect, even if you burn carbon and oxygen in perfect ratios to get CO2 you will still get CO, carbon monoxide, just do to the physical (and thus probabilistic) nature of chemical reactions. Even the strength of the bond between the two stands can work against it as f a mutation does slip in the DNA will still hold together, and if it gets replicated before an error correcting mechanism catches it it will stick around. The kicker is although a DNA is very unlikely to mutate, there is a lot of it so even the extremely unlikely still occurs, DNA also has to be split apart to be replicated, during which mutations are far less energetically unfavorable.
Cells actually have dozens of error checking mechanisms and chemical stabilizers to limit how many of these can get through or occur however again this is a physical chemical process, thus it will not be perfect. Even without these mechanisms DNA replications is still fairly reliable, but many organisms have gigantic genomes meaning even reliable as a swiss watch is still not good enough. It is simply impossible to create a perfect copying mechanism that has high turnover that operates in the real world there are just to many interactions. the fact many replications are happening at once does not help since sometimes these many disjointed strands can end up bonding together causing the error correcting mechanisms to cut out entire sections, or mix them up trying to fix it.

Mutations occur due to sudden and unpredictable changes in the structure of DNA. Radiations, particularly those of energies of ultraviolet and higher are capable of breaking the bonds that make up DNA. This fragments the DNA. While DNA has mechanisms to counter this, and reform as a complete strand, it’s not perfect and the original DNA might not be made. Oftentimes, a small error such as base pair swaps or a missing pair could occur. These changes are reflected as mutations.

As ultraviolet radiation forms thymine diamers due to free radical addition reactions, this is one of the environmentatally caused damage to DNA. There are various mutagens which do the same. Since DNA is a chemical molecule the fate of any chemical molecule is the tendency to undergo changes, even during normal conditions chemical reactions occur. Take for example the transformation caused by deamination of cytosine residues which changes it into uracil or deamination of adenine to form hypoxanthine. Another important reaction is hydrolysis of glycosyl bonds between sugar and nucleotides creating a DNA lesion more commonly called depurination. 10000 purines are estimated to be lost in 24 hrs in mammalian cells increasing concentration of acids by any random mechanism might also accelerate the depurination process. So DNA like any chemical material is subjected to changes though there are processes to check this process still it happens. Moreover during replication there are practical chances of error in spite of various check points. Depending upon the chemistry of the reaction DNA is undergoing at which point a mutation would occur might be studied, numerous biochemical process takes place simultaneously further complicates the precise location where a mutation might take place.


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Can plants get cancer?
I can't think of any reason why plants wouldn't be able to get cancer, but I've never heard of a plant growing a tumor. I've also never seen a plant with a noticeable abnormal growth. Can plants get cancer?

This is touched upon in this answer

This is a similar post.

Yes, plants of all sizes can have cancerous growths.
Agrobacterium tumifaciens, the causative agent of crown gall disease, produces what is called a tumor. See this link for detailed information on these growths. Alternatively, use a plant physiology textbook to look up the above terms. (Here, is where a textbook is better than a single abstract in PubMed.)
I am certain that you have seen such growths on trees, such as this. Other smaller versions can occur on smaller plants - on stems and leaves, for example. The plant builds up tissue around the A. tumifaciens infection in an effort to isolate and contain the infection and its effects.

Are there any examples of cancerous growths without infection, however?

the link is dead.

incidentally, a tumor is just a growth, or even, classically, a swelling (as in calor, dolor, rubor, tumor) . Tumors are not necessarily cancer.

Burls/Burrs are often defined as tree tumours, and as analogous to cancer in animals. There seems to be numerous reasons why burls are formed (more research is needed on the topic), which include wounds, insects, fungi, DNA changes, environmental stress and viruses. However, burls are localized and often relatively benign, and since plant cells do not move around they cannot metastasize (see e.g. "Can Plants Get Cancer?" from the New York Times). Since burls have multipe causes the 'Cancer/tumour' label might not fit very well to all types of burls, and in some cases normal shoots can sprout from burls that have been removed from the tree (indicating that the burl was not caused by damaged DNA).
Galls are related tumorous growths that are usually caused by parasites (insects, virus, bacteria, fungi), and are often induced by plant hormones (at least from insects/mites, see Insect and mite galls). However, in the case of crown gall caused by the bacteria Agrobacterium tumifaciens the tumorous growth is due to a DNA transfer, which will permanently modify the infected cells (Gheysen et al 1987).
As you can see, the answer to your question depends on if you are interested in tumorous growths in general (where many types of burls and galls should qualify) or cancer in particular (if defined as unregulated cell growth caused by permanent DNA damage).

Could not fit in a comment. The following is purely intuitive, I have not much knowledge in this field and no reference. I am just guessing and I'd welcome some corrections. I was thinking about three points which effect opposite each other.
1) In plants, there are no cells specialized in transporting stuff throughout the body (I think!) while there are many cells that travels a lot in animals. Therefore, I0d guess that plants cancer are much more likely to only remain localized while animal cancer are more likely to create metastasis. As a consequence, I'd expect that cancer would be more lethal in animals than plants.
2) The number of mitosis occurring in the lifetime of an individual is probably positively correlated with the occurrence of cancers. Because plants tend to be bigger than animals, I would expect more mitosis in plants and therefore, I would expect that cancer are more common in plants than in animals.
3) According to life history theory, the intensity of selection on a gene decreases as the ratio of the fitness pre- and post- expression of the gene. Because plants never really age and stop reproducing, I would expect that selection against cancer would be stronger in plants than in animals resulting in a less cancer in plants than in animals.


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Why are the largest land/air animals today smaller than in the Mesozoic?
The largest dinosaurs and pterosaurs seem to have been much larger than the largest animal terrestrial/avian species since. Was the Mesozoic somehow more hospitable to large animal species than today's world? Have subsequent evolutionary innovations shifted the balance towards smaller species?
Interestingly the still-existing blue whale seems to be the largest animal ever.

Closely related/maybe partial duplicate of What are the atmospheric requirements for large dinosaurs? and What was the reason for some plant and animals to become giant in course of evolution?

Although the specified question is not an exact duplicate, this answer pretty much covers my question.


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When did death due to aging first appear?
As I understand it, single-celled organisms that reproduce via mitosis essentially live forever. When a cell divides, one cannot say that either one of the new cells "is" the parent and the other the child, neither is older than the other, and we might say that the original cell is still alive as long as either of the cells resulting from the division is. With humans the pictures is very different, of course: we have no trouble telling parents and children apart and no one lives longer than about 120-something years.
When in evolutionary history did organisms stop living forever? Was it with the advent of multicellular life with differentiated cells? Sexual reproduction?

This is a similar question where the asker is confused about the difference between aging in yeast and in multicellular organisms. The comments back and forth got out of hand.

Whilst both a single-cellular and a multicellular both appear to age, this is only a rhetorical similarity. You are defining single-cellular organisms as immortal because the lineage doesn't die; this process occurs for the cells in multi-cellular organisms (we are all directly related to the ancestral cell -the lineage of cells is immortal) but the organism dies. I'm voting to close this question because it's unclear what you're asking given that there has never been an instance where an organism was immortal that mortal creatures evolved from (except that one damn jellyfish).

For the record, this is a good question in the sense that it highlights a common and easy to misunderstanding use of terminology since the media band around "immortal cells" a lot. However the SE Q&A isn't a good forum for ironing out the misunderstanding without a very specific question.

I think both @Roland and James are telling me that when a cell divides, we should consider the two resulting cells to have age zero rather than age equal to that of the original cell. Under this definition the question is, at best, poorly phrased. I suppose one way we might think about the daughter cells' age is by considering whether they inherit any age-related wear and tear from their parent.

(Not an evolutionary biologist, but I couldn't resist :)
I don't think your premise is correct. In (symmetric) cell division, we should consider that the old cell "disappears" and two new cells appear; neither of the two daughter cells is the parent cell, they are both descendants of it (hence the term "daughter cells"). The parent cell is gone. Therefore, at least for symmetric cell division, the lifetime of a cell equals the length of a cell cycle. So cells are not immortal --- only the cell lineage is.
Asymmetric cell division (as in stem cell division, not budding) is more tricky. Here it might seem as if there really is an immortal cell (the "stem cell") generating "mortal" offspring. But I think the situation is really the same as in symmetric cell division: most of the cell cycle mechanisms are identical, and again two new daughter cells are generated, and the parent cells disappears. The asymmetric part is that only one of the two daughter cells are "permitted" to continue the line. Again, the cell line is immortal, the cell is not.
But this is still true in higher organisms: the germline is an immortal line, while the somatic cells are not. So the key difference between higher organisms that have a clear life span and unicellular organisms is the appearance of cells that do not generate offspring, but instead support the cells that do.
I'm not sure there is a sharp transition from single cells to the germline/somatic cell situation. Intermediate cases are found in all sorts of single-celled organisms where certain cells "decide" that it's better to support their (genetically identical) neighbor in some way to rather than divide themselves; these are a form of "somatic" cells. All sorts of community behavior in bacteria and other microorganisms could be viewed in this way. During evolution this behavior has gradually got encoded into the DNA itself, with more and more sophisticated "support systems". Higher animals are really just the latest version of this, where the entire body is really just a support system to ensure survival of the germline.
I would suggest reading Richard Dawkin's books on this subject, especially The selfish gene. They are well written and quite accessible.

I too am not a specialist, but The Selfish Gene is pretty old fashioned and outdated often being referred to as one of the "blunders of biology". Eo Wilson who was amongst the developers of that theory and many others are outspoken on the issue of the "the selfish gene" mistake.

@James Say what? Who refers to The Selfish Gene as a blunder? Creationists?

@Alex I thought this was old news no? There is a large movement of evolutionary biologists, and I'm sure even Dawkins has different views based on new observations. ...also, for different reasons, creationists! From io9 article "To be clear, biologists like West-Eberhard and others are not saying genes and their selfishness aren't important. But they are merely one part of a much larger and more complicated mechanism, which involves inputs from the environment which affect how genes express themselves."

... From the mouth of the horse: https://twitter.com/RichardDawkins/status/408142568468119552?ref_src=twsrc%5Etfw I have read the book cover to cover and there are indeed holes and examples that contradict the model. Paper from the journal of physiology expands on this more than I can!

@James That a model does not explain every single part of reality does not at all invalidate it. I've read the book cover to cover as well, and it's a fantastic book for anyone wanting to learn the core concepts of evolution, even disregarding the selfish gene theory. If you want to call it outdated, a blunder and a mistake, be aware of many bs-filters engaging.

@Alex I used these words because that's what it has been described as by others who are paying closer attention than me. It's a fun book that did exceptionally well, but there is so much we have learned since then. 40 years in genetics is a long time! I wouldn't recommend it as a place to start learning about evolution. Just because it's written by Dawkins does not excuse it from scepticism. Furthermore, being sceptical of Dawkins et al 40 year old model does not make me a bs religious nutter, which could possibly be an accusation inferred from your previous comments :/

Well, regardless of controversy about how "selfish" genes may be, I think Dawkin's book presents the basic concepts in a good way, and in particular explains what "immortality" means in the context of this question. But please feel free to add a more recent reference!


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Physiology of skin and leather: why do salt borders occur?
I discussed a leather store about the white border aka salt border on leather shoes. They said that it is due to inner features of leather and you could try to add some fat/cream to push it back inside the shoes. I haven't yet understood physiology of skin here, "why does it act like that?" is the first doubt and then the second "does human skin act the same way?" -- I can see this kind of salt borders in gym clothes when they cry uncleaned but haven't seen them yet on my skin at least. The extra salty water from legs causes real damage, such as getting the inner fluids out, to the leather. When you do heavy training, the salty sweat in the human skin acts apparently the same way. So:

how to manage the skin in living human skin and how does it differ from leather maintenance? What is the common physiological background with the different kinds of skins?

I try to answer it myself:

leather: you can add the fat/cream/etc only externally
living human ski: you can add the fat/cream-etc both internally (fatty food) and externally (lotions)

The two processes are quite different: On leather shoes no active transport takes place. The salt either comes with the snow (most likely most of it) when the streets get salted to avoid ice. Your shoe soaks up the salt-water mixture and when the water dries up, the salt stays behind. The other possibility (more for new leather shoes) is that water goes into the leather and dissolves salts, which remain from the tanning process of the leather. With older shoes I have never observed this "snow marks" in the summer when the shoes got wet in rain.
Using a wet cloth removes the salt, subsequent treatment of the shoe prevents that water can enter the leather.
The skin is quite different: Here we have living cells and an active transport of water through pores when you body get warm. This is to cool you and prevent overheating and since the body fluids contain salt, so does sweat.

Why is salt used in taining process? To kill bacteria? To force other ions out or some other reason?

Its needed to preserve the leather. Salts are remnants of the process.

Salt is used in many points of tanning such as curing, liming and pickling (Wikipedia). So yes the salt coming from leather seems to be totally different thing to the salt coming from the living organism. So the leather maintenance only requires some fats to keep it nice, not salt additions? Then again an athletic person requires all kind of inputs such as salt, hydrocarbons, protein, oils, etc after training.

Yes, leather needs to get some fats to keep it nice. As athletes are living organisms, they need much more stuff for proper "maintenance", as they loose or metabolize the stuff they take up.

One thing I cannot fully understand: why does the leather only require some fats to keep it nice? Why not something more? The observation of the salt borders made me wonder whether leather requires some salt additionals, for instance.

Leather is dead material. So we need to protect it from too much moisture so it will keep its current state. If its permanently wet, it will finally get colonized by funghi and bacteria which will break it down.


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Image Processing Suite for bacterial microscopy: Schnitzcells or MicrobeTracker?
I am looking to start doing some work tracking the size and growth of individual bacterial cells in the microscope. In order to analyze the images I need software that can segment the cells, accurately determine their shape, and track cell lineages on a 'movie' of images collected from one experiment. Given the constraints of my microscope setup, the easiest thing for me to do is to use a strain of bacteria constitutively expressing GFP and segment the cells based on fluorescent intensity. This is functionally equivalent to segmented phase-contrast images of wild-type cells, i.e. I'm not that interested in changes in fluorescence or using fluorescence as a gene expression reporter, though my needs may head in that direction.
I don't want to reinvent the wheel (and I think that it's better if the community consolidates around a few programs that everyone uses so that experiments can be more comparable), so I'm looking for a previously published package that is robust and easy to use. Flexibility at measuring fluorescent tracking is nice, but at this stage is not crucial. The two packages that I have seen are Schnitzcells from the Elowitz lab at CalTech and Microbetracker from the Emonet and Jacobs-Wagner groups at Yale. Unfortunately they were released at the same time and don't provide a good comparison of the pros/cons of each tool.
Finally, my question is

What are your recommendations for an image analysis suite (from the two packages above or another package you have used)?

Let me know if I can make my criteria more clear or anything else. Thanks!

Although I haven't done live image tracking and analysis myself but I know the main method that people use is through Matlab, which means programming/coding so you would have to find someone to help you with some coding if you haven't worked with it before. Otherwise I suggest looking at fiji Image-J since it has a wide variety of open source plug-ins. I personally use image-J very very frequently and I'm very happy with it.


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Assay for Beta-galactosidase activity in single cell microscopy
I'd like to be able to measure the activity of $\beta$-galactosidase in living cells with simple optical (maybe fluorescence) microscopy. Ideally I'd like to do a minimum of genetic engineering, and use this assay with strains I already have (that have a WT lactose system), i.e. a fluorescent lactose-mimic would be ideal. Additionally, it would be nice if the lifetime of the fluorescent byproduct of $\beta$-gal activity was short, so I could detect a decrease in $\beta$-gal activity as well as an increase. Does such a fluorescent analog exist? I'm hoping to look at the switch from lactose to glucose utilization under the microscope, so I want lactose-using cells to light up and glucose-using cells to be dark, or vice versa. It does not have to be fully quantitative--a qualitative sense is fine.

Here is a link to on the Invitrogen/Life Technologies webpage detailing various probes to detect the activity of glycosidases, including $\beta$-galactosidase. These include DDAOG as mentioned by @Alan Boyd, as well as Fluorescein Digalactoside, Resorufin Galactoside, and  Methylumbelliferyl Galactoside, among others. NB, this is an Invitrogen/Life Technologies website, so all the reagents they mention are ones sold by the company; there may be others not mentioned here. Of these, DDAOG is very stable, which would allow for measuring the initiation of $\beta$-gal activity, but might not work to measure decreases in $\beta$-gal activity (without bleaching the dye). Resorufin Galactoside is sensitive and stable at physiological pH, allowing measurement over a long period of time. Fluorescein Digalactoside is the most sensitive assay, but since it requires the removal of 2 galactose moieties for full fluorescence it's activation time may be slow.
For my particular usage (limited access to near-red frequencies), I think that Resorufin Galactoside or Fluorescein Digalactoside might be the best choices. However, given the cost of these probes, I might be better off just finding some lab with a strain with gfp under the lac promoter in the chromosome and asking them for a sample!

I found this paper.

Zhang GJ et al. (2009) In vivo optical imaging of LacZ expression using lacZ transgenic mice. Assay Drug Dev Technol.7:391-9. doi: 10.1089/adt.2009.0195.
Abstract
beta-Galactosidase (beta-gal) (encoded by the lacZ gene) has been widely used as a transgene reporter enzyme. The ability to image lacZ expression in living transgenic animals would further extend the use of this reporter. It has been reported that 7-hydroxy-9H-(1,3-dichloro-9,9-dimethylacridin-2-one)-beta-d-galactopyranoside (DDAOG), a conjugate of beta-galactose and 7-hydroxy-9H-(1,3-dichloro-9,9-dimethylacridin-2-one), is not only a chromogenic lacZ substrate but that the cleavage product has far-red fluorescence properties detectable by in vivo imaging. In an attempt to noninvasively image lacZ expression in vivo, we applied fluorescence imaging to a G protein-coupled receptor (GPR56), knockout (KO) mouse model, in which the lacZ gene is introduced in the GPR56 locus. Compared to wild-type (WT) mice, GPR56KO/LacZ mice showed three- to fourfold higher fluorescence intensity in the head area 5 min after tail-vein injection of DDAOG. beta-Gal staining in sections of whole brain showed strong lacZ expression in homozygotes, but not in WT mice, consistent with lacZ activity detected by in vivo imaging. The kidneys were also visualized with fluorescence imaging both in vivo and ex vivo, consistent with beta-gal staining findings. Our results demonstrate that fluorescence imaging can be used for in vivo real-time detection of lacZ activity by fluorescence imaging in lacZ transgenic mice. Thus, this technology can potentially be used to noninvasively image changes of certain endogenous molecules and/or molecular pathways in transgenic animals.

The work in the paper is cited in a more recent paper which reports beta-gal-based chemiluminescent imaging in mice.
It's unclear if any of this would be successful at a single bacterial cell level.


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Why does max heart rate decrease with age?
I have heard that max heart rate declines steadily with age, and can be approximated by the equation Max Rate = 220 - Age.
What is the physiological reason for this decline, and how is it consistent with the fact that most endurance athletes reach their peak cardiovascular performance at around age 30?

There are many reasons why the maximal heart rate decreases with age.
The most prevalent is the heterogenous thickening of the walls of the heart.
Cardiac output is stroke volume times heart rate.
When the wall thickens, the heart needs more energy to achieve the same pumping (bigger stroke volume) or it needs to increase heart rate at rest.
Because of physical limitation, the stroke volume cannot be increased.
Heart needs to also rest which it does before the action potential reaches the AV conduction system.
Note the long time just after the action potential reaches AV node.
However, the heart cannot increase its maximal heart rate if the elasticity of the walls have decreased in ageing.
Ageing often leads to heterogenous thickening of walls of the heart.
If this is the case, then T wave gets high fast; which causes the risk of bleeding when exercising.
Doing sport or just feeling tired can cause a long-standing pain in the heart area in the chest.
Sport then again leads to dynamic hypertrophy of the heart tissue, which increases the maximal heart rate.
Ageing then again does not have such a dynamic changes.
There are secondary reasons caused by ageing

hormonal changes
decreased metabolism
decreased physical activity
...

which are associated with decreased maximal heart rate.
Why most endurance athletes reach their peak cardiovascular performance at around age 30?
Human's best age is at about 25 years old physiologically.
Muscles grow in rest.
When practicing at that age, recovery time of muscles is short.
It takes long time to improve cardiovascular performance (1-5 years), since heart muscle improves slowly.
I think the slow hypertrophy of heart musculature and the best physiological age of human are the reasons why the most successful endurance athletes are about 28-30 years old.


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Hypovolemia and orthostatic hypertension
What is the physiological mechanism behind the occurrence of orthostatic hypertension in the presence of hypovolemia?

it would really be helpful if you could like to some external references for terms like this :)

Orthostatic (=postural) hypertension is an excessive increase of blood pressure upon standing up. Hypovolemia is a reduced total blood volume (i.e. lack of plasma). This question is perfectly on-topic.

The pathophysiology of orthostatic hypertension has not been elucidated. It is believed it involves activation of the sympathetic nervous system [1], vascular adrenergic hypersensitivity and diabetic neuropathy [2]. High levels of plasma atrial natriuretic peptide and antidiuretic hormone were observed in children [3].
Hypovolemia causes:

baroreflex-mediated increase in muscle sympathetic nerve activity [4]
release of epinephrine and norepinephrine [5]
activation of renin-angiotensin axis [5], thus increasing ADH levels

All these reactions result in vasoconstriction and blood pressure raising. But not up to absolute hypertension.

Orthostatic hypertension is diagnosed by a rise in systolic blood pressure of 20 mmHg or more when standing [6].

This is possible. A raise of 20 mmHg from hypotension could result due to vasoconstriction.

References:

Fessel J, Robertson D. Orthostatic hypertension: when pressor reflexes overcompensate. Nat Clin Pract Nephrol. 2006 Aug;2(8):424-31. doi: 10.1038/ncpneph0228. PubMed PMID: 16932477.
Chhabra L, Spodick DH. Orthostatic hypertension: recognizing an underappreciated clinical condition. Indian Heart J. 2013 Jul 5;65(4):454-6. doi: 10.1016/j.ihj.2013.06.023. PubMed PMID: 23993009.
Zhao J, Yang J, Du S, Tang C, Du J, Jin H. Changes of atrial natriuretic peptide and antidiuretic hormone in children with postural tachycardia syndrome and orthostatic hypertension: a case control study. Chin. Med. J. 2014 May;127(10):1853-7. PubMed PMID: 24824244.
Ryan KL, Rickards CA, Hinojosa-Laborde C, Cooke WH, Convertino VA. Sympathetic responses to central hypovolemia: new insights from microneurographic recordings. Front Physiol. 2012 Apr 26;3:110. doi: 10.3389/fphys.2012.00110. PubMed PMID: 22557974.
Wikipedia contributors, "Shock (circulatory)," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Shock_(circulatory)&oldid=612494727 (accessed June 26, 2014).
Wikipedia contributors, "Orthostatic hypertension," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Orthostatic_hypertension&oldid=603984647 (accessed June 26, 2014).

I presumed you meant orthostatic hypotension.
Blood pressure falls on standing and is caused primarily by increased gravity causing blood pooling in the legs. This reduces venous return and subsequently cardiac output and therefore arterial blood pressure. Usually however standing doesn't usually cause a massive fall in blood pressure as standing immediately triggers vasoconstriction (baroreceptor reflex), pressing the blood up into the body again. However when there's a secondary factor reducing blood pressure such as hypovolaemia, the fall in pressure is higher than the body may sometimes be able to compensate for. This causes symptomatic orthostatic hypotension.

No I meant orthostatic hypertension, which apparently can also a symptom of hypovolemia.  For instance, look at the 5th cause on the list on wikipedia http://en.wikipedia.org/wiki/Orthostatic_hypertension.

Ah okay. Orthostatic hypertension: Sometimes the above mechanism can overdo it in whats thought to be through an alpha adrenergic system. This is rare and medical communities doubt its existence.


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Under what conditions does the body burn fats, proteins and carbohydrates?
Searching the internet, I have found lots of conflicting information from various fitness sites concerning when the human body burns fats, proteins and carbohydrates.
My basic understanding was that the body will first utilize glucose and glycogen stores, followed by fats and finally proteins once the fat and glycogen stores become depleted.  Also I believe there is some overlap in this process.
However many fitness websites claim that during high intensity physical activity, the body will prefer to burn protein over fat.
Scientifically speaking, when does the body ordinarily burn the following food groups (proteins, fats and carbohydrates) and how does exercise influence this process?
If you are able to provide graphs or data to back up your answer this will be extra helpful because I am bored of all the speculation I see on other sites.

I do not know about exercise but I can tell you that in case of starvation, body first uses glycogen/other carbs as energy source and then fat and lastly proteins(as proteins have other important functions,too). I also want to point out that proteins might be used for the first week of starvation but then fat takes over and only after all the fat has been consumed is protein utilisation started substantially.

Even though I am not sure, it seems ridiculous to me that "protein is used during heavy exercise" as proteins are generally the last resort and they have other more important functions.

Introduction
The system that regulates body energy store consumption is hugely complicated, but is mainly a cooperation between hormones released by the pancreas (insulin - lowers blood sugar and glucagon - raises blood sugar) and the liver (as the bodies main glycogen store and factory for various energy related tasks).
Fed State
In the fed state (high blood glucose e.g. after a meal), the body produces a large amount of insulin.  When the ratio of insulin:glucagon is high (≈0.5):

Dietary glucose is absorbed by the liver when glucose concentrations are over 8mM.  This glucose is then either

used in respiration by the liver
converted to glycogen to be stored in the liver
converted into fatty acids which are then transported out to the periphery in very-low-density lipoproteins (VLDLs)

Adipose tissue (fat tissue) takes up glucose in the blood.  This glucose is then:

used in respiration by the adipose tissue
converted into fatty acids then tri-acyl-glycerols (TAGs) - fat.  VLDLs from the liver can also be absorbed by adipose cells to be used for this.

Skeletal Muscle again directly absorbs glucose from the blood

During contraction glucose is used directly in respiration to fuel the activity
In preparation for future contraction it is converted into glycogen and stored in the cell
Amino acids are incorporated into cellular proteins though if they are superfluous then they can be used in respiration

The brain directly absorbs glucose and uses it in respiration

Early Fasting State
Where the insulin:glucagon ratio has dropped to around 0.15

In the liver

Glycogenolysis is activated to release glucose from stored glycogen to compensate for falling plasma glucose levels (signalled by elevated glucagon)
Triglycerides in the liver are preferentially broken down for hepatic respiration - fatty acids are transported in from the blood to meet the livers own energy demands
The liver begins the process of gluconeogenesis - making glucose from non-carbohydrate precursors

Adipose tissue

Rapidly starts lipolysis - stored fats are broken down into free fatty acids and glycerol.
Some of the free fatty acids are used for the adipose tissues own respiratory demands
The majority is released to the periphery to be utilised by other tissues
The glycerol released can't be used by most tissues, but is taken up by the liver where it can be used to make glucose by gluconeogenesis

Skeletal Muscle

Uptake of glucose from the periphery is reduced to preserve glucose for cells that can't easily use other fuels - e.g. the brain or red blood cells
Free fatty acids become the main fuel for skeletal muscles to conserve the glucose for elsewhere
Unlike in the liver, glycogenolysis is not activated as there are no glucagon receptors in muscle tissue.  This means glucose is only produced from glycogen when muscles are actively contracting, as before.
At this point proteins can start to be broken down,  their skeletons used as an immediate source of energy and amino acids released to be taken up by the liver and used in gluconeogenesis

The brain directly absorbs glucose and uses it in respiration.  Fatty acids can not be used as these do not cross the blood brain barrier

Late Fasting State
If there has still been no glucose intake, the insluin:glucagon ratio falls even further, to around 0.05.

Liver

No further glucose has entered the liver and within 24h all hepatic glycogen stores have been depleted
Gluconeogenesis becomes the principle source of all plasma glucose - the liver creates new glucose from:

Amino acids - muscle & liver protein breakdown
Glycerol - from adipose tissue
Lactate - from red blood cells and muscles

High amounts of fatty acids are converted into Acetyl CoA to be used in respiration by the liver, but too much Acetyl-CoA is produced.  The remainder is converted into ketone bodies that are useless to the liver, so jettisoned to be used by other tissues (esp. the brain)

Adipose tissue

As the fast continues into a few days, adipose tissue adapts to producing large amounts of free fatty acids.  This becomes sufficient for most body tissues
These fatty acids are used preferentially by all tissues that can use them, conserving glucose for the brain

Skeletal Muscle

Fuelled almost entirely by fatty acids and ketone bodies from the liver and adipose tissue
Protein breakdown continues to release carbon skeletons and amino acids for gluconeogenesis - but this is inhibited in the presence of high levels of ketone bodies to prevent unnecessary muscle wastage (still allowing the human to hunt)
Amino acids are incorporated into cellular proteins though if they are superfluous then they can be used in respiration

The brain

Once ketone levels reach a critical level, they can cross the blood brain barrier to be used as a supplementary energy source
However, it is not sufficient alone, so a net source of glucose is needed from somewhere in the body

Progressing to starvation
This process can continue for a number of weeks, with the body eventually exhausting fatty acids in adipose tissue and being unable to produce ketone bodies in the liver, losing the inhibition of proteolysis causing a last ditch response of muscle breakdown for energy.  Death is usually from heart failure resulting from cardiac muscle breakdown.
Summary
This chart might be useful in summary, it shows where the glucose levels in the blood are coming from at various stages, the gluconeogenesis line indicating protein and fatty acid breakdown:

Exercise
Exercise has to be very intense to have any effect on this system in normal situations.

Resting Muscle metabolises stored fatty acids for its own energy.  Glycogen stores are replenished from glucose ready for more vigorous contraction.
Brisk Walking fatty acid metabolism again provides almost all the energy
Sprinting Glycogen stores are used, respiration is almost entirely anaerobic as blood vessels are constricted by the muscle activity and ventilation has not had time to increase.  Lactic acid is produced, which can be used by the liver for gluconeogenesis
Middle distance running: aerobic metabolism takes over as the body adjusts to the higher oxygen demand.  Lactate is still the major end product

One example of where this may be more noticeable is during a marathon.

0 Mins - Muscle is resting at the start line, as above.
10 mins - Muscle and liver glycogen released to power muscle contraction
2 Hours - A marathon requires roughly 700g of glycogen to complete, however the liver can only store around 500g.  This is largely depleted after roughly 20 miles.  Blood glucose levels fall rapidly and the body switches to fatty acid metabolism.  This only provides around 60% of the power output and pace falls off (known as hitting the wall).  At this point, virtually every reserve power source is being used simultaneously to keep the body going.
Finish - Muscle and liver glycogen are entirely depleted. If glucose levels haven't been maintained by other means, hypoglycaemia results causing confusion, hallucinations and even coma and death.

Thanks for your informative answer.  Let us say someone is on a calorie deficit diet, and undergoes exercise that night.  They would supposedly have low glycogen stores, and would rely on gluconeogenesis.  What proportion of gluconeogenesis will be fatty acids, and what proportion will be from protein?  Is this ratio always the same or is it dependent on intensity?

@Chris I would anticipate greatly more from fatty acids than protein breakdown until one runs out of fat.  You'll be able to release enough energy through fatty acid usage for any intensity of exercise assuming that you still have fat stores available.

@Chris The only gluconeogenesis that is possible from fat breakdown is that derived from the glycerol of the triacylglycerol. Fatty acids are metabolised to acetyl CoA, and it is not possible to synthesise glucose from them because for every acetyl group that enters the TCA cycle, two CO2 molecules are lost before the 'start' of gluconeogenesis (oxaloacetate). A starving subject would rely on fatty acids (directly and as ketones) and glucose derived from glycerol, lactate and amino acids. Despite the switchover to using fat, a net loss of protein is unavoidable.

Dear @RoryM i really liked your answer and just want to kindly ask you further readings (even technical) about this field of human nutriton.

The answer should cite its sources, crucial for fact checking and good science. Where's the graph and the table from, for example? That said, this answer is top notch and the missing references are small fry. Well answered.


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Is the empty GI tract a hollow tube with air inside, or is it generally collapsed until food is eaten?
I have heard that "air in the GI tract" results in flatulence and burping etc, however I initially assumed that the "empty" GI tract was a hollow tube filled with air anyway.
So on an empty stomach (or "empty" GI tract rather), does the GI tract collapse due to the pressure in the surrounding cavities, or is the GI tract normally a hollow tube filled with air, and flatulence merely a result of "excess" air?

Under normal circumstances the stomach and GI tract have very little "gas" in them - whether it be flatus, air, CO2, or anything else - and so are essentially collapsed with the walls against each other. However, gas is continually being produced by the microorganisms that inhabit our gut, and can also come from swallowing small amounts of air, fizzy drinks, etc., so the environment is never 100% gas-free. A typical person produces on the order of 500-1500 ml (0.5-1.5 liters) of gas per day.
If you're interested, the Wikipedia article on flatulence is a good introduction.

If you look below you can see two X rays. One with bowel obstruction on the right and a normal on the left. On an X ray air bubbles are black as indicated. Under normal circumstances as you can see there is very little air in the stomach and GI tract, although more frequently there will be some in the stomach due to fizzy drinks or reactions involving stomach acid producing gas in our stomach. That air later on in our GI tract tends to be a mix of carbon dioxide, methane and other waste products that bacteria in our gut have made. As Matt said, we produce quite a substantial amount of gas (500-1500 ml) per day. In an obstruction all of this can collect and further increase as microogranisms are in contact with the food for a longer duration as well as more enzymatic breakdown. And this can be seen in Figure 2.


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Why is weight gain a symptom of Cushing's Syndrome?
Cushing's syndrome results from increased levels of cortisol in the body.
Cortisol as I understand it however, promotes the breakdown of glycogen and amino-acids in the process of gluconeogenesis, to increase blood sugar - opposing the action of insulin.
Why then does Cushing's syndrome lead to weight gain rather than weight loss?

Cortisol is released when body goes through stress situations like while working out in gym, physiological activities outdoor etc. As you have already mentioned about what Cortisol does, it accumulates in the body after the stress situation and then with the intake of food and other nutrients it replaces the consumed carbohydrate and fat in the body i.e. a kind refueling. So this is how Cortisol maintains the body weight normally if our body gets enough exercise or has proper metabolism.
Whereas in Cushing' syndrome which comes usually by taking glucocorticoid drugs, or diseases that result in excess cortisol, adrenocorticotropic hormone (ACTH), or CRH levels. In this case Cortisol content will be more than the normal level which in turn requires more carbohydrate. So cortisol metabolizes the food and reefuels the body even when there is no requirement within the body. So because of excessive cortisol content body simply gets excessive fat accumulated in various parts which mainly results in obesity.
One more explanation from High level of Cortisol effects:
Chronically high levels of cortisol plays a big role in the development of obesity.

Cortisol helps the body handle stress; so, when stress goes up,
  cortisol also goes up. Cortisol stimulates fat and carbohydrate
  metabolism during stressful situations. This leads to increased blood
  sugar levels required for fast energy. In turn, this stimulates
  insulin release which can lead to an increase in appetite.

Adrenaline increases alertness and metabolism by helping fat cells release
  energy. When the immediate stress is over, the adrenaline levels
  return to normal. But, cortisol lingers to help bring the body back
  into balance after stress. One of the ways it gets things back to
  balance is by increasing appetite to replace the carbohydrate and fat
  used for the flight or fight response.

The problem is that in today's society, stress-causing situations do
  not really require the body to use up a lot of energy. So, cortisol
  ends up causing the body to refuel after stress even when it doesn't
  really need to refuel. This excess fuel or glucose is converted into
  fat resulting in increased storage of fat.

"So cortisol metabolizes the food and reefuels the body even when there is no requirement within the body. So because of excessive cortisol content body simply gets excessive fat accumulated in various parts which mainly results in obesity." doesn't really make sense to me, if it metabolises the food, it should lead to weight loss.  Also your answer is mostly about stress, but I'm interested in cushing's syndrome.

In Cushing's syndrome when the cortisol level goes up, it makes body to consume more food which in turn leads to fat build up. This is unnecessary fat which body gets when it does not need it. I gave stress as an example but higher level of cortisol was the main highlight which results in fat.

why does cortisol make you consume more food?

How different hormones are interrelated and What is the potential link between stress, cortisol, and appetite?

I read this somewhere. In Cushing's syndrome the excessive cortisol disables metabolism of proteins and fats rather than increasing it ( I don't know the reason). Hence, fat gets accumulated, mainly in the abdominal region resulting in weight gain

Can you please add some references?

http://www.3fatchicks.com/how-cushings-syndrome-can-contribute-to-weight-gain/


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Why does caffeine consumption cause one to urinate more?
What is the physiological mechanism behind the diuretic effect of caffeine?

Caffeine inhibits the secretion of the antidiuretic hormone (ADH), so it increases diuresis, but this effect is small and transient.
http://en.citizendium.org/wiki/Vasopressin
Caffeine in amounts up to 400 mg/day (~4 cups of coffee) does not results in net dehydration, since the amount of water lost due to slightly increased diuresis is much smaller than the amount of water in coffee.
http://www.ncbi.nlm.nih.gov/pubmed/19774754
In some people, caffeine may irritate the bladder and thus trigger more frequent urination, but this is not increased diuresis and the total volume of the urine is not increased.