text:
How does HCl not burn our stomach?
How does the digestive acid (HCl) not burn the surrounding membrane of our stomach? It digests the majority of raw food we eat but how does it stay safely in our stomach?
Also, how does the stomach maintain the ability for a human body to retain HCl for all lifetime?

What do you mean by "how does the stomach retain the safety procedures for a human body to retain it for all lifetime"?

Just as a note, ulcers occur when stomach acid does break through the mucus layer.

Mucous-producing cells at the neck of the gastric pits create a layer of protective mucous covering the stomach lining. This mucous layer includes bicarbonate ions which act as a chemical barrier against the protons in gastric juice.  See here for some evidence.
The stomach lining stays protected because the mucous layer is continuously replenished.

This is why stomach acid will burn and break your stomach after you die - the mucous layer is no longer replenished then. Since it isn't any enzyme but acid that is breaking down the organs, I don't think this can be called autolysis though.

Cause of this secret are tight junctions and mucous.
As Wikipedia explains:

Tight junctions, or zonula occludens, are the closely associated areas of two cells whose membranes join together forming a virtually impermeable barrier to fluid. It is a type of junctional complex present only in vertebrates. The corresponding junctions that occur in invertebrates are septate junctions.

They perform vital functions:They hold cells together.Barrier function, which can be further subdivided into protective barriers and functional barriers serving purposes such as material transport and maintenance of osmotic balance:They help to maintain the polarity of cells by preventing the lateral diffusion of integral membrane proteins between the apical and lateral/basal surfaces, allowing the specialized functions of each surface (for example receptor-mediated endocytosis at the apical surface and exocytosis at the basolateral surface) to be preserved. This aims to preserve the transcellular transport.They prevent the passage of molecules and ions through the space between cells. So materials must actually enter the cells (by diffusion or active transport) in order to pass through the tissue. This pathway provides control over what substances are allowed through. (Tight junctions play this role in maintaining the blood–brain barrier.) At the present time, it is still unclear whether the control is active or passive and how these pathways are formed. In one study for paracellular transport across the tight junction in kidney proximal tubule, a dual pathway model is proposed: large slit breaks formed by infrequent discontinuities in the TJ complex and numerous small circular pores.1In human physiology there are two main types of epithelia using distinct types of barrier mechanism. Dermal structures such as skin form a barrier from many layers of keratinised squamous cells. Internal epithelia on the other hand more often rely on tight cells junctions for their barrier function. This kind of barriers is mostly formed by only one or two layers of cells. Until recently it was not clear whether tight cell junctions also play any role in the barrier function of the skin and similar external epithelia, recent research suggests that this is indeed the case.

In the next step mucous protect epithelial cells from released HCl.
Here  you will find more things.


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What causes adenosine build up in the brain when awake?
Adenosine is an important hormone in sleep regulation.  It is postulated that when a person is awake, there is a build up of adenosine in the brain, which inhibits the neurons in the brain, and produces tiredness.  (See answer for more information:  What causes humans to be sleepy?)
However, I am wondering what specifically causes this adenosine build up.  I understand ATP (adenosine tri-phosphate) is broken down to ADP in the brain to produce energy.  I thought this ADP would then be used to re-generate ATP again etc, so I'm not sure how adenosine is built up in the brain over a day.
Basically I am unsure how Adenosine itself, as opposed to ATP or ADP, is produced during the waking state?
My theory is that during the high demand waking state there is insufficient energy to convert ADP back to ATP, and the excess ADP is broken down to adenosine somehow.
I would appreciate an explanation of how this build up occurs, and also an explanation of how this in turn how it induces sleepiness would be a plus.

You may find this interesting, although it is not directly related to your question: http://www.scq.ubc.ca/eyes-wide-open-dispelling-myths-and-uncovering-truths-behind-caffeine-consumption/. Also, I retagged your question - you might find these tags useful.

Adenosine causes humans to become sleepy. But how ?

During day time we consume food which is broken down into glucose. This glucose is broken down by "Glycolysis" in cell's cytoplasm during which ATP is produced. This produced ATP is is then used by body as an energy supplier. ATP breaks down into ADP and then AMP with the release of energy which our body consumes for doing work.

(Fig 1- Structure of Adenosine to ATP)
Adenosine is produced continuously and starts to accumulate around and in Adenosine receptors such as A1, A2a, A2b and A3 (as shown in fig below).Adenosine inhibit signal propagation and energy production in at least A1. (Not all the receptors induce sleep when they receive Adenosine.) "A1 receptor" receives adenosine and induces sleep. A1 receptors are implicated in sleep promotion by inhibiting wake-promoting cholinergic neurons in the basal forebrain.

Continuous inhibition of A1 receptor by Adenosine slowly induces sleep by relaxing the brain and muscles but without substantially weakening their abilities!
How is Adenosine metabolized ?
During sleep the accumulated Adenosine is metabolized by Adenosine deaminase enzyme which catalyzes the irreversible deamination of 2'-deoxyadenosine and adenosine to deoxyinosine and inosine. With the reduction in the Adenosine content the body is excited from sleep slowly.
So in short summarize:

The accumulation of adenosine during waking periods is thus associated
  with the depletion of the ATP reserves stored as glycogen in the
  brain. The increased adenosine levels trigger non-REM sleep, during
  which the brain is less active, thus placing it in a recovery phase
  that is absolutely essential—among other things, to let it rebuild its
  stores of glycogen.
Because adenosine is continuously metabolized by the enzyme adenosine
  desaminase, the decline in adenosine production during sleep quickly
  causes a general decline in adenosine concentrations in the brain,
  eventually producing conditions more favourable to awakening.

(Refer this page: MOLECULES THAT BUILD UP AND MAKE YOU SLEEP)

Glycolysis requires ADP to make ATP. So if all the ADP and AMP is becoming adenosine and getting hydrolyzed by ADA, where does new ADP come from?

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What is the cause of muscle cramps?
According to Wikipedia, muscle cramps are caused by the inability of myosin fibers to break free from the actin filaments during contraction, resulting in a prolonged contraction.
A lack of ATP would obviously produce cramping, as myosin requires ATP to become free from actin.
However, I have heard that potassium and sodium are useful for treating cramps and that their deficiencies can lead to cramping.
So, how does a deficiency in sodium or potassium result in the inability of myosin fibers to break free from the actin filaments during contraction?

check this article. It is not accessible to me.

The quick and simple answer:
Cramps of a hypokalemic origin are much more common than those of a hyponatremic origin because the Na-K pump is more effective at moving potassium in comparison to sodium.
At the onset of a muscle contraction, the presence of calcium triggers the opening of the Na-K channels in the membrane. Potassium is a calcium inhibitor, so as the potassium flows out of the cell, it eventually reduces the presence of calcium. This causes the closure of the Na-K channel (negative feedback mechanism). In a hypokalemic state, the lack of sufficient K doesn't inhibit the calcium channel, and in turn doesn't properly terminate the muscle contraction at the cellular level.
The continued presence of calcium, which has a lot to do with nerve impulses, means that the nerves keep firing, and in some cases such as a 'charlie horse', these impulses fire fast and continuously. The body at this point is reaching a small local state of metabolic acidosis resulting from the extremely high oxygen consumption, increasing levels of CO₂ (the acidosis component) and reducing blood partial oxygen levels. Since the oxygen is no longer as abundant as it was, it inhibits the bodies ability to locally produce the ribose and phosphate necessary for ATP. Less ATP = more myosin that can't be disconnected from actin = continued muscle cramp.

still doesn't answer why low sodium causes cramps..
the exercise cramps dont happen because of hypokalemia.. potassium is hardly lost in sweat.. Potassium is not a calcium inhibitor.. calcium release in muscles in voltage gated, which is triggered by sodium influx

"Muscle cramps, notably nocturnal leg cramps, are common symptoms experienced by general medical patients, particularly the elderly. Their etiology is varied; most commonly, these cramps are idiopathic. With the notable (and relatively rare) exceptions of serious electrolyte imbalances including hypokalemia, hypomagnesemia and hypocalcemia, these cramps are typically benign in nature." So electrolyte imbalances are not a common cause of cramps, even in the elderly.

And (same source): "The second recent study to challenge the notion that diuretics are a common cause of muscle cramps was a cross-sectional survey of 365 general medical patients. Although the prevalence of leg cramps in this cohort was 50%, no associations were found between these cramps and any medication except analgesics that were used to treat the cramps." (Most diuretics lead to a loss of potassium through urine; there are some potassium-sparing diuretics but they were not distinguished in this study.)

Furthermore the [review] paper says "Interestingly, potassium‐sparing diuretics, such as amiloride, are also associated with cramping."

And a more recent (2012) investigation: "Physicians may be surprised that potassium-sparing diuretics have a stronger link to cramp treatment than loop diuretics. Yet, hyperkalemia facilitates neuronal excitation, and hypokalemia suppresses motor neuron activity." So I'm having doubts that your claim that cramps of a hypokalemic origin are much more common [...] has a basis in epidemiology.

Muscle contraction occurs when the brain tells the body to move. The brain then starts an action potential down the motor neurons, until it reaches the terminal bouton. At the terminal bouton, it releases the neurotransmitter, acetylcholine, which travels through the myoneural junction and into the myoneural cleft. ACH binds to the receptor, which causes an action potential in both directions along the cell membrane.
    The action potential repels the potassium, which travels down the cell membrane until it falls into a transverse tubule. K+ continues to fall into a transverse tubule and accumulates, which increases voltage (-70 to -50 mV). The voltage change causes the calcium gates to open and to diffuse the calcium.
    Calcium then binds to troponin, which in turn binds to tropomyosin and pulls it, exposing the g-actin binding site that allows myosin and actin to bind. The myosin head changes shape (called power or working stroke) and pulls the actin towards the M line, and the muscle contracts. Similar to a tug of war, the myosin heads (your hands) pull on the actin (the rope) to contract a muscle. Like team members in a tug of war, the myosin heads alternate between pulling and holding on to the actin; the only way that myosin will release actin is to add ATP, which forces the two apart and thus relaxes the muscle (as mentioned above).
Now, a lack of potassium, sodium, or calcium would prevent the muscle from contracting but won't relieve a muscle cramp. The common advice of eating a banana actually does help relieve cramps but not because of the potassium. Bananas also have sugar and fat, which are converted into ATP.
Muscle cramps are primarily caused by a lack of ATP in the body. ATP forces the myosin to release the actin; thus, the muscle relaxes and the cramp is relieved.
Another cause could be the lack of magnesium, which helps the ATPase sodium/potassium pump, which, in turn, returns the voltage to resting potential and relaxes the muscle.

Anaid, welcome to Bio SE, and thank you for resurrecting this question with an answer. If you can try to add in line citations as mentioned in the help section.  I also think there are some more topics that might should be covered here like Ca2+-ATPase.

None of these answers makes sense, and there some minor errors in them. I know that action potentials may continue to fire down the axon. One reason may be because acetylcholinesterase is not coming to the rescue and cleaning up all the acetylcholine in the synaptic cleft. But that usually happens if there are drugs involved. So, in terms of natural muscle cramps, it really does not make any sense whatsoever.
A really good reason is mainly because of a lack of potassium. The function of potassium inside the muscle cell is to repolarize the membrane. However, if there is not enough potassium, the time it takes for it to repolarize is very slow. On the other hand, sodium is used to depolarize the membrane. As a result, since there is an unequal distribution of sodium to potassium, less potassium flows out the membrane while more sodium flows into the membrane, causing it to depolarize faster than it repolarizes. Since the inside of the cell is becoming more positive with the help of sodium, and since the outside of the cell is becoming negative with the help of potassium, the inside of the cell is pulling back the potassium. But, again, there is an unequal distribution of potassium compared to sodium, so it will never achieve that electrochemical equilubrium (resting membrane potential). Since electrochemical equilibrium can not be achieved, sodium is flowing inside the membrane, causing it to depolarize across the membrane and to form an unfused tentanus at a rapid rate.
The rate in which this is happening is so fast that it won't let the myosin head detach from actin for a long period, so it is continuously making the sacromere shorter, causing a pain receptor to travel toward the CNS. This is my hypothesis.

Can you please expand your answer with some references?

One possible reason why low sodium levels induce cramps may lie in the cation selectivity of the nicotinic acetylcholine receptor (nAChR), which is an ion channel. When ACh binds to the receptor site on the nAChR protein, the protein changes shape to open a pore formed by the protein in the cell membrane. This pore allows the influx of both sodium and calcium ions, which induce depolarisation (a positive shift in the membrane voltage) to trigger the voltage-dependent ion channels responsible for action potentials.
A reduction in sodium ions would mean more calcium is able to enter the cell through the nAChR. The calcium ion carries greater charge as it is formed by the loss of two electrons from its outer shell, while the sodium ion is formed by the loss of one electron. This means that, each time the nAChR channel opens, the cell undergoes greater depolarisation. The muscle response is harder and faster to the same neural stimulus, which results in a depletion of energy stores.

One of the things that I would like to point out is that ATP detached the myosin head but does not control the powerstroke! If there are no more ATP being produce, then rigor mortis results. You will just be really tense/sore because the myosin head is not being released, and it's staying contracted (perhaps a fused tentanus), but it does not make the sacromere shorter if ATP are no longer able to be produced. And if there are no more ATP being produce, it can't be hydrolyzed into ADP and inorganic phosphate (Pi).
That would help to create the cross bridge. In addition, inorganic phosphate, not ATP, is the essential compound when you want the power stroke to happen.

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Determining limiting nutrients from a graph
The question was
Which of the following statements is supported by these data?
A. Phosphorus was the first limiting nutrient followed by nitrogen.
B. Nitrogen was the first limiting nutrient followed by phosphorus.
C. Phosphorus was limiting but nitrogen was not limiting.
D. Nitrogen was limiting but phosphorus was not limiting.
E. Neither nitrogen nor phosphorus was limiting.

The answer was B: Nitrogen is the first limiting nutrient followed by phosphorus, but I do not know why. I thought it would be only phosphorus as the Nitrogen values are always greater than the control values.

The control graph shows the baseline against which we can compare the other graphs. It is the graph without any changes, and hence is the graph in which one of the nutrient is limiting.
In the graph for +P, there is no rise in biomass and the graph resembles the control. This shows that Phosphorous is not the first(initial) limiting nutrient, as its addition did not affect the biomass production.
The +N graph shows a significant rise in biomass, indicating that N was indeed the initial limiting nutrient. On its addition, the biomass production increased.
The +N and +P graph shows a higher biomass than +N and the control. This indicates, that while  N was established to be the first(initial) limiting reagent, addition of Phosphorous also significantly improves the biomass yield, and hence P must also have become a limiting nutrient once N was added and its limiting effect removed. That is the reason why +N+P graph is higher than just +N graph. If phosphorous would not have been limiting even on addition of N, then the +N+P graph would have resembled +N graph.


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Tap vs. mineral water for drinking
I was told a human should drink a small glass (0,3 liter) of mineral water per day to get the minerals. What is the rationale behind this? What is the difference between tap water and mineral water in terms of nutrition facts and effects on human health?
Values for tap water in my area:

How good are the values regarding nutrition facts?

it all depends on where you live and how your neighborhood water supply is..

You physician is the best one to answer questions about the rationale behind this recommendation.

We spent all but the last few thousand years or so of our evolutionary history exclusively drinking mineral water so it is reasonable to suspect there may be things that benefit us in naturally-occurring, mineral-laden water. If you live in the US there is also a lot of discussion about the health effects of chlorine in tap water as it may be a carcinogen and have a lot of other possible bad effects. I could also write a book about the tremendous amount of incompetency I have witnessed surrounding the management of public drinking water. I try to consume tap water in moderation.

@Kozuch I propose you change this question to discuss about necessary minerals and their role with necessary hormones in human body. The only necessary hormones are Insulin (glucose), Parathyroid hormone (calcium) and aldosterone (Na ad K). Pay attention to Calcium especially. Please, see this http://ajcn.nutrition.org/content/71/4/999.full

The mineral content in tap water differs from area to area as well as the source. The mineral content in bottled water is regulated by the companies that manufacture them, in particular the Mg and Ca content(reference).

Death rates tend to be lower in areas with tap water containing higher
  levels of Ca and Mg. It has been shown that deficiencies in magnesium
  are capable of producing heart disturbances, including 215,000 fatal
  heart attacks in the U.S. each year, and as many as 20,000,000 fatal
  heart attacks worldwide (reference).

Different brands of bottled water will differ in their mineral content as well (reference). The place where you stay might be lacking in a particular mineral that your body requires which is why your doctor has specified the use of a particular brand of mineral water.

The main minerals in tap water are calcium and magnesium, which determine the hardness of water. The main minerals in mineral waters are calcium, magnesium, sodium, chloride, carbonate and sulfate. Tap water from different regions and various brands of mineral water can contain very different amounts of minerals, so it is impossible to make a general recommendation to drink more mineral water.
Mineral water high in calcium or magnesium can be a good source of calcium and magnesium for people who do not get enough calcium from foods. Foods are much better source of calcium and magnesium than water, though.
Researchers from the World Health Organization (WHO) claim that water hardness (calcium and magnesium content) has no effects on health (positive or negative).
Foods high in calcium, beneficial and harmful effects of calcium and references to claims I made:
http://www.nutrientsreview.com/minerals/calcium-ca.html
Calcium concentration in bottled and mineral waters (US, Europe):
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2488164/table/Tab2/

Agreed, if foods high in calcium and magnesium are touted as "super foods" then it is illogical to reprimand water for the same thing. its all going in the same place lol


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What is the name of the smallest self-replicating thing?
Some time last year, I found an article on Wikipedia about the smallest something to be able to reproduce.
I don't remember exactly what it was, but I am fairly certain that after the initial discovery another of the previous organism (this one slightly smaller) was discovered.
I think that the smallest something might have been the smallest self-replicating protein, or smallest self-replicating molecule, or something like that.
It was not mentioned in this thread: Which organism has the smallest genome length?
It had a strange, stand-out name and I believe it was discovered in the 90s.

Also see http://en.wikipedia.org/wiki/Smallest_organisms

You're probably thinking of the Spiegelman Monster. It was actually discovered in 1965, but it was discovered that it became shorter over time in 1997.
It also wasn't included in that thread, and it has a strange name.
http://en.wikipedia.org/wiki/Spiegelman_Monster

I don't understand how this fits the criterion of 'self-replicating' since it seems to require the addition of a replicase enzyme to the in vitro system.

@AlanBoyd Neither do I, but it seemed to fit (some of) the criteria, and I thought it was worth a shot. Apparently it was correct!

A research team (Lee et al.) has discovered what maybe the smallest known self replicating RNA molecule - actually a 32-unit-long "a-helical peptide" whatever that is. It is based on the yeast transcription factor GCN4. The 32 peptide sequence is so small, that one could describe it in text form simply as:
ArCONH--RMKQLEEKVYELLSKVA-CLEYEVARLKKLVGE--CONH2
ArCONH--RMKQLEEKVYELLSKVA-COSBn
H2N--CLEYEVARLKKLVGE--CONH2

Two of those lines are likely to be pre-cursor molecules required (the food), and one is likely to be the RNA sequence, I think the final line.
This is a lot smaller than the smallest known or simplest genome, which could be Carsonella ruddii, which lives off sap-feeding insects, has taken the record for smallest genome with just 159,662 'letters' (or base pairs) of DNA and 182 protein-coding genes.
Source: https://www.nature.com/news/2006/061009/full/news061009-10.html
Also, it's likely you should checkout this study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4187685/ "Systems Biology Perspectives on Minimal and Simpler Cells
"

The first part of this answer is complete nonsense. It talks about RNA and shows a peptide sequence, refers to a precursor as food, and quotes something called the journal of creation.

Although this answer cites "creation.com" as the source and (as David says) includes some obvious gibberish, the actual source is a 1996 Nature paper A self-replicating peptide. It is, obviously, about a peptide rather than RNA. It is not particularly responsive to the question, but may still have some relevance.

Fair call, I was too excited to quote that sequence, which I like a lot. It was good to learn about Spiegelman Monster, I should have taken a squiz at that: I'd agree the dwarf genome with only 218 bases AFAIK would be likely correct, because it is a organism whereas mine is just..... a "thing". Half correct. The question is wrong! :)


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What is the definition of a stringent/relaxed plasmid?
I have found a publication which proposes some definitions, including a definition for strict and relaxed replication. The definitions are:

Relaxed control of plasmid replication. Relaxed control should be used in reference to plasmid replication that is not obligatorily coupled to chromosome-replication.
Stringent control of plasmid replication. Stringent control should be used in reference to plasmid replication that is obligatorily coupled to chromosome replication.

However, the publication is from 1976. Are these definitions current? If no, what is the current definition?

In short, yes, the definitions are still correct:
The number of copies of a plasmid in the cell is determined by the mechanism of its replication: whether it is synchronized with the replication of the bacterial chromosome or is independent of it.
In the first case, the initiation of replication is performed by the same mechanisms of replication of the bacterial chromosome. This means that the origins of replication, as well as all proteins involved in the initiation of replication, are shared between the plasmid and the bacterial chromosome. For plasmids, which replication is synchronized with the replication of the bacterial chromosome are under stringent control of replication. The stringent control of replication is characteristics of plasmids with low copy number. These plasmids contain DNA regions called par-locuses (from partition) that control the correct division of the plasmids in the two daughter cells.
Plasmids with high copy number are under relaxed control of replication. These plasmids are replicated independently of the replication of the bacterial chromosome. They have individual mechanisms for initiation of replication. The plasmids themselves encode the initiation factors for replication, which are mainly RNA molecules. Once the plasmid replication is initiated, it continues with the same machinery used by the bacterial chromosome.
Reference (Textbook): Bacterial Genetics, Margarita Pesheva (2000)


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DNA as an acid?

Possible Duplicate:
Does DNA react in all of the ways most other acids do?

Even if DNA is made up of nucleotide bases, it is said to be an acid. Why is this?

voted to close.

First of all, DNA is not made up of "nucleotide bases" but of nucleotides. These consist of a sugar bound to one of the 4 nucleobases Adenine, Cytosine, Guanine or Thymine (Uracil in the case of RNA) and a phosphate group.
When these bases are bound to a sugar (2-deoxyribose for DNA), they form the nucleosides Adenosine, Cytidine, Guanosine or Thymidine respectively:

When the nucleosides are bound to one or more phosphate groups, they become nucleotides. The general structure of a nucleotide is (source):

Finally, nucleotides are joined together through their phosphate groups that form phosphodiester bonds between the third and fifth carbon atoms of adjacent sugar rings. This polymer is what we know of as DNA:

So, after this long introduction, the acidity of DNA is caused by the presence of the phosphate groups which are themselves acidic. You can see this by comparing the structure of DNA to that of Phosphoric acid:

As explained very well here:

If you compare the structures of phosphoric acid (Figure 1) and a
  short strand of DNA (Figure 2), you’ll see that in the latter, two
  protons of phosphoric acid are replaced by carbon atoms either in, or
  attached to, the five-membered ring. In chemical terms, such a group
  is called a phosphate diester. The remaining proton is now quite
  acidic, and is relatively easily lost, thereby giving DNA its acidic
  character. Indeed, under neutral conditions, DNA is deprotonated at
  this site, and the oxygen atom bears a negative charge. Despite the
  fact that DNA does contain many basic groups, their basic properties
  are masked somewhat because of the fact that they hydrogen bond with
  each other to form base pairs. Hence it’s the acidic part of the
  molecule that dominates, and that is why we know DNA as an acid.

Could we say that the weakening of O-H bond is due to -I effect of the sugar groups?

DNA is made of three types of molecules in equal proportions - basic nucleotides, sugar deoxyribose and acidic phosphate groups. The bases are on the inside of the helix and partly hidden from the outside. Deoxyrybose and phopshates are on the outside, forming a backbone.
Though the proportions are equal, the nucleotides are weak bases, so the overall pH is acidic.


text:
How Scientists sequence, assemble and annotate plant genomes?
I previously read this question and this paper and learned good things about this topic. my current question is that scientists use which tools, algorithms, soft wares... to sequence, assemble and annotate plant genomes?
For each genome project do they develop new tools and algorithms or there are some tools that are useful for (almost) all genome projects?
Are there any comprehensive site, book or paper that have plant genome sequencing and annotation protocols?

Given the C-value paradox (where there may be massive amounts of non-coding DNA, much of it often repetitive), and the fact that polyploidy seems more frequent in the plant kingdom than in animals, (e.g., bananas, wheat), I can imagine some challenges at the assembly step, but I am not aware of a specific tool or approach that is only used by plant genome projects. DNA is DNA for every kingdom, and eukaryotic genes are eukaryotic genes, regardless of species, right? Software and algorithms don't care where the DNA comes from.

But I think algorithms will consider long repeats in plant genomes

Let's try and answer all three parts of your question.
Sequencing
The general method is the same. Sequencing is just sequencing. But as for every single sequencing, there are factors to consider and protocols to be selected.
One important thing is, that you might want comparably long reads to cope with the repeats and the general large size of plant genomes. To get long reads, you need long input DNA sequences. Therefor you would want to follow a suitable protocol for high molecular weight plant DNA. That might be hard, because plant DNA can be difficult to extract based on the plant and tissue you have, as most easily put you have to "crack open" the cell wall in the very beginning.
After that, it is general sequencing. Although, as I already said you might opt for long reads (PacBio) and/or good coverage. If that is not at all feasible, you might choose to do targeted sequencing and only capture the whole exome (or only the genes you are interested in) to reduce both cost and analysis complexity.
Assembly
Now you have probably accumulated a lot of sequence and also potentially long sequence. There are multiple tools you could use for assembly and generally you can use the same for plants that you might want to use for example for a human genome assembly. One example that works well on large plant genomes is MaSuRCA, another is Allpaths-LG. There are some assemblers designed to cope with long repeats, but quite often you just assemble and then try figuring out the repeat regions later, for example by improving a shotgun read assembly with long reads from another technique.
Annotation
This one definitely has specific tools for plant genomes. Well, large genomes. The main thing in annotation is finding potential genes and comparing them to databases to annotate them with function. Plants do splice and plants can have long introns, even ones including long repeats.
One gene prediction software example that works on plants is Augustus, but for some model organisms there are even organism-specific pipelines and tools for this task. And of course, on the database part you would choose to rely on a plant specific database (if you do not use NCBI-NR anyway). Those can also be species or genus specific like the ones you find on the TAIR (Arapidopsis) project.
TLDR:
It's in fact complicated. On one hand, there is a need of specific tools and databases, on the other you might go well with standard tools, but would have to adapt parameters, do additional pre- or post-processing steps and so on.

Thank you. very use full answer. I have a question: in annotation part, if I have a set of assembled sequences, how can I compare (align?) all them with databases like NCBI or TAIR to find possible matches? Are there automatic ways or I'll code or do that manually?

There is a variety of alignment tools, the most used and most widely known is BLAST. There is a web server at http://blast.ncbi.nlm.nih.gov/Blast.cgi but for complete plant assemblies or even all proteins found in one plant you would have to install and run it locally. In case you are not aligning pre-predicted protein sequences but want to align against RNA or protein databases, you would need a spliced aligner.


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Is there any kind of immortality in plants?
I asked a question about immortality of hydra and learned good things about senescence. Now I would like to know about immortality in plants, if there is some kind of immortality in plants and how this occurs - how does it protect itself from senescence?

Hi there. There is a somewhat similar question here (http://biology.stackexchange.com/questions/2055/do-trees-age-on-a-microscopic-level/) that I have posted an answer to.

Just found this amazing example of a really old tree - >4000 years old! http://www.ncbi.nlm.nih.gov/pubmed/11295507

I can find no examples of immortal plants, but then again immortality is rather hard to prove, it's rather like trying to prove that space will never turn in to a pony - as long as time exists it could still occur, only if you go beyond the end of all time would you be able to say that it has or has not happened but then time would no longer exist and nor would space/the pony.
However, for examples of long lived plants it is perhaps best to look at trees - there are some species that live a long time and they can easily be aged. Here is a list of oldest known trees. It is difficult to tell how old these trees can become, and thus whether they are "immortal", because anything that lives that long is likely to encounter sources of extrinsic mortality during it's lifetime - predation, deforestation, extreme weather, erosion, natural disasters, contaminants, humans, disease, parasites etc. (rather than intrinsic dying of old age).
A lot of plants go through some kind of apoptosis, where cells are programmed to die. Plants such as annuals, biennials etc. die after a few months or years in a programmed way. It is difficult to say whether long lived species of trees would do the same after a few thousand years of life, because we just don't get to see many reach that stage of life, or if the mechanisms causing it have been suppressed (which could explain their long life).
Luke has posted a very thorough answer on the cellular and genetic aging of plants here. And to quote him:

"...it seems to me likely that plants may also have enhanced maintenance
  against other cellular stresses than DNA damage, such as build-ups of
  aberrant proteins. It therefore appears that in a protected
  environment some plants could live indefinitely"

Wikipedia has some very good pages on the evolution of senescence & aging. This article has also a good section on plant aging and I hope you can access it.
and finally, if you want to have a laugh, take a look at this entry on plant immortality and aging from creationwiki.org...

"Plants are actually or potentially immortal organisms that will live
  indefinitely provided their environmental requirements are met. In
  striking contrast to plants, humans and animals have a maximum life
  expectancy regardless of whether their needs are fulfilled. Although
  it is true that some plants grow as annuals, all plants are actually
  perennials by nature, and have adapted to a programmed life cycle in
  some instances to match growing seasons. Otherwise, plants only die
  because of biochemical starvation or disease. If their physical
  requirements are met, plants will grow indefinitely."

Some great clear science there, well done creationists... but it's just plain wrong.

Since meristems (the parts of plants from which growth happens) are constantly creating new stem cells, plants have a theoretical capacity for immortality. Of course, in practice, the vast majority of plants still senesce and die. But there are some notable exceptions such as bristlecone pines and quaking aspens which live for thousands of years. If you consider new individuals produced through clonal reproduction to be extensions of the original individual, then even more plants could be seen as immortal.

In addition to the above answers, the answer to your question also depends on your definition of immortality. There are a number of clonal organisms (the most famous of which is probably Pando, a quaking aspen https://en.wikipedia.org/wiki/Pando_%28tree%29 ) where there is a large area, sometimes multiple square miles, where individual shoots are sent above ground, giving anyone in the area the impression of a forest, but all of the trees are connected underground in one single large root system.
Such an organism could certainly be considered immortal, as its stems will constantly die off and be replaced by new organic material, enabling the network as a whole to live for tens of thousands of years (so far).


text:
Determine which gene is in the middle complementation

Possible Duplicate:
Crossing mutant strains on minimal media problem

I'm studying this problem for my genetics final:

My Attempt:   The answer for part B is met2 and the answer for part C is Df1.  Met2 and met 1 both have 1 no so i'm not sure how met2 is in the middle.  I didn't even know complementation tests could tell gene location. I think the answer to part C is because df1 has the most NOs, which means it's missing the most DNA.  (If it had that DNA, it would complement).

Please don't ask a duplicate question, you can just edit your own posts to add more information. I copied the content of this question into your older one, and will delete this one soon.


text:
What determines the thickness of Cornea?
In eye-operations such as Lasik and Femto, the thickness of cornea is key decision factor whether the operation is feasible. A normal thickness is between 500-600 µm. Cornea consists of a very special tissue having no blood supply and no vessels so it gets nutrients through diffusion of tear fluid and oxygen directly from air (hence in a way, it has its own respiration system not dependent on lungs).
Now I started to think the following questions:

I. What determines the thickness of cornea?

Helper questions

II. Is the thickness of cornea determined genetically so twins have the same cornea thickness?
III. Is the thickness determined by the environment and psychological things? Eg. how does diving affect cornea? Look it cannot get oxygen anymore through the air with the mask. What about drying? Does cornea gets too much nutrients all of a sudden from eye fluids?
IV. Does Homo Sapiens have more this kind of independent tissues? What about other animials? What determines the thickness of Cornea there?

"What determines the thickness of cornea? " - As you mentioned the efficiency of diffusion is the main size limitation factor here. I don't know much about the topic btw.

The corneal thickness is genetically programmed. There are multiple genes that induce the final corneal thickness:
USP37, Chromosome 2;
GPR15, 3;
TIPARP, 3;
CWC27-ADAMTS6, 5;
RXRACOL5A1, 9;
LCN12-PTGDS, 9;
FGF9-SGCG, 13;
and at least 6 other genes.
source
other questions had to be asked as separate ones


text:
What does breathing through the mouth have to do with cracked lips?
https://www.healthline.com/health/mouth-breathing#symptoms3

Symptoms in children
Children who breathe through their mouths for most of the day may also have the following symptoms:
...
...
dry, cracked lips
...

Why can breathing through mouth result in dry, cracked lips?

Breath is humid. Constant addition to humidity to lips and then the drying of that humidity will dry up the lips, similar (but not as quickly) as licking the lips does.

breath varies in humidity and with temperature. lips crack fairly easily. increased airflow can cause dehydration. it's vague guidelines

You may notice waking up with chapped lips at times. It may be because of sleeping with your mouth open. So, of course you breathe through your mouth all night, leaving it exposed to continuous flow of your breath. Continuous airflow around the mouth region can cause chapped lips in many individuals.


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Hardy Weinberg Equilibrium after 5 Generations
1
There is a population not at HWE where red eye = $a^+$ (dominant) and white eyes = $a^-$.
If:
$a^+/a^+ = 0.6$
$a^-/a^+ = 0.1$
$a^-/a^- = 0.3$
what are the frequencies of the $a^+$ and $a^-$ alleles?
My attempt: So if it's not at HWE then I should divide the heterozygotes equally to get $a^+ = 0.65$ and $a^- = 0.35$.
2
We are now at HWE.  What are the frequencies in the next generation?
My attempt: so if $a^+ (p) = 0.65$ and $a^- (q) = 0.35$ then $p^2 = 0.42$ and $q^2 = 0.12$.  Then using $p^2 + 2pq + q^2 = 1$, I can figure out that the heterozygotes make up $0.46$.  So the frequency of the $a^+$ allele is $0.42 + 0.46 = 0.88$, and then $a^-$ should be $0.12$ (because they should add to 1)
3
What is the frequency 5 generations later in HWE?
My attempt:  Wouldn't it be the same answer as #2. I'm not sure how more generations in HWE would change the allele frequencies.

You are almost correct, but with a few modifications/comments.

The calculations in Q1 are independent of HWE, and are just calculating the current allele frequencies in the population based on genotype frequencies (i.e. would be the same irrespectively of if the population is in HWE or not).
In Q2 it is unclear if the questions is asking for genotype frequencies or allele frequencies. Your answer of genotype frequencies of $p^2=0.42$ ($a^+a^+$), $q^2 =0.12$ ($a^-a^-$) and $2pq =0.46$ ($a^+a^-$) is correct if you assume the allele frequencies from Q1 and HWE. However, your allele frequencies are incorrect and should be $p = 0.42 + 0.46/2 = 0.65$ and $q = 0.12 + 0.46/2 = 0.35$, i.e. the same as in Q1. Remember that the allele frequencies shouldn't change under HWE.
Yes frequencies should not change in Q3. This is the textbook definition of HWE, i.e. that allele and genotype frequencies remain constant between generations in the absence of evolutionary forces (i.e. under the HWE).

thanks.  for #1 I thought that i calculated the correct allele frequencies (im given genotype frequencies).

@Kirby Yes the numbers in Q1 are correct, and I was only commenting on that you wrote "So if it's not at HWE then I should ...". The calculation of frequencies (as $p = f(a^+a^+)+f(a^+a^-)/2$ and $q = f(a^-a^-)+f(a^+a^-)/2$ ) is valid with or without HWE.

ok.  for #2 you said that p^2 = 0.35, but isn't that just p and p^2 would be 0.42?

@Kirby Yes correct. That was a typo on my part. Allele freq $p = 0.65$ and genotype freq $p^2 = 0.42$ ($f(a^+a^+)$).

@Kirby Feel free to mark an answer as 'answered' if you find it satisfying.

At generation 1, the frequencies of $a^-$ is $p=0.35$ and the frequency of $a^+$ if $q=0.65$.
Assuming random mating (and no change in allele frequency) after any number of generation is given by $p^2$ (=0.1225), $2pq$ (=0.455) and $q^2$ (=0.4225).


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Have creatures ever evolved to become less intelligent?
Inspired by https://worldbuilding.stackexchange.com/questions/58533/is-intelligence-the-natural-product-of-evolution , I'm wondering if creatures have ever become less intelligent as a result of natural selection and evolution.
It seems plausible, because the brain can use a lot of energy, and I've heard of other aspects of an animal atrophying because they're not useful any more, such as vision in the Mexican blind cavefish.
One possible candidate I can think of is the koala: it's described as having a low brain to body mass ratio, doesn't have a great need for intelligence, and may have a need to minimise energy usage.
I'm mainly interested in cases of natural selection, as opposed to artificial breeding - I wouldn't be surprised if we selected animals to be less intelligent.

Unfortunately, measuring intelligence (assuming we would have a strict definition) is not a thing that can be done from fossil record or genetic data. The only thing one can do is to compare brain mass (or at least size of the cranial cavity) from fossil record. In this regard, no need to go very far for an example, humans are an example. From wikipedia

The evolutionary history of the human brain shows primarily a gradually bigger brain relative to body size during the evolutionary path from early primates to hominids and finally to Homo sapiens. Human brain size has been trending upwards since 2 million years ago, with a 3 factor increase. Early australopithecine brains were little larger than chimpanzee brains. The increase has been seen as larger human brain volume as we progressed along the human timeline of evolution (see Homininae), starting from about 600 cm3 in Homo habilis up to 1500 cm3 in Homo sapiens neanderthalensis which is the hominid with the biggest brain size. The increase in brain size topped with neanderthals; since then the average brain size has been shrinking over the past 28,000 years. The male brain has decreased from 1,500 cm3 to 1,350 cm3 while the female brain has shrunk by the same relative proportion.

Note however, that wikipedia does not cite any reference and I failed to find one!
Note, also that one should not confound cranial cavity (the thing that is actually measured) with brain size and more importantly no confound brain size with intelligence. Wikipedia goes on saying

However it is argued that another essential element of brain evolution in humans is rearrangement (Hoffman et al. 2004). Larger brains require more wiring, but more wiring can become inefficient (Hofman 2001). The brain has therefore become reorganized for efficiency. Furthermore, the average body size of nethanderthals was larger which led to bigger brain size (see Brain-to-body mass ratio).

I could not find the Hofman papers but I probably just did not look hard enough (and am a bit tired right now)! One might want to read Healy and Rowe 2007 for a criticism of the inference that can be done from measures of cranial cavity.

Domestication is often given as an example, though it seems to be debated.
I'm guessing almost all parasites have become less intelligent in their evolution to parasitism, you could probably find some slam-dunk examples there.
More specific but anecdotal and possibly opinion-based, I recall in the book "Adventure among the Ants" the author draws a line between the size of an ant society and how competent and intelligent its individual members are. He specifically talks about how ants evolved, how the species with the biggest colonies are comparatively recent, and how there is an inverse correlation between an individual ants' size, brain size, complexity of behavior etc and the size of the colony it's a part of.
In other words, the evolutionary history of ants involved the evolution of larger and larger colonies, and in the lineages where this happened, as the species evolved to exist in larger colonies, the individuals in that species evolved to become simpler and less intelligent.
You could plausibly find examples if you look for examples of organisms that evolved to be smaller - if only because that can involve smaller brain size.

Yes, there is one great example just off the top of my head,Tunicates which have evolved to lose their brain as they mature. The simple reason this happens is brains are expensive they cost calories and material that could be spent elsewhere so just like anything else under the right conditions (when they are not helpful (such as in sessile filter feeding sea squirts) a reduction and/or lose will be favored.


text:
Improving throughput of CFU plating?
In a separate question I've described my general experimental setup where I need to measure the number of live cells in a growing bacterial culture in a fairly rapid and high-throughput manner. In that question I'm asking if there are any alternatives to the gold standard of CFU plating for making this measurement. As I wrote that question, it occurred to me that if I could just make CFU plating easier to do with lots of samples (esp. using fewer plates), then this method could work just as well. So my question here is if there is a way to make CFU serial dilution plating easier when I have to measure the number of live cells in 7+ different growth conditions every hour of growth?
Thanks!

see my answer on your previous question - I'm not sure you'll be able to get much more high-throughput than that :)

Thanks, @MattDMo. I agree that the Cedex machine is more high-throughput, but I am looking for any neat tricks people have tried to make CFU plating more economical. For example, one idea would be to put agar in each well of a [12 well plate][1] and do 12 samples at a time; then the question would be if people have tried this and the reduction in available area for counting made the CFU counting significantly less reliable. Or something like that. [1]:http://globebio.com/plates/multiwell-plates/suspension-culture-sterile-multiwell-plates/12-well-cell-culture-plate-with-lid-sterile.html


text:
Why aren't D-amino acids used in proteins?

Possible Duplicate:
Why are amino acids in biology homochiral?

Why are only L-amino acids used in protein construction, and not D-amino acids?

We already have a question about the number of amino acids used in proteins, so I edited your question to be only about the second part of your original question.

We also have Why are amino acids in biology homochiral?

I personally (not base on Lab works) think, maybe structure of  translation related proteins and RNAs, is the cause of these. I'll carefully read your suggested links.

I could give citations of where D-amino acids are in fact used in proteins; however I'm not sure that would count as an answer to this question.


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Why does having cold hands hurt?
(1). Why does having cold hands create a painful sensation?
Is it a physical effect, maybe a protection mechanism from evolution?
(2). Why, if one's hands are cold, does it feel as if they are more susceptible to pain?
Note: I have (2) as a separate question because the painful sensation in (1) refers to that from the coldness, whereas in (2), I mean that certain 'ordinary tasks' would feel painful, for example, holding a shopping bag.

You may want to have a look at: http://biology.stackexchange.com/questions/371/how-is-temperature-sensed/

For question 1 it's just a biochemical response from thermoreceptor nerves in the skin, temperatures that are likely to cause lasting damage from prolonged exposure cause a neurological response - in this case it's pain.
In address to question 2 it is most likely down to the physiological response of vasoconstriction.
When the body is cold the body undergoes constriction of the blood vessels in the extremities to preserve core temperature where it is more essential for the proper functioning of vital organs. By constricting blood flow to the extremities (in this case the hands) there is less volume of blood present, because of this nerves present in the hand are closer to the surface and thus more sensitive to pain.

It doesn't matter if its hand or any other human body organ, cold would hurt, the reason being that we humans being warm blooded animal require an optimal temperature-pressure balance to be maintained for our nervous system to work in its natural order.
So when we have, in your case, cold hands its like a thermal shock to our hand as the above mentioned functional optimality is hampered, and just similar to a hot ceramic cracking due to cold water poured on it, our hand(would not crack, however might in extreme cases) reacts to  this with the sensation termed as Pain.
This is a common answer to your questions, cold is directly proportional to pain being felt during our daily engagements(like holding a bag).
Pressure plays a vital role in this too as when your hand is cold the pressure exerted to the epidermis is at a reduced rate, which is another reason for the same.
Hence commonly my conclusion would be the Temperature-Pressure Factor.

It has to do with the way that body parts are more rigid when it is cold. This makes them less flexible and more prone to superficial injury....even without frost nip setting in. In the event that actual frost nip set in, this would be even more sensitive, as you have tiny crystals beginning to form in your cells, like little shards of glass......and, smacking them, rubbing them, or scraping them would be like SMACKING, RUBBING, or SCRAPING your neutral temperature hand against shards of glass.
When it is cold, your nerves are very sensitive to the temperature, as it isn’t numb yet, and still....blood flow is slowed down tremendously. In fact, your body has begun "vaso-constricting" all blood flow away from your extremities, resulting in nerves being pressed upon by the less supple skin and vascular tissues.


text:
I photographed a couple of butterflies and birds in Argentina but can't identify them. What are my options?
I photographed a couple of birds and butterflies in Argentina and tried to identify them. I tried online species identification tools, looked in books, and just tried to find pictures on Google with similar animals. This worked for some of the pictures, but for others I couldn't find the correct species. So as a layman, what options do I have?
Here are the ones that I couldn't identify so far
1 (There seems to be a bird and a beetle in this picture. The bird could be a Thraupis Episcopus)

2 (A hummingbird but which one?)

3 (Seems to be the same hummingbird)

4 (No idea)

5 (No idea)

6 (No idea)

7 (No idea)

8 (No idea)

What most people do to identify is, well, Google "Birds (or butterflies) of Argentina" and narrow down the categories by beak type, tail type, etc. I know you have a dove, a hummingbird (should be easy), what I believe is a vulture, and one of the most common of parrots. That should start you off.

To 1: I am not quite sure if this is a beetle. It could be a piece of banana that was stuck to the tree. possibly to attract birds. Something black is sticking out of it close to the "center". And the bird also has this "don't touch my food"-look.

Each of these would probably be a good question by itself, but asking for 8 separate identifications is too broad for a single question. I think this should be broken apart into separate questions.

First, I think it is more useful to post separate questions, at least for each taxonomic group (birds, butterflies etc). To make a question a dumping ground for all sorts of species determination pictures is a bad idea.
That said, the butterflies seem to belong to the families Nymphalidae,  (nr 5) and Papilionidae (Swallowtails) (nr 7), judged by overall apperance. I'm not directly familiar with South American butterflies, but two likely species are:
Doxocopa agathina (Nr 5), or related species in the Doxocopa genus.

(from wikipedia commons)
Papilio thoas (Nr 7)
This is the King Swallowtail, your specimen probably of the subspecies P. t. brasiliensis which is found in Argentina. Sometimes the name Heraclides thoas is used. Pictures of subspecies can be found here: Butterflycorner.net. Your speciemen have lost the tail appendages (could be due to wear-and-tear or bird attacks). A related similar species is Papilio astyalus, which is also found in Argentina (pictures), but it usually has a broader yellow band.

(from wikipedia commons)
The bird in nr. 6 looks like a Black vulture (Coragyps atratus).

To answer your question as written, the best option I have for species ID is still to post to fora (such as this one), where experts (or interested amateurs like myself) can manually identify them. Computer identification, although much better nowadays, is still some way away from being able to recognise all species.
4 looks very much like a Mourning Dove Zenaida macroura, although its range seems to be limited to North America.
Going up its taxonomy I found the Eared Dove Zenaida auriculata which does live in Argentina.

8 looks like a collection of macaws, with the Blue and yellow macaw and the Scarlet macaw being visible.


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How to use mechanical microstrainer to extract tissue proteins from human?
Background:
There are many methods to extract proteins form human tissues out there. The majority of them use an extraction buffer containing variable concentrations of detergents and protease inhibitors to preserve the extracted proteins as much as possible and keep them functional until being analyzed by downstream applications, like western blot, ELISA, etc. One drawback of this chemical extraction is the interaction of the buffer components with antigen-antibody binding in the analysis. The interaction is sometimes difficult to predict, therefore, validation of the sample matrix is necessary before going into the real analysis, e.g., for ELISA, spike-and-recovery, linearity-of-dilution are two known validation assays to this effect. For more info about these two assay you may find this answer useful.
One optimal way would be to avoid such interaction by avoiding the use of extraction buffer altogether and using mechanical methods plus protease inhibitors, instead. I don't know the drawback of this method, but one may be it is not as effective to get cytokines out their vesicles to be accessible by assay analysis.
Questions:

How to use Microstrainer as a mechanical substitute for protein extraction in human gastric tissue?
What are the pros and cons of using the Microstrainer?
How effective is it to measure human cytokines from tissues?

what is a micro strainer?  is this an idea you have or a reference to a specific piece of equipment?   several methods of the sort you have described may be used, but i've not heard of a microstrainer...

@shigeta, it is some sort of milli-pore filter that would disrupt tissue by vortexing. I have never used it, here  you can find a reference that used it.

thanks - never used it so can't comment - sounds cleaner and more $$$ than a hydraulic press, a bead beater or other similar methods.. :)


text:
Carrying or packaging capacity of SAD B19 dG rabies virus
I'm wondering about the carrying capacity also referred to packaging capacity or loading capacity (how many base pairs can be packed efficiently into virions) of the pseudotyped rabies virus SAD-dG as described in the Wickersham, Callaway publications.

Wickersham, I. R., Finke, S., Conzelmann, K.-K., & Callaway, E. M.
(2006). Retrograde neuronal tracing with a deletion-mutant rabies
virus. Nature methods, 4(1), 47–49. doi:10.1038/nmeth999
Wickersham, I. R., Lyon, D. C., Barnard, R. J. O., Mori, T., Finke,
S., Conzelmann, K.-K., et al. (2007). Monosynaptic Restriction of
Transsynaptic Tracing from Single, Genetically Targeted Neurons.
Neuron, 53(5), 639–647. doi:10.1016/j.neuron.2007.01.033

I have gone through quite a number of papers using this virus, but I haven't found any definite answer on the maximum insert length. There is an indirect answer, though. The two articles cited below both report possible insert length of up to 3.7kb without any experimental problems. This insert length results in a viral genome which is about 1.9kb longer than naturally occurring. So at least 3.7kb insert length are possible, if longer inserts can also be used, needs to be tested.
References:

Design and generation of recombinant rabies virus vectors.
New rabies virus variants for monitoring and manipulating activity
and gene expression in defined neural circuits.


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What's the percentage similarity between human individuals (and other primates) when comparing only exons?
In popular science books and articles, I often see it stated that humans are >99 % similar to each other (wikipedia has it a 99.5 %, referencing Craig Venter and this PLOS Biology article) and ~96-99 % similar to chimpanzees or bonobos (Smithsonian Institute, National geographic). I have previously thought that this referred to the entire genome, but the wording on the Smithsonian Institute page I linked, makes it appear that it might refer to genes only, which also seems to be the case according to the answers to this post Do apes and humans share 99% of DNA or 99% of genes? What is the difference?.
How big are these percentages when comparing only the coding regions (exons) instead of entire genes, both within our species and compared to other species, such as primates? And, not as importantly, what are these numbers when including the entire genome with all non-coding DNA?

One of the references to the chimpanzee genome paper linked by Maximillian is Inferring Nonneutral Evolution from Human-Chimp-Mouse Orthologous Gene Trios, where the authors seems to have focused on exons only:

Here we apply evolutionary tests to identify genes and pathways from a new collection of more than 200,000 chimpanzee exonic sequences that show patterns of divergence consistent with natural selection along the human and chimpanzee lineages.

They conclude that:

Perhaps the best way to understand the relation between DNA sequence divergence and the differences between human and chimpanzee physiology and morphology is to compare these differences to the variability among humans. Human-chimp DNA sequence divergence is roughly 10 times the divergence between random pairs of humans.

Unfortunately, they didn't compare this to the fold-difference of non-exonic DNA, so the comparative quantification between coding vs non-coding regions remains to be determined.
However, this does directly answer the question of how big the genomic differences are between individuals of the same species vs those of other species, when comparing only coding regions. I also found it useful to quantify the differences in these relative terms in addition to the previously stated percentages.

This paper seems to have relevant estimates for human-ape divergences. Note again that it isn't using the entire genome, but selected regions of exons, introns, pseudogenes, etc. The chimpanzee genome paper has a nice bullet-point list towards the beginning of relevant statistics for you for that species specifically, that is on the order of 1% overall. The section on "gene evolution" has some specific numbers for coding sequences.
For among-human variation, there is a bionumbers page on that subject based on 1000 genomes project numbers, that comes out at 0.1% divergence among humans.

Correct me if I missed something (didn't read the entire paper), but doesn't the first paper you linked specifically not use coding regions? From the abstract: "...we selected 53 autosomal intergenic nonrepetitive DNA segments..."

The chimpanzee genome paper states: "When CpG and non-CpG sites are considered separately, we find that both CpG sites and non-CpG sites show markedly lower divergence in exonic synonymous sites than in introns (~50% and ~30% lower, respectively)." To me this indicates that the interspecies differences within exonic regions would be smaller than within intronic regions...

...My understanding is that this is due to the survival constraints put on exonic regions, i.e. some exonic mutations kills the organism and will not be passed on to the offspring, while mutations in non-exonic regions don't impact survival to the same extent. This is not my area of expertise though, so I am happy to hear if I have misinterpreted something.

First comment: note that Table 5 of the first paper compares coding region distances. Again, probably not the best example because it's only selected regions; but in my experience these estimates tend not to change that dramatically with sample size.

Comments 2+3: You are correct that the mechanism for the lower rate of divergence in exons is due to selection. Indeed, the inference of functionally important chunks of sequence by comparative analysis depends on this; see for instance http://compgen.cshl.edu/~acs/phylohmm.pdf. But that didn't seem to be part of the original question. There is a very large literature on this subject, but for a concise review by a well-known author you could look at http://www.sciencedirect.com/science/article/pii/S0959437X02003489. Note that among-site variation in divergence is also important in proteins.


text:
Why would mutation rates increase in a tumour?
This article describes a tumour:

Swanton found that even the primary tumour was surprisingly varied. He found 128 mutations among the various samples, but only a third of these were common to all of them. A quarter of the mutations were “private” ones – unique to a single sample.
The tumour had also split down two evolutionary lines. One area – part of R4 in the picture – had doubled its usual tally of chromosomes and seeded all the secondary tumours in the patient’s chest. The other branch had spawned the rest of the primary tumour. Even though this tumour looks like a single mass, whose cells all descended from a common ancestor, its different parts arehave all  evolved independently of one another.

My understanding is that if non-cancerous cells normally had such a rate of mutation it would be lethal to the cell if not the organism.

What about tumour cells would lead to a higher incidence of mutation?
How are these cells able to survive when non-cancerous cells would perish?

You should read "Hallmarks of cancer: the next generation" by Hanahan and Weinberg - it's a great open access review that covers your question http://www.ncbi.nlm.nih.gov/pubmed/21376230

All cells perhaps have the same likelihood to be affected by some deleterious mutation. When you say "the cancer survives", you do not talk about all the cells in the tumour tissue. Eventually, there may be a few cells that survive and they expand the population.

Cancer cells generally lack the "safety mechanisms" or "check points" that prevent normal cells from replicating, and some of these mechanisms are also involved in ensuring that DNA replication proceeds without serious errors. Inactivating these safety mechanisms lets cancer to cells divide rapidly, but at the same time also causes their genome replication to be "sloppy", introducing various errors.
The P53 protein is probably the most well-known example of such a "safety mechanism". In normal cells, P53 arrests the cell cycle if breakage occurs in the DNA strands; but cancer cells often inactivate P53, and consequently they tend to proceed with DNA replication even if DNA is damaged. A consequence is that DNA is often in a state of disrepair in cancer cells. (A review of P53 here.)
This lack of proper "quality control" can lead to loss of large pieces of the genome, even entire chromosome arms. While it may seem strange that the cells can survive this, keep in mind that the genome encodes information to support the complex working of an entire organism. Loss of a chromosome arm would indeed be lethal to the organism as a whole --- perhaps it would disrupt brain development, or the immune system. But for single cell to survive and develop, most genes are actually not essential, likely because there are so many redundancies. This is frequenly seen in genome-wide RNA interference screens, for example this paper. Remarkably, cells can even lose the entire mitochondrial DNA (which means they cannot even respire anymore!) and still survive.
It is not clear that "non-cancerous cells would perish" if they would similarly lose DNA. They would likely arrest and turn senescent because they detect DNA damage, precisely because of these safety mechanisms --- but that is different. The loss of genes in itself may not be lethal to a normal cell, it's rather that normal cells "choose" not to continue when this happens. But this distinction is probably difficult to test experimentally.


text:
What is the connection between sleep requirement and age?
By this question: Is the human biological clock genetically programmed or learnt? we discussed that the sleep requirement depends on the age of the individual.

- Figure 1. - Sleep requirements by age - ref
I thought I ask the question, why?

I believe the current theory is that it is related to cell loss in the intermediate nucleus of the human hypothalamus. They have shown sleep disruptions due to lesions of the hypothalamic ventrolateral preoptic nucleus in rodents, and found that the intermediate nucleus in humans is homologous and shows a reduction in size in older adults that is correlated with sleep disruptions. http://brain.oxfordjournals.org/content/137/10/2847

Has any causation been shown on this correlation?

I'm late to this answer, but this seems incredibly simplistic (especially given how unsettled the scientific understanding of sleep is) and not really related to the issue of sleep "need" but simply a single possible explanation for age related sleep disruption. You could have sleep disrupted and yet need sleep, or have sleep not disrupted and yet not need it per se - they are completely separate dimensions.


text:
Why does mud therapy work by some pain related diseases?
Apparently, some users here agree there is no ion exchange through the skin. Mud therapy has some therapeutic effect for pain related diseases. As an anecdotal example, I experienced pain relief by treating my sport injury using mud therapy. If it is not ion exchange, then what is the mechanism behind mud therapy?

Never underestimate the power of the placebo effect, especially in pain related disorders. Treatment can change neuronal signaling, which can in turn influence gene expression. It may be as simple as the increase in buoyancy relieves force on the affected tissue, and this in turn allows a different series of neurotransmitters to be released. The article you linked to makes it sound like there is a significant immunological component, so if you can influence the chemokines in the area of injury, you may be able to reduce inflammation to a certain degree.

@AMR Placebo is about 3%, it is significant, but you cannot explain everything with it. At least show some placebo controlled study in the topic, if you claim, that it is only placebo.

it is my opinion, that is why it is a comment and not an answer. However anything that can change cell signaling has the potential to change gene expression, and the study linked to apparently showed a change in levels of protein products that was statistically significant.

Here is a review article that asks the question "How can placebo effects best be applied in clinical practice?" You will likely have to dig into the references to find quantified studies, however, in the their summary, the authors state "Placebo effects have been demonstrated in a number of experimental trials and clinical studies. These effects cause physiological responses, such as reduced activity in the pain-sensitive areas of the brain."

The answer on the linked question is apt: transdermal administration of medications or other compounds include exclusively lipophylic compounds, i.e. uncharged 'fatty' materials, such as nicotine, opiate-bases and steroids. Minerals, like those found in clay, are highly hydrophylic and are therefore unlikely to be taken up by the skin.
A search through a bunch of articles makes me believe that mud therapy has mainly a thermal effect, i.e. a mud pack heats the underlying tissue and thereby relieves muscle spasms and pain (Espejo-Antúnez et al., 2012; Liu et al., 2013).
References
- Espejo-Antúnez et al., Rheumatology (2012); 258: 1-10
- Liu et al., J Int med Res (2013); 41(5): 1418–25

I heard/read from a non scientific resource that mud with high sulfur content was the only cure of lead poisoning in the old times, because of the Pb2+ + S2- = PbS type of reaction. I have not found any proof of this. It is hard to find old articles in the topic. :S If Chris is true (and I think he is), then this type of reaction does not happen, because there is no ion exchange, so mud therapy did not help by heavy metal poisoning. Unless... I don't know. :D Maybe if the heavy metal is not in an ionic form, e.g. Hg can be absorbed through the skin.

@inf3rno The most toxic forms of mercury are the organomercury compounds, for the exact reason that they are hydrophobic and can thus pass through the skin and into fat stores where they bioaccumulate. I don't know how easily you could draw them back out through the skin, but if possible, then sulfur chelation might work.

@Filipq I'll try to find some evidence about this kind of mud therapy later. Currently I have other things to do, maybe next weekend.


text:
Sewall Wright for dunces
[This is one more post in my growing "X for dummies/idiots/morons/etc." series.]
I've been enjoying Provine's The origins of theoretical population genetics for the last couple of days, but I must confess that I find his description (on pp 127-8) of the logic behind Sewall Wright's (and W. Castle's) selection experiments with "hooded rats" about as clear as if it had been chiseled in Linear A...
Which is really bumming me out, because I'd love to understand these experiments.
Does anyone know where I can find a description of these experiments aimed at those with only a very limited grasp of classical genetics?  (I took a graduate-level genetics class a billion years ago, and I did not find it easy.)

I think there might be several places to read a description of these experiments, but they are discussed extensively in a book by historian-philosopher Lindley Darden, entitled "Theory Change in Science: Strategies from Mendelian Genetics", parts of which are available online.  See p. 112 of Darden's book for references to other accounts of these experiments by historians E.A. Carlson (1966) and W. Provine (1988).
Everyone knows what Castle did but his aims have been obscured by "Synthesis Historiography" (i.e. making things turn out right for Ernst Mayr and his homies).
What Castle did was to breed rats in the laboratory and implement selection on coat patterns, with such success that he has able to get a large seemingly continuous range of forms. Imagine breeding oreos, with one line of selection of darker forms, and one of lighter, and achieving the success of getting both pure-black or pure-white oreos, and then lining up all the oreos from black to white to show the continuous range of forms.
The story that we hear from people like Wright and Provine is that this proved that selection can work on continuous variation, an idea that the "mutationists" allegedly rejected, paving the way for acceptance of Darwinism.
Yet, while the experiments may have helped one version of Darwinism, they also represented the dying gasps of another form of Darwinism-- the form that Darwin proposed and Castle was (partially) defending.
You can get an inkling of this from p. 143 of Provine's book, where you will find a curious confession, made in passing.  Provine is explaining why Pearson did not want to publish Fisher's famous 1918 paper.  He writes "Pearson claimed, and Darwin would probably have agreed, that the continuous variations in a pure line were heritable and that continued selection in a pure line should be effective."
Why would Pearson believe-- 17 years after the rediscovery of Mendelian inheritance-- that the environmental variations in Johannsen's pure lines were suitable material for selection?  The reason is that this is what Darwin believed, and Pearson was a follower of Darwin.  Darwin's "indefinite variability", the fuel for modification in his theory of "natural selection", described in Ch. 1 of the OOS, is clearly a description of environmental variation-- it is always present and emerges anew every generation in response to "conditions of life" (see Winther, 2000).  Darwin knew about "definite" single variations or "sports", which could be inherited perfectly (whereas indefinite variations were inherited by blending), but he didn't think they were important for evolution.  Darwin bet on the wrong horse, as Johannsen showed in 1903.
Pearson, Castle, and others defended Darwin's original view well into the 20th century.  They were not satisfied with the idea that selection merely sorted out stable Mendelian factors that undergo rare mutations.  Instead, they held out hope that there was some other form of heredity, or that the Mendelian units were squishy and underwent continuous shifts in potency under conditions of selection.  Thus Castle and Phillips in 1914 argued that "the unit character for hooded pattern is itself variable"
Muller, Sturtevant and others from Morgan's lab disagreed, arguing instead that there were simply various Mendelian modifying factors in the background affecting coat color.  There was a long-running dispute over the proper genetic interpretation of Castle's results.  If you want a very clear statement of the dispute, go to a 1916 article by Jennings, p. 287:

"Castle finds that in rats he can, by selection, gradually increase
  of decrease the amount of colour in the coat, passing by continuous
  stages from one extreme to the other.  As to this, he holds two main
  points:

The change is an actual change in the hereditary characteristics of the stock; not a mere result of the recombination of Mendelian
  factors.  This is the general and fundamental point at issue.
More specifically, he holds it to be an actual change in a single unit factor; this single factor changes its grade in a continuous and
  quantitative manner.

On the other side, the critics of these views
  maintain that the changes shown are not actual alterations in the
  hereditary constitution at all, but are mere results of recombinations
  of Mendelian factors.  And specifically, they find a complete
  explanation of such results as those of Castle in the hypothesis of
  multiple modifying factors."

A few years later in 1919, Castle recanted his earlier view and accepted the multifactorial theory (the development of which is described by Kyung-Man Kim, cited below).
And finally, the idea that the "mutationists" rejected selection on quantitative variation is mistaken.  What the mutationists rejected was selection on non-heritable environmental variations.  Johannsen's 1903 results were revolutionary because scientists at the time understood that they refuted Darwin's theory.  We don't "get" this today because "Darwinism" has been redefined to disentangle "natural selection" from Darwin's errant views of heredity-- see Jean Gayon's "Darwinism's Struggle for Survival" for more explanation.
References
Kim K-M. 1994. Explaining scientific consensus : the case of Mendelian genetics New York: Guilford Press. xxiv, 239 p. p.
Gayon J. 1998. Darwinism's Struggle for Survival: Heredity andthe Hypothesis of Natural Selection Cambridge, UK: Cambridge University Press.
Winther RG. 2000. Darwin on Variation and Heredity. Journal of the History of Biology 33:425-55.

I don't have access to Provine's book, and I can't describe the details of the hooded rat experiments, but here is an attempt to explain the importance of the work.
Darwin published “Origin of Species” in 1859. He proposed that modern species were all descended from ancestral species, and that evolution proceeded by natural selection. He believed that evolution proceeded gradually by an accretion of small changes (gradualism). The origins of hereditary change were, of course, unknown to Darwin.
Mendel’s work (published in 1865) was rediscovered in 1900, and gave rise to a school of thought referred to as mutationism.  Mutationist theories emphasised the importance of single factor changes with large effects, and placed these “leaps forward” at the centre of the mechanism for the generation of new species. This was in contrast to the biometricians who argued, in the Darwinian tradition, that natural selection acted on populations in which there was continuous variation. Extreme mutationists believed that continuous variation within a species had no relevance to the evolution of new species. Their view was that within a species most genes were fixed (100% wild-type allele), and that only mutations could create new species (‘hopeful monsters’). T.H. Morgan, for example, was a strong proponent of the mutationist theory, so this wasn't some minor controversy.
Sewall Wright joined the laboratory of W.E.Castle as an assistant in 1912, when he was 23. Starting with black and white hooded rats (white rats with black ‘hoods’) they instigated breeding programmes and showed that they could progress gradually, through a number of generations, towards all white or all black rats. The importance of this work was that it demonstrated that there was underlying genetic variation within this strain of rats that could be acted upon by selection (selective breeding) resulting in  gradual changes in coat colour. This provided strong evidence for the gradualist school.
By the 1930s the modern synthesis began to emerge, which combined mutationist and gradualist ideas: natural selection acts upon populations (gene frequencies etc.) but mutation provides the raw material that creates new variations in the population. Key to the acceptance of the modern synthesis was the development of a mathematical treatment of population genetics. This led to the current view of phenotypic  traits influenced by multiple loci, with natural populations harbouring genetic variability which can be acted upon by selective forces. We have all accepted this and so of course it is difficult to think ourselves into the controversies that existed in genetics at the beginning of the twentieth century.
Here is an article in which Sewall Wright refers briefly to his work with Castle, placing it in historical context. It also describes subsequent work with guinea pigs. This is a quotation from the article which underscores what I have written:

From assisting Prof. Castle, I learned at firsthand the efficacy of mass selection in changing permanently a character subject merely to quantitative variability. Because of this and a distaste for miracles in science, I started with full acceptance of Darwin's contention that evolution depends mainly on quantitative variability rather than on favorable major mutations. Thus, I have assumed that species are typically heteroallelic in tens of thousands of loci in which the leading alleles differ only slightly in effect, a situation that is maintained in a continually shifting state of near-equilibrium by the opposing pressures of recurrent mutation, diffusion and weak selection. Only a few loci at any time can show fairly rapid changes in allelic frequencies from strong selection.

Thanks for this summary (BTW, the first half of Provine's book is a chronicle of the biometrician/mutationist battle), the link, and the quote by Wright.  His is a clarity of understanding that we seem to have lost somehow.

@kjo So, you could have probably written this better yourself! Hopefully it will help other readers of your question and maybe you'll get the answer that you are looking for. I agree about clarity - it reminds me of the writing of AD Hershey, a "founding father" in a later generation of geneticists.


text:
How to obtain bacteria samples at home?
As the original question went from hold to closed, I thought I would write up a more appropriate question.
How should one go about getting bacterial samples to look at under a microscope at home?  How do professionals do it?  What if I want to look at cool pathogenic species like Salmonella bongori, Escherichia coli, or Bacillus anthracis?

Interestingly enough, PLOS just published an article about culturing Salmonella and other bacteria in field conditions. Here's the link to that paper by Andrews et al., and here's the Scientific American summary

There's nothing "cool" on killers such as Bacillus anthracis. The use of the word "cool" in association with B. anthracis suggests this is probably a kid, wanting to experiment. Or worse. With all the possible dangers involved. I strongly oppose releasing any information on how to culture it and I suggest the answer here being erased.

This is kind of pointless, since this knowledge is not secret. Anyone with access to a well-sorted library or microbial science publications can find out the conditions. Besides that, the real problem is doing this work without training. Most likely nothing (or only contamination) will happen.

I know, but then let them search it from themselves. That kind of "cool" knowledge shouldn't be provided to kids on a golden plate. I will be the first to plea for scienc education for kids, even if that involves some risk. But helping a kid culturing antrax? With all the risks it involves? Him being infected only being the least concern? No.

@guest did you actually read the post? You'll note that there's not specific instructions on culturing anthrax. That language in the question came from the comments and back and forth from the original post. I don't know if it would be on topic but if you wanted to make this a question, maybe a meta, I'd be happy to refute in detail. I don't think that there's any point denying that people will perceive more highly pathogenic species as "cool."

First, and I cannot stress this enough, you should not go seeking out human pathogens if you don't have the appropriate equipment to handle it at the right safety level.  That goes for all pathogens, even ones you might find around your house.
In a professional lab, you might get samples from collaborators, clinical samples, vendor, or really an number of other professional resources.  A well respected vendor as an example is ATCC, but the general public wouldn't be able to "shop" there.
But you really don't need to go far to get a whole host of microbes to study, you can grow them all at your house.  The basics of bacteria culturing can really be broken down to three steps: (1) get a source of bacteria, (2) put some of the bacteria in an environment where they can grow easily, and (3) harvest them to do something useful with them.
(1) Is fairly easy, bacteria are everywhere.  You can swab nearly any surface of anything in your house and come up with microbes (note you might also get some mold/fungi).  In this case (3) is easy as well.  Once you have culture you can streak it across a slide to view it under a microscope (you could also use several proper mounting techniques).  After all, looking at microbes under a microscope is the real goal here!
The only part of this plan that will take some real elbow grease is making your own culture dishes at home, but it's not as hard as you might think.

Making your own culture dishes:
1) The "plates" themselves.

I recommend getting the smallest Tupperware like containers your can
  find that are microwave safe, dishwasher safe, and really make a good
  seal (water tight at the least). They really don't have to be big, and
  you will make your life easier if you buy a bunch to match. They need
  to be super clean. After running them through your dishwasher at home,
  put them all in a boiling pot of water until you are ready to pour in
  your "medium." A mid-low simmer will work

Note that you won't probably be able to have perfect sterile technique at your house, but you should try to do what you can.
2) Your "Medium" or Broth

I highly recommend using pectin as your gelling agent if you can't get
  your hands on some agar. After that comes plain unflavored gelatin,
  but I recommend pectin. You can get it at almost any grocery store and
  my recipe is made assuming that. You can determine how much you want
  to make, just scale up the ratios. I'm going to list things as rough
  volume by volume so you won't need a scale.
i) Make the powder first:

45mL of pectin;
4 bouillon cubes ground as finely as you can (you can get different
  types and results depending on if you start with vegetable, beef, or
  chicken. I recommend starting with vegetable.);
125mL of refined white sugar;
Additives (more on this later)

ii) Mix the powder into 500mL of water.
Before you mix in the powder, heat the water to 50-75oC (mid low heat), but not boiling. Mix the powder in while stirring until
  dissolved.
iii) Bring the mixture up to a boil. Let it boil for about 2 min,
  stirring all the while.
iv) Cover the pot and let it cool for 4-5 min.
You by no means want it to cool down to room temperature, you just want
  to get it a little below boiling. If you are at 55oC or below it's
  definitely time move on.
v) Dip/fill your "plates" 1/3 full of media using clean/sterile
  utensils and seal while hot but not boiling.
You may have noticed this seems an awful lot like canning, and that's
  because it is. Again you want to be as clean as possible in this step
  and of course try not to burn yourself on anything.
vi) Let your media plates set and chill over night in the
  refrigerator.
You really probably only have to wait a few hours if you are anxious
  to get going. You are going to want to store the plates that you are
  not using in the refrigerator anyway. Also if you made a bunch of
  plates, let the cool on a counter before you put them in the fridge so
  that you don't raise the temp of your fridge too much.
Remember the thing about additives? You can play around with adding
  different amounts and different types of salts, vitamins, food, or
  other items to see how they affect the cultures you get to grow. All
  kinds of fun there. First go round, leave them all out.

Now you have your own home made culture plates! The above recipe was empirically tested by my childhood, and repeated by my son's. Not all pectin from the store may be equal, this is with Ball Classic (I have no relation to the company). I'd love to know people's results in trying it, because I might need to re-think how/what I'm doing to get it to work.
Go around your house swabbing things with sterile swabs (you can get these at a drug store), and then streak them out on plate. While it will be a little different with a swab and homemade plate, the idea is similar to what is done here.
Leave your plate in a warm wet place, but not in direct sunlight. Ideal temp is going to be around 37, but you can leave them above and below that and still get things to grow. On top of our dryer is where I leave them.
After a day or so you should have colonies you can streak out on a slide and look under a scope. You will find all kinds of things this way. If you want a more formal way to put things on a slide, you can check out dry and wet mounting from a Google search.
You are actually quite likely to run into E.coli if you sample enough "areas" this way. Obviously don't eat or huff the stuff that ends up growing. Maybe you can post some fun pictures of this if you try it.
As pointed out in the comments, if you successfully get bacteria to grow, then you will need to successfully get rid of them.  I should point that a good set of rubber gloves (that you can bleach and wash after use), or disposable gloves are a really good idea when handling plates that have grown bacteria.

Clean Up

First off, I want to clearly say that this stuff can clog a pipe.
If you tried to grow something on a plate, and you didn't get a colony that you can see with the naked eye (note some microbes might make CLEAR growths) you can probably just scoop the gel into the trash.
Note that I said probably.  If you swapped any part of your body, waste, or that of an animal you must decontaminate even if you didn't see anything grow.  On the plus side decontamination is easy.
If you did see something grow, or you otherwise need decontamination:
First make a 20% bleach solution in a large Tupperware like container (probably don't want to do this is a nice metal pot, but could do it in a junk one).  You can go as low as 10% bleach solution if you sure your bleach is NOT a cheap already watered down brand (like something bought at dollar store).  But just to be sure, I recommend 200mL of bleach in 800mL of plain tap water.
Drop your plates and lids into the bath (with the lid off) and let it sit for 10-15 min.  Then, working under/in the bleach solution with your gloves on, use a fork/spoon to get out the medium (it will be like thick jello).  Do this for all your plates, and you can do more than one at a time this way.
Once you have all the medium out and floating in the bleach, take the plates out and put them in the dishwasher.  Strain out the bleach/medium/funkiness you grew through a cheap colander (I recommend dishwasher safe plastic like PP).  Put what get's caught in the colander in the trash and take the trash out.  Wash the plates, lids, colander, and large container you used for the beach bath.
Slides
Slides present extra caution because they can break or shatter to create sharp edges.  For the most part, if you cover your sample with a cover slip, and seal it with nail polish, you can actually keep your slides indefinitely with little risk.  If you do decide to dispose of them, they should first go into a thick Ziploc bag (use an expensive freezer guard type bag for this) or into a Tupperware you don't mind throwing away.  If you never sealed your sample to your slide, you should also decontaminate the slide in bleach first (as above, with extra caution to not cut yourself).
If you are sophisticated enough to get microscopic photos of the microbes you see, by all means post them up and we'll try to ID them as best we can (many look very similar, and we use genetic or protein markers to get a true ID).

O wow, the formatting did not copy paste well.  If no one does it earlier, I will probably be able to work on the formatting tomorrow night.  I just don't have time right now.  If someone does it for me, thanks in advance.

Just wondering @Atl LED, pectin is of course a solid, so what is the concentration of the pectin solution that your recipe is based on. I've seen a 10% solution - does that sound ok? Or do you mean 45 ml of powder?

@AlanBoyd Crazy enough, I mean 45mL of powder.  If you look at most home cooking recipes they are given v/v, as is the recipe. For example, add 2 tbsp of sugar is a volume measurement.  I think most people won't have good scales at home.  Surely I won't be accosted for going metric here :).

I think this answer needs some information about safe disposal. I don't think you should be growing bacteria without knowing how to get rid of them safely.

@JackAidley Good point.  Decon & disposal added. +1 for the foresight.  Also thanks to the editors, you really saved me some time.

Have you considered growing the bacteria at 25°C to reduce the likelihood of pathogenic bacteria growing?

@MarchHo, Holding a temp accurately close to room temp is much harder than an elevated or refrigerated condition.  Our lab dropped some serious cash for an incubator that can really accurately maintain even 30oC.  At people's home, I just don't think you're going to get that kind of accuracy.  You'll note I said I put them on top of my dryer which tends to be 27-39oC (family is almost constantly doing laundry).

@AtlLED What I mean is that wouldn't it be safer to not place the bacteria in a heated environment, and just leave them in a cool, dry, shady area?


text:
What's the maximum pressure inside a bombardier beetle?
This question got me wondering about the pressure inside a bombardier beetle.
Lots of articles mention pressure, but don't specify the amount of it:

One study records the velocity of the spray to be within a range of 325 to a stunning 1950 cm/s.
  [...]
  Once the muscles around the reservoir squeeze the first amount of
  reactants through the valve into the reaction chamber, the resulting
  explosion causes the pressure to rise rapidly in the reaction chamber,
  forcing shut the one-way valve. The products of the reaction then exit
  the chamber with a pop and a puff, and the pressure inside the
  reaction chamber lowers again, falling below the pressure of the
  collection reservoir, which is still being squeezed by the reservoir
  muscles.

Calculating from the spray characteristics is beyond me.

According to this study, model data shows a maximum pressure of 110 kPa, that's 16 psi and only 1.086 atm:

The three-phase process involved in the beetles explosive secretory
  discharge (ESD) process. The inlet size is shown as a proportion of
  the inlet radius. During the first phase of refill and heating (blue),
  only the inlet valve is open. During the second phase (red), the
  chamber is closed. Finally, the third phase (marked by an arrow) is
  the exhaust phase, when only the outlet valve is open. This phase is
  significantly shorter than the first two phases. This cycle then
  repeats with phase 1 starting at approximately 5.1 and again at 7.8
  ms.