text:
Did cats evolve from monkeys ? or vice versa?
Did cats evolve from monkeys? or vice versa?
How similar are the genes of cats and monkeys?
What is the proof that they are related or that they are not related?
Most monkeys climb in trees and there are other similarities but I could not find any evidence on the internet.
Do cats and monkeys have a common ancestor?

I've +1'd this question because this question seeks a clarification in bold way from a common-people's view on the concepts of evolution, classification and similarities. To my views it is the common problem to many-other students because these concepts are often taught in a very unclear way any many people contains innumerable misconceptions about phylogeny trees and classification trees.

Cats and monkeys have a common ancestor, both are placental mammals, so at the very least they must have both evolved from the first placental mammal. Cats are members of the Laurasiatheria group and primates are members of Euarchontoglires. These groups of mammals probably split off from each other about 100 millionish years ago. For more information about mammalian phylogeny, look here.

"Evolving from another species" versus "Most Recent Common Ancestor (MRCA)"
One cannot say about two extant species that one evolved from the other. It just doesn't make any sense. It is not only true for cats and chimpanzees (just to pick one species of monkey) but it is true for any pair of extant species. One extant species has never evolved from another extant species.
However, one can say from any pair of species (Eventual exception with viruses but don't pay attention to them now) that they have a common ancestor. Again, it is not only true for cats and chimpanzees but also for yeasts and ants or for chestnut trees and reticulated pythons. The interesting question is always, "when did the MRCA live?" or if you prefer "when was the time when the lineage that will one day yield to cat and chimpanzee was living?"
Do cats and monkeys have a common ancestor?
Yes! All life on earth shares a common ancestor. The question of interest is when did the Most Recent Common Ancestor lived between cats and monkeys lived?
Please consider having a quick look to this post for an introduction to phylogenetics.
Chimpanzee and cats evolutionary relationships
This question has been answered by @user137. Cats and chimpanzee are both mammals. Their most recent common ancestor was therefore also a mammal and this most recent common ancestor lived about 100 million years ago. This is the kind of information you can get with DNA comparison.
How do we know that?
@user137 already linked to an article that shows when the most common ancestor of cats and chimpanzee has lived. If you want, you can learn more about how such inferences can be made. As you like mathematics (I read from your profile), you might be not too scared (although it will take some time) of statistics and algorithmic to have a look at those Wikipedia articles:

Phylogenetics - generality about phylogenetics (=the study of the evolutionary relationship between organisms)
Computational phylogenetics - How to build a phylogenetic tree
Molecular clock - One method to estimate the length of the branches in a phylogenetic tree.

To understand the stats, you may need first to follow a stats course, such as this one from Khan Academy but again it will take some time. Of course, aside from the multitude of tools that one can use to infer time to MRCA from genetic data, one can also make an inference from phenotypic comparison although this method is generally much less accurate.

'One extant species has never evolved from another extant species.' Are you sure about that? What about Homo erectus and other hominin species a few tens of thousand of years ago? H. erectus is both basal in the tree to H. sapiens and co-existed.

@AlexDeLarge Yes, I am sure of that! The examples you are given are those of sister species, not cases where one is the ancestor of another one.  This whole concept can be blurred by how inaccurate is the concept of species (see [here](How could humans have interbred with Neanderthals if we're a different species?)) but it is by large very much considered as if a species give rise to more than one species, then we ought to use two different species names for the descendents and therefore an "ancestor species" cannot live in the same time as a "offspring species"

I'm not convinced. If species A gives rise to two founder populations that, according to whatever species concept, maybe even quickly evolve into species B and C then B and C evolved from A. There is no necessity for A to get extinct or evolve into something like species A* in that reasoning.

A does not become extinct, it becomes either B or C if you want. The whole issue is an issue of how you decide to group lineages into species but pretty much everyone does the same. When there is a speciation event, the two extant species are both considered different from the ancestor species. This is mainly to avoid confusion and avoid to fail to recognize that all extant species have evolved for the same amount of time. Calling one an ancestor make it feel like some extant species would have less time to evolve.

It might be confusing, but the way you put it in your answer is not correct. In the example I give, A, B and C are all extant but the ancestors of B and C are members of A and this is by no means impossible.

Before answering the question; I need to become clear about the concept of common ancestry.
All groups of organisms seem to have only 1 common ancestor (earliest ancestor of all life-forms on Earth), as generally accepted.
While discussing about evolution; when people frequently talk about "common ancestry";
firstly, they talk about latest common ancestry. If we pick any 2 species without any basis (for-say a pea plant and a dog); and try to search back their latest common-ancestor; there should exist some-or-some life-form (usually extinct, commonly hypothetical).
secondly; that latest common ancestry too;  would must 'exist' between any 2 randomly chosen life-forms. Latest common ancestry is of not much use if we think it in a present-or-absent way.  It only makes sense when we use it in a quantitative way ("how much common or distant") within 1 particular lineage-of-interest.
Example:  in the following sample * phylogenetic tree;
Fig-1.

(* drawn on basis of this, this and this)

People often informally say "Macaca mulatta monkey and human have a latest common ancestor" or "cats and human have a latest common ancestor" but that would not make any useful sense. But it will make a proper sense only if we say "monkeys share more close common ancestry with a human than cats" or "cats share more close common ancestry with a human than plants". or more elaborately; "cats share more closer-distance of common ancestry with human than the distance of common ancestry cats share with plants."

An answer to your main question(s);

We can say neither of "cats evolved from monkeys" or "monkeys evolved from cats" in a true sense. They evolved from a certain group of organisms (their latest common ancestor) that doesn't exist today.

Here is a diagram from http://genomewiki.ucsc.edu/ (slightly modified by marking the cat and monkey)
Fig-2.
( original file,  page)
(Rhesus macaque is common-name of Macaca mulatta monkey)
The website http://evolution.berkeley.edu/ has wonderfully explained, evolution proceeds like a tree, not like a ladder.
Fig-3.
Still, we can argue that, at the branching-point, out of 2 evolving groups,  only one evolving group could have shown alteration and another group was just unaltered parent group, like this;
Fig-4.
Still, we could not apply that for cat and monkey; because if we consider one of the 2 branches after red circle at fig. 2 (for argument say it is on cat's side) exact same as parental-species; we could not say "monkeys had arrived from the cat". That ancestor could neither be considered as a cat or cow or horse etc.

Cats and monkeys have enough similarities. Each of both contains 2 eyes, 4 limbs, 1 tongue, skin hairs, ear-pinnae and such and such. Is it too difficult to recognize?

Yes, we have mainly 2 tools to recognize common ancestry...
A. similarity (including macroscopic through biochemical to molecular-genetic);
and
B. Fossil records, which are much difficult to find (mainly structural, also ancient-DNA evidence nowadays doing great help ** )
And yes, establishing common ancestry from similarity, is difficult, because there are lots of exceptions caused by 'convergent evolution'. But still, there is a strong correlation between similarity and closeness of ancestry; and it needs our discretion about which one similarity could be really due to same origin, or which one is due to convergent evolution or due to just a superficial similarity or coincidence.

Reference:

Understanding Evolution website: http://evolution.berkeley.edu/ and their section on understanding evolutionary tree (http://evolution.berkeley.edu/evolibrary/article/evo_05).
** The Evolution of Plants by K. J. Willis and J. C. Mc.Elwain/ Oxford: that includes an elaborate discussion about ancient DNA in animals too.

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Does creatine-phosphate (CP) supplementation regenerate NADH?
I have the following facts:

It is possible to convert ATP <-> creatine vice-versa. (ref - non scientific)
CP supplementation protects against metabolic syndrome. ref1 ref2
Fructose digestion depletes NADH via TG synthesis. ref

I assume that CP supplementation regenerates not just ATP, but NADH, if it is depleted, and so it restores the redox balance in the liver. Both ATP and NADH are similar energy storing molecules, so I guess there is a biochemical pathway which converts ATP to NADH, or there is a pathway, which regenerates NADH using CP. Am I right, if so, which pathway is it?
note:
I might be wrong. From one of the references:

Taken together, this study provides direct evidence that creatine reduces lipid accumulation in hepatocytes by the stimulation of fatty acid oxidation and TG secretion.

So maybe ATP is enough to prevent TG accumulation in the liver.

Creatine itself is never converted into ATP. Creatine-phosphate on the other hand can donate its phosphate group to ADP, phosphorylating to form ATP and creatine. This is a buffer system for high-energy phosphates, and is very important in organs with rapid ATP turnover, notably muscle.
The mechanism of the findings described in the papers is not fully understood yet I think. But it is not via ATP, because the supplementation is not creatine-phosphate, but creatine itself, which does not yield ATP.
Regarding NADH: ATP is very different from NAD/NADH in terms of molecular structure, and the two are not interconverted by any pathway that I know of. (Probably this is not what you meant, but just to be clear.) But it is certainly true that reducing power in the form of NADH can be used to phosphorylate ADP into ATP; this is the task of the mitochondrial respiratory chain, where NADH is oxidized to NAD by complex I. On the other hand, I am not aware of a physiologically relevant process that uses ATP to reduce NAD into NADH.
The liver is a main site of synthesis of creatine itself, and this syntesis consumes methyl groups donated by the S-adenosylmethionine system. The authors of your ref1 seem to suggest that reduced synthesis of creatine following supplementation is a possible mechanism. Similar effects have been observed with choline supplementation, but again this effect is not well understood and a current research topic. A recent review is found here.

Creatine supplementation maybe increases the high energy phosphate reservoir. By "stimulation of fatty acid oxidation" I think they mean that the hepatocytes degrade fatty acids to produce energy for the conversion of creatine into creatine-phosphate. It would be interesting to check the regulation of CP synthesis, but I have no time for it currently.

I agree with @inf3rno that the creatine supplementation might increase the high-energy phosphate reservoir – this is the physiological basis for creatine supplementation in athletes. However, I know of no study whatsoever that has ever shown that we have been able to increase the reservoir of creatine phosphate by supplementing with creatine in the diet – this is the reason athletes take the supplement but there's no data (That I am aware of) actually suggest that it works the way we think it does

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Why *morning walk*?
My PT teachers professes working-out/training in early morning hours is the best time to do so. A quick search on benefits of morning walk (or similar phrases) reveals a lot of information which seem to be backed by sound scientific evidence. In fact it is common wisdom around the world, across all cultures.
Okay - accepted. But why is it beneficial in first place? Because there is plenty of oxygen in the morning; or is it?
After long hours of darkness (plants respirating at night) when first light comes plants would have just started photosynthesis, that too at a pretty slower rate (owing to lower intensity of light at dawn). In fact I remember having read something about compensation point

The (light) compensation point is the amount of light intensity on the light curve where the rate of photosynthesis exactly matches the rate of respiration. At this point, the uptake of CO2 through photosynthetic pathways is exactly matched to the respiratory release of carbon dioxide, and the uptake of O2 by respiration is exactly matched to the photosynthetic release of oxygen. SRC

So now, obviously, we can establish the fact that concentration of oxygen should be/is much lower than carbon-dioxide in early morning hours.

So why morning walk or early morning exercises?
If oxygen content is important why not exercise in early evening hours because not all people would like an endurance drill at theoretically perfect time of noon :)?
Is there some other mechanism makes oxygen content more than carbon-dioxide content in the morning?

Personally - I do feel more fresh in the morning hours but maybe that is because of my internal biology, correct me if I am wrong.

P.S. I am not a biology student, so pardon my ignorance.

Personally, I would argue with the premise that it's more beneficial.  Of course I have no data to support this, because (bar a long-ago stretch in the military) morning exercise is just not something I'm going to do.

1: The only benefit I've heard of scientifically is to do with the circadian rhythm. I heard a talk that basically said a dose of bright light in the morning can help set hormonal levels to a daily rhythm. This seems to suggest the same.
2 and 3: I think the overall oxygen levels would not be significantly different at different times of day, but pollution levels might be, this might be relevant.
edit: didn't realise this was such an old thread...

I am going to play the devil's advocate here.
I don't know if working out within the first three hours of waking is necessarily the best time to do so. In the morning, we have what is called cortisol awakening response which is where the body releases cortisol. Cortisol is a by product of the sympathetic nervous nervous system. Dr.s James E. Muller, Geoffrey H. Tofler, and Richard L. Verrier in their article Sympathetic Activity as the Cause of the Morning Increase in Cardiac Events said that early morning activity is a likely culprit but only circumstantial in sudden cardiac infarction [1]. However, Dr.s Douglas P. Zipes and Hein J. J. Wellens in their article Clinical Cardiology: New Frontiers Sudden Cardiac Death found that:

Time of day is also important, with more sudden cardiac deaths, strokes, and myocardial infarctions occurring in the morning on arising from bed, perhaps related to increased sympathetic discharge in response to venous pooling that then triggers increased blood viscosity and platelet aggregation [2].

In Exercise and Acute Cardiovascular Events in Collaboration With the American College of Sports Medicine and Dr.s Paul D. Thompson, FAHA, Co-Chair; Barry A. Franklin, FAHA, Co-Chair; Gary J. Balady, FAHA, Steven N. Blair, PED, FAHA; Domenico Corrado, N.A. Mark Estes III, FAHA; Janet E. Fulton, Neil F. Gordon, William L. Haskell, FAHA, Mark S. Link, Barry J. Maron, Murray A. Mittleman, FAHA, Antonio Pelliccia, Nanette K. Wenger, FAHA, Stefan N. Willich, FAHA, and Fernando Costa, FAHA, felt they that didn't have enough data on claiming early morning exercises and sudden cardiac death (SCD); however, early morning SCD occurred in adults whereas for teens it SCD occurred in the afternoon [3] but "vigorous exercise, however, transiently increases the risk of acute myocardial infarction (AMI) and SCD, even in exercise-conditioned individuals, and several strategies are recommended to potentially reduce this risk"

Active individuals should know the nature of cardiac prodromal symptoms and seek prompt medical care if such symptoms develop.

That is, I wouldn't claim victory for working out as soon as you rise the best choice. However, I am not suggesting that you don't work out in the morning either but just be carefully about it. The best time to workout is the time that will allow you to be consistent, get in at least 30mins, and keep you motivated. If that time is the morning, just be aware of what is going on in the body.
Additional article found in support of afternoon/evening training
Serendipitously, I stumbled across an article on swim performance and time. The article found that the best performance was afternoon to evening and not in the morning [4]. This was published in 2007 in the Journal of Applied Physiology.

I would offer the counter point that this has to do with energy availability. (I'm on my phone so I can't put in references just yet). But there was just a great recent study published in Science (I'll go find it), in which a group looked at plaque deposition as a proxy of overall cardiovascular health of groups of mice exercised before and after food intake. They find that exercise under fasting conditions, which would be akin to morning running, appears to be significantly more protective against cadiovascular disease than exercise after feeding. This is also consistent with some human data suggestive of fasting exercise benefits as well. In a separate experiment the mice were fed the same number of calories per day, but those that were exercises after sleep and before eating were significantly leaner and had less plaque deposition in their vasculature.
In part the idea is that after a period of fasting exercise will promote scavenging of residual cholesterols in the vasculature as well as cellular autophagy (which promotes "fixing" of current cells rather than just replacing them). To the layman, Resveratrol from red wine is probably the most commonly known way in which autophagy might be promoted. But in general think of periodic fasting and feasting as protective because it can help maintain metabolic homeostasis and prevent unnecessary cell turnover.
Hopeful that helps lead you in the right direction. Metabolics and aging is a huge and exciting field and this question could be answered with a small textbook. But you should at least understand that this field is far from being well understood. And that your PT teachers may end up being right, but this field still quite primitive, and this is not accepted yet or really understood by the scientific community.

Did you forget to look up the links? I am rather interested in looking up this study that you have cited.

You know, I've looked and I can't seem to find it. Unfortunately, not being my field of concentration I never saved the reference. I'll keep looking but I can't seem to find it in science, so it may have been in nature or cell, though I looked and can't seem to locate the study. Sorry.

If walking in the morning is truly more beneficial than walking at a different, it certainly wouldn't be related to atmospheric oxygen content. The oxygen content of the atmosphere fluctuates on the timescale of years, not hours. And keep in mind that when it's morning where you are currently, it's going to be noon somewhere else, and dusk somewhere else.

W.r.t. keep in mind that when it's morning where you are currently, it's going to be noon somewhere else, and dusk somewhere else - But the distance between morning & noon would be several longitudes, oxygen, under the effect of diffusion or even torrential winds, wouldn't normalize its concentraion so quickly.

Morning walks are preferred because the sunlight that falls on the earth in the morning is good for your skin for producing Vitamin D.
and also it is said that morning walks are good for:

Strengthening Bones and Joints
Weight control

and also independent of the time of the day, due to exercise and walking you keep moving your joints an this improves your Blood circulation.
And also as you keep moving your muscles too which improves Muscle Strength .
this was from my knowledge.If you want to know more :
Click Here(link 1) ||
and here(link 2)
Share your thoughts with comments,
Any suggestions and questions welcomed,
Anurag .

This is nothing I would attribute only to a morning walk. Vitamin D will be produced as well in all other parts of the day during sun exposure, the training effect as well.

Ditto, there is no difference in the sunlight hitting the earth at different times of day. edit, other than intensity.

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Book/source for learning bioinformatics, focused on genomics?
Does anyone know of sources for learning bioinformatics, focused on genomics? I would like to learn a lot of skills I could apply potently in the workforce if I ever became adept at the fields. My computer science knowledge is weak, and my biology knowledge is mediocre, but I find the topics to be interesting.
I have read "The dynamic Genome, A Darwinian Approach", by Fontdevila, and it was a bit rough for me. I have also read some of a introduction to genomics textbook, by Arthur M Lesk, and found it to be very "academic".

Hi, There are some bioinformatics introductory courses on "coursera" ..cud be useful to u...

Unix and Perl to the Rescue by Keith Bradnam and Ian Korf is an excellent introductory book and guide for bioinformatics (Linux and Perl) in genomics. It includes exercises and starts with the very fundamentals. You will still need some basic understanding of genetics and biology though.

Beginning Perl for Bioinformatics by Jim Tisdall http://shop.oreilly.com is quite good, in my opinion, and his sequel, Mastering Perl for Bioinformatics is also great. The focus is largely, but not exclusively genomics.

Elementary Sequence Analysis by Brian Golding and Dick Morton is a good starter. Online resources can be found here:http://helix.biology.mcmaster.ca/courses.html
Here's a great online tutorial for sequencing techniques, with introduction, examples and everything.
http://bioinf.comav.upv.es/courses/sequence_analysis/sequencing_technologies.html

While not a book per se, the edX Lifesciences course has been really useful for me, it does a great job of covering the entire pipeline of genome analysis that one would need to use. The link containing all 8 classes is here, scroll down a bit and you can see links to all of the classes in this module:
https://courses.edx.org/courses/HarvardX/PH525.3x/1T2015/dffde833663e4f71ab64246ebe5598d1/

A Primer for Computational Biology is a great open-access book with intros to Unix, R, and Python. As the title says, it's focus is computational biology (e.g., applying a variety of methods and analyses) rather than strictly bioinformatics (the development of novel methods and analyses), but I've found very valuable both for myself and for teaching others.

I strongly suggest you to take a free course on courseraThere are many valid courses focused on bioinformatics for beginners and they offers slides, notes and everything is necessary to start. If you are looking for a nice book to get started, then I suggest you this one

This is a book being worked on by some people at biostars.  It's being constantly updated
https://www.biostars.org/p/225812/
Perl is a good place to start if you don't know any coding, but when you want to use already written libraries, you'll want to know R or python, if not both.

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Cell energy consumption and food intake
I am wondering if each cell in human body starts consuming ten percent more energy, how much food one has to consume compared to normal intake?

The answer is relatively simple: About 10% more (assuming that there is not much loss in the uptake and conversion).

Does efficiency of digestive system play a part? If it is 10% efficient, then consumption should be doubled.

Compared to IV injection, consumption via the digestive tract gets about 80% of administered drug. So it may be that you would need to multiply that by 1.2 so you get 12% more food intake. But this question really is not physiologically going to ever happen like you phrase it.


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If oxygen deficiency is bad even for a short while, why do people swim?
This may be trivia to many of you.
Textbook says the oxygen deficiency, even for a short while can injure our cells. Then why do people go for sports like swimming? (where rhythmic breathing is required yet, there's a practical possibility of holding the breath longer than usual inhale exhale process) I am looking for a reasoning from cellular biology/patho-physiology/respiration aspect. And not because swimming or any other such exercise is anyone's choice/preference.
So my question is: during sport like swimming, does the oxygen level in our blood drop below a critical level, that cells might suffer from lack of oxygen?
Also found some relevant information here.
Currently referring to this online text : Swimming Fastest: Physiological Responses to Exercise.

My best guess is simply that holding your breath for short periods does not lower your blood oxygen to levels were cells die of asphyxia. It will take some time for your blood to reach critical levels of oxygen, i.e. acting as some sort of buffering.

I've edited your question to avoid closure. Please feel free to revert my edit at any time.

In this paper the authors measured decrease of arterial blood oxygen saturation in healthy and patients with sleep apnae (this latter part is not really relevant only the measurements in healthy individuals).

They found that fall of oxygen saturation depends on the initial saturation rate, but is not affected by the breath-holding time. As you can see on the graph at high initial saturation the fall rate per second is quite low. Here is the info in a table format:

At high initial saturation only mean 0.16% saturation drop occurs per second, thus in average a healthy individual looses 1% oxygen saturation approx every 5 seconds (I'd also like to note that the urge to breathe does not come from the lack of oxygen when holding breath, but from the accumulation of CO2). According to wikipedia normal oxygen saturation is between 100-95%, and only below 90% is considered hypoxemia /hypoxia (a medical condition where blood oxygen level is low). So if we look at the data in the table, it is safe to say that it takes approx 20s until the blood saturation level drops from 97% to 93% and another 5-6 seconds until it drops to 90% (with approx 0.5% saturation loss per sec at 93% initial saturation).
People who are conditioned by exercise have larger vital-capacity (they can breathe more air in for a single breath), thus have means to acquire more oxygen can compensate for the excess use of oxygen. During heavy sport activity like swimming it is unlikely that anybody will hold his/her breath for several tens of seconds.

I am going through your post and will revert once I have understand it enough to ask few side questions.

I don't mind reverting my edit, but be cautious not ask too many sub questions as it may make your question too broad or unclear. If your have side question that are not tightly related to the main question of your post I'd advise putting them into separate post. But encourage you to edit your post to fit your curiosity, and if needed I'll edit my answer to fit the edited question.


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DNA length and annealing kinetics
I have a mixture plasmids and undesired short linear fragments that share the same sequences. During denaturation and annealing, I would like the plasmids to 'find each other' before annealing to the shorter linear fragments. Assuming the concentration of shorter fragments is significant, is there a temperature profile to bias towards re-annealing of longer DNA?
More specifically, this is for a variation of the Surveyor Mutation detection assay, where re-annealed DNA with mismatches are digested, leaving non-mutant DNA intact. I would like to keep non-mutant plasmids for E. coli transformation. However, some linear fragments  ~10-50% of the length of the plasmid have escaped exonuclease treatment and would compete with the plasmids during annealing.

it is unclear what you ask. And why not transform e. coli with your mixture, only circular plasmids will propagate and linear pieces will be degraded/purified-out

If the linear fragments anneal to the circular plasmids instead of the complement, the resulting DNA would only be partially double-stranded, which I assume would render it unusable by bacteria. This would lower the transformation efficiency.

did you think of just using DNAse that targets ssDNAs? For example, Mung bean nuclease. There should be another enzymes with similar activity, e.g. S1

I'm using PlasmidSafe which is a cocktail of exonucleases that do that. It's just not 100% efficient and I wanted to leave no room for error.

Short answer is that higher temperature favors annealing of longer sequences. There are number of ways to calculate melting temperature, but all of them produce similar results: longer polymers require more thermal energy to melt. Hence, quick cooling from higher (say, from 95C thermocycler can cool in 10-12 sec) to RT/4C will favor re-annealing of circular strands. Slower cooling should allow more ssDNAs to bind.
But again, if end goal is to select for circular dsDNA, simple transformation should take care of that.

Thanks for the answer! How about slow annealing down to slightly below the melting temperature of the plasmid and then snap cooling on ice from there?

Also, unlike oligonucleotides, longer DNA is flexible and contains local regions of higher and lower melting temperatures. Would the the overall melting temperature be accurate in this case in describing that half of the ssDNA molecules have completely annealed? In other words, would it be common to have two ssDNA molecules incompletely annealed to the same template, where one of the molecules is partially blocking the other one?

I don't know, what is really possible. What is true, is that at any temperature interaction that includes more bases is more favorable. Think about it as a dynamic equilibrium: at each moment ssDNAs will bind/try to bind and unbind. However, it takes only dozens of bases to unbind whole oligo, whereas circular DNA is on order of KBs. So oligo will unbind and go into solution much easier than second strand of circular dsDNA


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What are the factors on which protein-protein interaction depend?
Does protein-protein interaction only happens when one of them is basic and the other acidic? Do protein interactions also depend on the protein structure? Are there more factors?

Proteins are not acidic or basic per se. It depends on the environment - if this is acidic, than some aminoacids can be protonated, while others cannot. But in a given environment proteins are either acidic or basic, but not both.

so two acidic proteins can interact in an environment?

Yes. Acidity or basicity of a protein is an overall property. What's important is the charge of residues at the interface where the proteins interact (amongst other things).

what are the other things?

Your question seems too broad and dupllcates these: http://biology.stackexchange.com/questions/2965/what-role-does-a-proteins-size-have-on-protein-protein-interactions?rq=1, http://biology.stackexchange.com/questions/1404/what-are-the-various-types-of-protein-protein-interactions

http://biology.stackexchange.com/questions/2965/what-role-does-a-proteins-size-have-on-protein-protein-interactions

possible duplicate of How does temperature influence the rate of protein degradation?

It depends both on structure and charge. Binding sites of proteins are essentially formed by amino acids placed in a particular conformations such that it will match the binding site of their counterpart protein or substrate. This is commonly referred to as the lock and key model of protein binding. This is similar to how two puzzle pieces fit together, the pieces are exactly the same shape at the point at which the puzzle pieces connect. At a protein binding site amino acids are clustered together to form the matching shape to the appropriate binding partner. This however is not just dictated by 'physical shape' of each amino acid but also their charges. This is important because negatively charged amino acids will repel other negatively charged amino acids, and attract to positive amino acids, thereby modulating the exact 'shape' of the protein binding site.

so negative;y charged amino acid will bind to positively charged amino acid. Similarly cant we say the same for proteins as a whole?

apart from charge and structure, is there any other feature on which the binding depends??

so the charge in the binding site of protein is being considered for binding and not the entire charge of the entire protein. Am I right?

Yes you are correct.


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Why do we get tired
At the end of a day full of work, it is general for people that their eyelids start to feel heavy. Laziness takes over and  we begin to yawn. We all know that we're tired at that time, but why people get tired?

I took the liberty to remove all personal references to yourself to avoid being flagged as personal medical question. Please feel free to revert my edit at any time if you wish.

Also in this question the regulation of sleep is quite well answered and in your case I'd look for the homeostatic regulation of sleep (that is the accumulation of adenosine in the brain due to the depletion of energy sources in neurons after a long period of wakefulness).
http://biology.stackexchange.com/questions/28123/length-of-sleep-time/31305#31305

Muscle fatigue

google that

It is yet to be discovered by scientists. But there is a new study that finds that brain cells called astrocytes supply the urge to sleep by releasing adenosine a chemical known to have sleep-inducing effects. The chemical accumulates in the brain during waking hours, eventually helping to stimulate the unique patterns of brain activity that occur during sleep.
You can find more about it in this link bellow  http://healthysleep.med.harvard.edu/healthy/matters/benefits-of-sleep/why-do-we-sleep


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"bead" on a string theory of genetics, source?
Thomas Hunt Morgan was a pioneer in genetics and proposed the now false model of genes being "beads" on a string. These beads being indivisible and responsible for a single phenotype, if I understand correctly.
Does anyone know of a good, reputable source of information on this theory that would be sufficient to use as a citation? I would use wikipedia, but it is disallowed.

I found this reference on the Thomas Hunt Morgan wikipedia page. It uses the "Beads on a String" phrase and may be more appropriate material for your homework. I would recommend you read the references on the bottom of that page for more information on his work and hypotheses.

If the Cold Spring Harbor Laboratory is considered a reputable source (it should be), you can check out their Defining the gene page which has an overview of the beads-on-a-string theory, and how it was disproved by Seymour Benzer. You could also try to find Benzer's original paper, although it doesnt seem to be available online.
Related and possibly helpful:

Benzer's page on Cold Spring Harbor website
Evolution of Genes and Genes in Evolution - very interesting paper from 1959 on genes/genetics, look on the fourth page (marked 18) for the bead-on-string theory


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How does the brain cool itself?
Thoughout life everyone tells you that brain is essentially a computer but just like computers your brain would create immense amounts of heat by being in use, so if that's the case how does it cool down.
Is like liquid cooling where the blood transfers the heat away? and if so what is the critical temperature when your blood can no longer cool your brain? Also at what temperature are you at risk of brain damage?

http://en.wikipedia.org/wiki/Countercurrent_exchange    might be of some help.

You may have to define "critical temperature," because many biological systems do not fail with a sudden transition from "perfectly fine" to "dead."  They usually have several layers of limited functionality.  Consider a nasty fever, which can cause unusual psychological states, but not death until a higher temperature.

At what temperature are you at risk of brain damage.

Brain has liquid cooling. Some liquids like blood or CSF flow around it and cools.

Computers rely on cooling mechanisms like heat sinks( an aluminum alloy mounted over the micro integrated chip) and fan. So far none of these mechanisms are utilized by nature, but analogies like cooling mechanisms in elephants which are in turn considered to be a model quite like the fan.
As the largest land animal, elephant's ears have crucial role in regulating homeostasis. When we see an elephant, it always wave its ears in order to reduce the brain temperature. On the other hand humming birds which are very smaller in size reduces its temperature by flowing blood to its wings. Humming birds wings flutter 90 times a second and it allows them to exchange much of its heat to the environment and the cooled blood is driven back to the brain.
The  carotid rete or rete mirabile in birds have been developed for heat exchange. In mammals, a pool of the cool venous
blood  returns from the nose or
head skin, exchanges the heat with
warm arterial blood of the carotid artery.
These arteries are sub divided into hundreds of
small arteries forming a net like structure which significantly improve the
heat transfer in brain.

Vascular retia mirabilia are also found in the limbs of a range of
mammals. These reduce the temperature in the extremities. Some of
these probably function to prevent heat loss in cold conditions by
reducing the temperature gradient between the limb and the
environment. Others reduce the temperature of the testes increasing
their productivity. In the neck of the dog, a rete mirabile protects
the brain when the body overheats during hunting; the venous blood is
cooled down by panting before entering the net.Reference

In Humans,

The net effect of heat production in the brain and brain cooling
keeps the brain cooler than the rest of the body and is achieved by
surrounding and bathing the brain with venous blood that has been
cooled outside the cranial vault, by bone and fat acting as
insulation, by the veins of the face and scalp through conduction,
convection, sweat and evaporation and by cooled venous blood flowing
through the cavernous and suboccipital cavernous sinuses cooling
incoming blood in the internal carotid and vertebral arteries before
it enters the brain. The combined effect of the brain cooling system
keeps the temperature inside the vault and brain about two to three
degrees cooler than the rest of the body. The effect is important
enough that some physical anthropologists attribute the extra-large
size of the human brain more to its exceptional cooling capacity than
to the increase in arterial blood flow that comes with upright
posture. Anthropologists refer to human encephalization due to
enhanced brain cooling capacity as the "radiator theory".
Reference

Also yawning and panting are considered to be mechanisms to reduce brain temperature.


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Why are clementines easier to peel than oranges?
In my experience, clementines have been significantly easier to peel by hand than and orange.  The skin of the orange seems to cling to the rest of the orange much more so than the skin of the clementine does.
What causes this?  Wikipedia (Clementine) merely mentions that they are easy to peel, but leaves it there. What is different between the way the skins are attached?

I think it all comes down to the thickness of the skin and how it's attached to the fruit itself.  For me, it depends on the variety of oranges and/or clementines, mandarins, etc. that I'm peeling.  Usually fruits with thick, hard skin are easier to peel whereas fruits with softer more delicate skin are harder to peel off in one piece.  Factors like growth climate and ripeness effect the skin quality.
If you roll the fruit on a hard surface under your palm before peeling, it makes the skin easier to peel off in one piece.

I'm not as concerned with getting everything off in one piece, but I feel like I really have to put a lot of effort to get the skin of an orange to separate.  Do you know more about how the different skins are attached? (And should I add that to the intent of my question?)

@BrianJ the ultimate arbiter of the way the skin 'attaches' (really it 'forms') is the genes of the plant.  Citrus fruit skins' all form by the same process of  cell differentiation and growth, which are controlled by the genes of the plant, which are in tern controlled by other genes, hormones, environmental factors, etc.  So, the oranges' genes may code to produce more fiber between the flesh and fruit, making the 'pull' easier or harder.


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Help me identify this insect
Over the last week or so as warmer weather has arrived, I've noticed small insects crawling around in the bathroom. I'm located in western Europe. They are perhaps 1mm in length, quite difficult to see without a magnifying glass. I used a macro lens to capture these pictures. What might they be? Ticks? Aren't ticks larger? Why are there so many?
Note: these pictures are heavily magnified (they are on an old wooden door with cracking paint), and I've applied lighting auto correction. Actual size of each insect is 1mm or less.

I can't tell if those have 6 legs and large antenna, or 8 legs and no antenna. If 8 legs, then I suspect some sort of mite.

At the moment, my guess is louse or first instar nymph cycle of a bed bug. Can you obtain better pictures?

It looks like 6 legs and large antenna to me.

@rozmarin Yeah, the last 2 images show it better.

Definitely a spp of mite. And definitely not a bed bug. Sick of people always suggesting that small unknown insects are bed bugs -_-. Need bus do have their own distinct appearance...

After a long hunt it seems they are Dermanyssus gallinae. It appears I have a pigeon's nest somewhere near my building.
http://en.wikipedia.org/wiki/Dermanyssus_gallinae

You should add the picture.


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Applying kiwis on gelatin
Kiwis have the enzyme actinidain. This enzyme will break the peptide bonds from the gelatin. Making gelatin with raw kiwis will not work, because the peptide bonds in the gelatin will be broken down.
But what if you would make plain gelatin, and apply raw kiwis to it? Do the enzymes break down the gelatin when the gelatin already has set?

It's ok, you did the edit, and now everything is fine.:D One more thing can you link a reference that kiwi truly has that enzyme and it does what you say it does. It's not known to me.

Do you mean actual kiwis (a family of birds native to New Zealand), or the fruits that are marketed as Kiwifruit?

@jamesqf just grab the bird and rub it on the gelatin.

@user137: One would first have to kill & dress it before slicing.

According to the (non peer reviewed) scientific experiment found here, simply placing a piece of kiwi onto gelatin that has set will cause the gelatin to be hydrolysed by actinidain.

This experiment aims to show the effects of Proteolytic enzymes on proteins and, subsequently, the effects of extreme temperatures on the proteins themselves. Petri dishes filled with gelatin, a derivative of collagen, were acted upon by kiwifruit samples overnight. Some samples were fresh and used as controls; others had been frozen or boiled for two, four, six, eight or ten minutes. The mass of digested gelatin was taken the next day. The results ultimately reflect the effectiveness of the actinidin, the kiwi’s Proteolytic enzyme, under normal conditions and after exposure to extreme temperatures.


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Why do spiders make their web near the ceiling and near a light source?
Why do spiders make their webs near the ceiling and near light sources ?
Is their an advantage for spiders in doing that? For example do they catch more insects when their web is near a light source because prey insects are drawn to it, hence giving those spiders with a well-lit web a better chance of survival?

probably...

same reason you put light inside of your bug lamp?

Possibly related?

Because many insects (their food) are attracted to light. This attraction is called phototaxis.
Hypotheses for why insects are attracted to light

The leading hypothesis for why so many insects are attracted to light is that before artificial existed, insects were using the light from the moon in order to navigate. They would keep themselves at a given angle relative to the light source in order to navigate straight.
Another hypothesis is the presence of light indicates that the pathway is clear.
A third hypothesis is that some insects may confuse artificial light source with the other sex. This appeared to be true for moths for example

These three hypotheses are not mutually exclusive.
How do spiders chose their habitats
For more information about the abilities of spiders to find a good habitat, have a look at this very interesting answer.


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Do we instinctially interpret birdsongs as a sign that there are no predators present?
I was outside today thinking how nice it was to hear the birds back from winter when I started thinking about the fact that we like bird song.  It makes us happy in a very basic level, the sort of level that usually implies subtle evolved instincts.  Thus I started wondering, why do humans all over the world naturally love the sound of birds?
The simplest explanation that came to my mind was because birds supposedly will flee or be quite when predators are around.  Thus the presence of birds singing may indirectly mean a lower chance of predation.  In other words it's less that were happy when birds are singing, as that were a little more on edge when they aren't singing.
However, that seems almost too easy an explanation.  Has anyone more intelligent then a random computer geek who's just happy to be away from the computer for a few hours put any more effort into considering this?  What is the generally accepted hypothesis?

I specifically don't really love bird songs (it is indifferent to me or sometimes quite irritating), I think I'm not the only one. Please don't think that I'm a horrible person. I just wanted to point out that your claims might be a bit wide....

Bird song appreciation is a thing that most (if not all) people experience at least some times and the question falls within the field of "evolution of behaviour" or more accurately "evolutionary psychology". I think it is a totally valid question.

I've never doubted that this is indeed a valid question. I just wanted to point out (with some self-irony) that not everybody loves bird songs. Nontheless this is an interesting question.

@poka.nandor sorry, your a horrible person and you will clearly be hunted down and burn on the stake any moment now  :)  yes I generalized a little bit, but I think the majority of people do in a way that suggest evolutionary influences, even if there are some (clearly horrible) outliers :)

I had a good laugh at your comment. Good to see that this site is full of joyful and friendly people. As i said earlier your question is totally valid in terms of what @Remi.b said.

There are plenty of birds that call and communicate in the presence of a predator, so I'm not at all convinced that we instinctual pay attention to their jabbering. Surely you learn that it's nice being in a park playing whilst the birds are tweeting.

Crows and gulls would probably also flee predators but their songs are definitely not really pleasant to listen to! I know it, they woke me up last week-end $\ddot \smile$. The canadian goose or the common starling (see here) are other examples of not really pleasant songs.
Too a selectionist view of evolutionary processes
It is important not to make the mistake to see anything as an adaptation (a result of natural selection only). Evolution is way more than natural selection and it encompasses tons of stochastic processes. This answer has a paragraph on the subject of not thinking of anything as a result of natural selection. This kind of over-consideration of adaptive processes in evolution is a common mistake especially when thinking about how human behaviour evolved.
Evolutionary psychology and evolution of appreciation of bird songs
The field of evolutionary psychology may interest you but note that it is a field that is sometimes still at the limit between psychology, philosophy and biology.
Appreciation of art as a by-product
Appreciation of art (like birds songs) and beauty is a pretty poorly understood subject yet. The first hypotheses came from Darwin and Gould. They pretty much argued that we enjoy sex, grasp facial expressions (kin recognition), have to like logical proof to appreciate learning and acquire language, efficient communication (cooperative hunting), appreciate put oneself into others thoughts (Machiavellian intelligence),  etc... As a result of those selection pressure, we may have evolved, so-called by-products. A by-product is a phenotypic trait that hasn't been directly selected for but that has been  selected via its correlation to some other phenotypic trait that is under positive selection and that is correlated. If this is true, then there would have a correlation between cognitive abilities and art appreciation and therefore a correlation between art appreciation and fitness.
Appreciation of art due to sexual selection
Some have argued that looking at the importance of art appreciation and intelligence in today's mate choice, it is likely that art appreciation may have been reinforced by sexual selection.
Either sexual selection may have reinforced a trait that was correlated to fitness ("evolution of appreciation of art as a by-product" hypothesis).
It is also possible that sexual selection may have selected for art appreciation without art appreciation being correlated with fitness but just because it asks for a big brain and lots of energy (brains consumes lots of energy) and being able to appreciate arts means that the individual has extra-energy to spare and is therefore very fit (handicap principle).

I understand your general point, but could you elaborate on what you mean by appreciation of beauty is due to having a big brain?

@dsollen It is a good point, it was indeed still unclear. I've been trying to develop the ideas a bit further. It is really not my field and I don't expect that my summary is a good review of the thoughts and evidences we have on the subject.


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Does DNA polymerase always go the same direction?
I read that mutations are more likely to occur on "the strand that DNA polymerase replicates discontinuously". Does DNA polymerase always replicate the same strand discontinuously and, if so, how/why?

Polymerization always occurs 5'->3'. Which strand is replicated discontinuously depends on the location of replication origins, but it doesn't change between replication cycles.

Summary:
In bacteria or organisms with only one well defined replication origin and a circular chromosome, yes for a given DNA region the same strand is replicated discontinuously.
In high order animals, which replicate chromosomes using several origins of replication (ori), this is less clear as the way ori are recognized is still not fully understood but seems to involve DNA structure. Chromatin structure is dynamic which means ori are also likely dynamic which results in defined regions of the DNA not likely to always be replicated discontinuously from a well defined strand (i.e. DNA replication might not always start at the exact same sites).

First off, as you probably know, DNA is always transcribed in a 5' to 3' direction. The why is nicely answered in this post.
DNA replication forks start at replication origins. Replication origins are recognized by origin recognition complexes. The way DNA replication occurs is by having two DNA polymerase complexes traveling in opposite direction (i.e. two bidirectional replication forks) from the origin as shown in the following schema:

This means that given constant origins of replication in an organism (like bacteria which usually only have only a single origin of replication) and given the DNA is replicated in a 5'-3' direction, same strands will be replicated discontinuously from the origin (i.e. in the schema, the bottom one on the left and the top one on the right). A global view of the replication at the chromosome level in bacteria is shown here below:

Now for more complex organisms, the origin of replication is not a single site but rather multiple ones across chromosomes (30'000-50'000 ori in humans). Where does DNA replication starts exactly, this is still not fully understood. DNA sequence is likely to play a role but no highly conserved consensus sequences were found and it is believed that origins of replication are linked to the structure of the DNA instead. In essence the chromatin structure is what seems to dictate where DNA replication starts and as the chromatin structure is dynamic within a cell, it is likely that origins of replication are also dynamic therefore making the identification of the discontinuously replicated strands very difficult (Méchali M, 2010).
Finally if you wonder what happens when two replication forks collide, well the answer is simple, replication stops and the two DNA polymerase complexes leave the DNA.


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What does it mean when a protein has a different excitation spectra than wildtype, but the same emission spectra?
We have a GFP mutant that displays a different excitation spectra with emission at 510nm than the WT. However, their emission profiles with excitation at 490nm are the same, and we do not observe the same trend.
We're confused as to what might be happening.

@AliceD What you said about emission/excitation is wrong. It is actually the opposite, the excitation is always shorter than the emission as shorter wavelengths are more energetic. The question is therefore valid in this regard. I think he is referring to an experiment they have done rather than a paper. Yet more informations would be indeed quite helpful for providing an answer. For example can you post the actual spectra? Also can you please provide the ranges you used for emission/excitation wavelengths in both experiments?

@cagliari2005 - yep noticed it, and removed comment. Thanks

emission spectra should not depend on excitation wavelength. Only scales.

@aandreev What? The emission spectrum totally depends on the fixed excitation wavelength... And vice-versa for a fixed emission wavelength.

in most practical applications shape of emission does not depend on excitation wavelength. (in range where $\lambda_{em}>\lambda_{ex}$) see here: http://www.olympusconfocal.com/theory/fluoroexciteemit.html

Hi, OP here, thank you guys so much for the help. It turns out there was a calibration error, and when we recollected the data, the symmetry in peak height was observed for both Wt and our mutant. Much appreciated either way!

Let me start from short description of fluorescence (since we talk about it here).
Fluorescence is one of the processes through which excited molecule can relax, lose its excessive energy. That is, quantum interaction between atoms in molecule (organic dye or complex GFP) create permitted energy levels. There is "ground state" $S_0$, for example, and excited state $S_1$. You "pump" your molecule with excitation light from $S_0$ to $S_1$. All this can be nicely illustrated as absorption in Jablonski diagram (look at a for now):

via http://micro.magnet.fsu.edu/
"Loss of energy" here is some process via which molecule returns to ground state. In case of GFP energy is released as an emission photon. Nature of fluorophores is that they tend to return to ground state as the state of less energy, and almost all systems tends to go to state with lesser energy.
Now, to your question. Why GFP can has different excitation profile but same emission? Notice, how in (a) molecule get pumped to highest state, then relaxes a bit to lowest of $S_1$ states and then go all the way to $S_0$? That initial relaxation is thermal relaxation. Some energy is lost, essentially, to water molecules around GFP. That is why emission is always "more red", i.e. has lower energy than excitation. Initial relaxation is why your GFP spectra also broad. There are many levels GFP can emit from, as well as be excited to. In crystals of GFP transitions will be very narrow, because much less of excitation energy will go not into fluorescence.
So, my point is following. Nobody prevents one from engineering a mutant molecule of GFP that could be pumped to some even higher level $S_2$, which then relaxes to $S_1$ via non-irradiative process (e.g. gives energy to water, but not into fluorescence!). Only requirement is that for mutant direct pathway from $S_0$ to $S_1$ would be forbidden (see b and c).
Another point is that whether your spectra are different in shape or only intensity. Different shape of spectra means there are differences in those levels and transitions.


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What is the magnification necessary to see pond life
My daughter is 5 and wants to learn about Biology. I thought a great start is to see life from pond water through a USB microscope. It would be great if she could see organisms like amoebas, flagellates and ciliates with her own eyes. The microscopes I have seen typically have a zoom range of about 40 to 400x.
Would this range be sufficient to see microscopic pond life?

+1 for awesome parenting and an intellectually curious child, as well as the good question.

It's advised not to start using a regular (meaning here transmitted light) microscope with kids under the age of about 10-12. It has to do with their brain being insuffiently developed to relate the two dimensional microscopical image with the three dimensional reality... I wouldn't know. I'm not a psychologist nor a neurologist, but however I am a dad of a 10 years old girl and an avid amateur microscopist with some 45 years of experience in that field. When my kid turned 8, I gave her one of my microscopes: a nice Zeiss Standard. The first time we did some pond dipping together, we found som

@mydaftquestion Mum teaches biology. she often had a pond slurry aquarium, which is  very interesting for children. they often harbor Cyclops, Daphne, Planaria, Cyclops, Snails and various types of algea. You can use a vase. For microscopes you can mix up some sticks and hay in a mug for 2 days. 10-100x is the best range.

2019-05-01 Edited: Updated dead links
From the comment section:
I would go with a cheap one with a magnification of ~40X. According to this source, 10-20X is already sufficient to see large protozoans and algae in a pond. Here some suggestions on what you could look at.

Both links are dead now.

@PiotrChojnacki Thanks for letting me know! The first link should be back soon (website is under maintenance). The second link is now restored (broke due to a change in the address name).

To me, microscopes are like pacemakers for your heart, they only come in two main categories, junk and not junk. The good news is pacemakers are way less complicated.
In short, 400x (on a $100 or so compound microscope) SHOULD certainly get you all the quality high school level bio class stuff a pond has to offer, without a lot technical skill to try to see it. BUT it is about CLARITY not just zoom. For pond watching, you want a compound (or phase) microscope with four main ingredients - a light condenser, a 10x objective piece, a 40x objective piece, and a 10x eyepiece. ?Why:
Most of the time, unless you are going to spend considerably more money on something that claims really high magnification (ie 1000x - 3000x etc) you wont get clarity and detail, which is everything.
to get best results for a beginner - First you have to look at what is called the "objective piece" (which is the nozzle looking piece that actually looks down into the specimen - it is a lens mechanism) your microscope MUST INCLUDE one objective piece with a 10x AND an object piece at 40x (but NOT so much a 100x - 100x is not needed and requires more work, 60x is good, but NOT 100x unless you are already expert level). These objective pieces should also have a minimum - lets say 'quality' - rating of "achromatic 160" or otherwise an "infinity" rating on what is called the "DIN rating" on that "objective piece." Decent quality microscopes usually have this rating printed right on the objective piece and objective pieces are removable and swappable. Usually, your good basic microscope has 3 objective pieces with different magnifications ranging 4x - 100x. The eyepiece (where you actually look into) should have at least a 10x magnification. The two of these together (40x X 10x), will give you an enlargement of 400x which is the benchmark for "good or quality."  This shopping list also gives you the best value for your money. In fact, you can spend 100 bucks or less for these essentials, while others will cost you 100 bucks or more and DO NOT offer these essentials even though they come in brighter, prettier colors. You can also spend $300 and get a microscope with these min standards that will last her until college (and is upgradeable). SECOND - assuming she is not doing anything like virus research yet - the compound or phase microscope should have a light condenser (which  would be a red flag if it did not).
The only other thing I think is important is to make sure it is a plug in - not just battery operated. That tends to go hand in hand with better quality, but doesn't necessarily mean more expensive.
The things that I mentioned are all the minimums that are inherent in microscopes that give a quality CLEAR image from most, if not all, of what you want to look at from a pond (but you can go much deeper). This can be had for $100 in the year 2020 or 2021. However, these very same microscopes that have these standards will typically include many more useful features (same price - all included).


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blue/white screening - results are opposite as expected
We inserted GFP-gene into plasmid Bluescript SK+, transformed E. coli with this construct, and then plated on an agar plate with Ampicillin and X-gal to do a blue/white screening. We got blue colonies and white colonies, and normally the white colonies are considered positive for the insert and the blue ones are negative for the insert.
The problem is that the results we got are actually the opposite. If we look at the plate under UV-light, we see that ALL the blue colonies are fluorescent, which means they actually produce the GFP, and ALL the white ones are not!! How would you explain this??
Thank you
Edit: i thought that maybe the insert could be in frame with lacz', so we get fusion proteins. However this doesn't explain why we got white colonies which are not fluorescent

What enzymes did you use to perform the insertion? Also, what happens if you transform the original non-cut plasmid?

i forgot this information. We used kpnI for the insertion, which does blunt-end cuts. We also plated bacteria transformed woth the non-cut plasmids and we got some white colonies and only one blue colony.. but none of them is fluorescent

KpnI is not a blunt restriction enzyme. Are you sure you didn't confuse it with another enzyme? Also, if your negative control is giving white colonies, then your plasmids are likely to be defective.

Oh yes pardon, kpnI makes cohesive cuts

If the antibiotic was not working for whatever reason, you could get growth of un-transformed bacteria.

Given the fact that the negative control uncut plasmids are producing white colonies, it seems that there have been significant mutations within the lacZ gene in the plasmid, causing the uncut plasmids to become white due to inactivation of the gene.
I would suggest purchasing a new batch of pBluescript, or if that is not possible for whatever reason, perform a miniprep on one of the blue colonies and sequence its multiple cloning site to verify that the MCS is present and not mutated before continuing. If you are not going to buy a new batch of plasmids, it would also be prudent to verify the plasmid's length using gel electrophoresis.
The most likely explanation is that the plasmids are mutated, and therefore you are getting bad results in the blue/white screen.


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Do non-enzyme catalysed reaction pathways exist?
Can their be a kind of chemical reaction pathway in a cell, that is catalyzed or regulated but NOT necessarily by enzymes? I could not find anything on Google.
I have almost no background in biology, and am only studying certain topics from a mathematical perspective.

If by enzyme you mean "protein" aka polypeptide, than there are such things as catalitic RNAs. Those are molecules of RNA that facilitate chemical reactions but don't change themselves (definition of catalyst). I think that, based on the discovery of such RNAs, it is now believed that life might have started from or with the help of catalytic RNAs (please forgive the speculative tone, see self-replicating RNAs).
You might find this article interesting: The Road to Non-Enzymatic Molecular Networks, which describes non-enzymatic networks. The problem with searching this topic is that most current publications, seem to me, to concentrate on way to transfer enzymatic reactions into inorganic catalysis systems--because those systems can be more clean and easy to expand--than purifying enzymes for biotech.

This should rather be a comment than a full answer in my opinion. You make good points, but i think this needs to be elaborated.

in what way? also, RNAs are only example of pure non-protein catalysts I can think of. Others involve coenzymes, e.g. vitamins while they are part of proteins. There is not much surface metal catalysis in cellular biology (Pt)

Well, in my mind I was thinking of enzymes which help in metabolism, regulate intracellular reactions and such..

@aandreev - In a way that you describe what catalitc RNAs or ribozymes are, how do they work, what reactions do they play roles in. Also some peer-reviewed article on the topic would be nice. I too use wikipedia as source for explaining basic things in my answers but for the main topic I think peer reviewed literature is more suitable.

@jablesauce Well, that is not very common, after all cellular biology is protein-centered. I wish someone with more insight will answer.

The article you linked is is non-free and might not provide much help as I think it is inaccessible to most users. Also posting google scholar search results does not show too much effort.

@poka.nandor I try to avoid answering in comments, even if there might no be much to say on topic. But I think that ribozymes are too googleable to expand on definitions/functions. In it I follow this meta@bio discussion: http://meta.biology.stackexchange.com/questions/552/comments-with-answers

That is fine, but then take time and put effort in it to be nice elaborate answer. It's better for everyone.

-1 for not putting real effort in answering the question.


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Does the biosphere have infinite resources and are they infinitely renewable?
Does biomass represent all of the resources of the biosphere and therefore it would be theoretically infinitely renewable (as long as we have the sun) since all the biomass is part of the carbon cycle?
Also, should I consider resources like gold to be part of the biosphere and therefore all the resources would not be infinite nor infinitely renewable?

Assuming no one burned any fossil fuels, the carbon cycle isn't perfectly recycled. Some organic matter would get trapped as coal or oil. But thankfully we have solved that problem by digging it back up and burning it.

No, it is not infinite.
The sun has not an infinite mass neither does the earth. So energy is not infinite. But we probably don't really care about that as it applies at a scale we're not really concerned with. What is important at our scale is the rate at which is the rate at which the biomass we're destroying (eating, building houses with) is produced. The rate at which we consume this biomass has to not overpass the rate at which this biomass is produced. Than, practically speaking, biomass will be produced infinitely. Of course, ecosystem stability is not that easy but it is not within the scope of the post to talk about that.

Obviously not infinite, since the Earth has a finite mass, and the sun has a finite lifetime.  Also the Earth continually loses some (very small) fraction of its atmosphere & water to space, so eventually it would wind up like Mars (which was warmer, wetter, and probably habitable a billion years or so ago).

This is an interesting page. Mentions that the weathering of rocks will most likely deplete most CO2 from the atmosphere by about 600 million years from now. Some plants may survive for a little longer depending on what carbon fixation method they use. This would probably happen sooner than loss of atmosphere to space. I think the expansion of the sun will happen before then.

@user137 The Wikipedia article on Future of the Earth referenced above has so many faults, studded with facts, that it's not even wrong.


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Help reading chromatogram
A genetic variation is found in this chromatogram:

It says that the "reference sequence" is the top line and that I can use the general genetic code to find the reading frame.
I can see that there are two N's instead of a G and a C. However I don't know what this means. I'm also not sure how I'd find the reading frame? I suppose I could look for a start and stop codon but I could read them both ways?
Last question: Is this change likely pathogenic? I'm not sure how to classify a variation as pathogenic or not.

So the two Ns that you see are not necessarily variants, but rather likely just poor quality reads. Essentially when you sequence DNA and the sequencer can't make a call as to what the base is, it will just designate it N meaning that the base could be any of the four DNA bases.
As for finding the reading from, if you know this sequence contains a stop codon, that helps, and just look for any of the stop sequences. If not, look for bases that match codon sequences and if you get a full strand of sequence that codes for amino acids you will likely be correct.
For reference here is a link to a codon chart that will help you decipher the reading frame.
Does that help?

Yes absolutely, could you tell me if you can, whether the mutation is likely to be pathogenic, though? And if so, why?

So as cagliari says above it does not look like you have any mutations. You cannot call N a mutation because this could be any base including the one from the reference genome.

The traces you have come from Sanger sequencing. N in genetics means nucleotide (surprising right?). N is used when the base at a given location is unknown (or could be any base pairs).
In your case you have Ns because the base-calling software is unable to determine the nucleotide. The first N is due to two peaks overlapping (G and A signals) and the second one should be a C rather than a N.
From what I can see, you have no apparent mutations so no those changes are unlikely to be pathogenic. A mutation can be called when you know a base in the reference is modified in your sample, which is not the case here (simply N -> G and a N -> C). The signals for your Ns look very similar between your reference and your sample therefore not suggesting a mutation.
For the reading frame, you have to look for a start (ATG) and a stop codon (TAG,TAA or TGA) to identify the open reading frame (ORF). Multiple software do that and here a link to an online NCBI tool called ORF Finder.
As you pointed out the ORF can also be in the reverse strand. You don't want to look at the reverse sequence but at the reverse complementary sequence. Usually tools to detect ORFs have the option to look at both strands.


text:
Help reading gene markers
I'm sorry if "gene markers" is not the correct word. An edit could be appreciated but I don't study in an English speaking country unfortunately.
Question overview:
In a family, there is a genetic, dominant disease. The father and a son is sick.
A gene marker analysis is performed with markers close to the assumed mutated gene on chromosome 11.

Marker D11S4088

Marker D11S1344

How do I read these and "What sort of markers are these"? I'm not sure what is going on here and I'm not sure what to search either due to language problems.
Thanks!

From what kind of experiment / machine etc do these graphs come from?

I have no idea. It doesn't say unfortunately. Could be a chromatogram?

@BjarniJóhannsson Those are not chromatograms from what I can see but rather a sort of counts per marker graph. "Genetic markers" is a better word. Do you know about linkage mapping? If not read this wiki and this post, it should help.

I was thinking the same, or some sort of sequencing read coverage. I'm still not sure.

Just googling, they are SSLPs.  You do PCR, and the different alleles make different length amplicons.  Looks like there is some kind of artifact that causes some of the amplicons to have peaks that look 2, or 4, or 6 letters shorter than the true length.
So for the top marker, the 211 bp long allele is linked to the disease, and for the other one, the 118 bp allele is linked to the disease.


text:
Modeling inclusive fitness
Consider a population of two altruist with coefficient of relatedness
$r$. The average inclusive fitness of this population will be
$w_{0} + br -c$. Like in this example, assignment of inclusive fitness
I've seen in books and articles follow the rule that you should
not count changes in inclusive fitness that result from the
action of your neighbor. For instance, in our example, the calculation
of average inclusive fitness include the increase in indirect fitness
to the actor (i.e., $br$), the costs (i.e., $c$), but do not include
the effects of the altruist behavior of the neighbor (i.e., $b$). That
is, the average inclusive fitness is not $(w_{0} + br -c) + b$.
My question is: why is it that, in inclusive fitness models, you do
not count changes in inclusive fitness that result from the
action of your neighbor? Wouldn't it make the model more accurate to
take into account the effects of your neighbor's behavior? In other
words, in our example, why isn't $(w_{0} + br -c) + b$ a better value
for the average inclusive fitness than simply $(w_{0} + br -c)$?

Note:
As @Corvus pointed out, if we include changes in inclusive fitness that result from the action of your neighbor, we will double-count benefits. Consider the example mentioned above once again of a population of two altruists with a coefficient of relatedness $r$:

If we write $w_1 = w_2= (w_{0} + br -c) + b$, the help of 1 on 2 appears as $rb$ in $w_1$ and as $b$ in $w_2$. If we write the fitness in the right way, $w_1 = w_2= (w_{0} + br -c)$, the help of 1 on 2 is only counted once (i.e., $br$ in $w_1$). However, I cannot help but ask "Why not count the help of 1 on 2 twice?" We are counting the help of 1 on 2 twice, but each time we are assigning it to different individuals, 1 and 2.

This is a very good question and in short the answer is that inclusive fitness is only an approximation or what natural selection maximizes. That said, the quantity you propose is not a better explanation; it ends up double-counting benefits.  I'll try to write up a more detailed description soon.

It is good to have questions about social evolution. It is a superficially easy field that very quickly gets quite complicated when you dig into it. +1

@Remi.b Initially I thought that it wouldn't take me long to have a good grasp of the basic models of social evolution. I was sooo wrong.

Generalities
There are plenty of ways at looking at phenotypes that affect the fitness of the carrier and of other individuals. One of them is group selection and another one is kin selection. Those two concepts are just two different ways of looking at the same processes. Now let's consider only the kin selection way of looking at these processes.
You can either consider the impact of the phenotype of a focus individual to neighbour individuals or the impact of neighbour individuals to the focus individual. Looking at it both ways, would yield to count the effect of your phenotype on twice. It doesn't make much sense to talk about the mean inclusive fitness of a population. You can only talk about the mean fitness of a population.
The confusion
The reason for all these confusion boils down to what $B$ and $C$ really mean. One of the issue is that you confuse $B$ and $b$, $C$ and $c$. The formulation $rB>C$ is a oversimplification of the reality. Hamilton did not use this formulation at first and interpreting $b$ as the benefit for the carrier might be misleading. It is important to understand Hamilton's rule in its original formulation and it is important to understand the evolutionary game theory that underlies the evolution of social traits.
What is Hamilton's rule
One cannot study the evolution of social traits under the kin selection framework if (s)he doesn't understand the underlying game theory. $rB>C$ assumes that the game we're playing is the Prisoner's dilemna. You can learn more about game theory. You can learn more about evolutionary game theory on wiki or in this book. Here is a Khan academy video on Prisoner's dilemna
Let's assume we are playing prisoner's dilemna. The fitness of an individual which cooperate is by definition $w_o + b - c$ (note the letters are not capitalized). If you cooperate and the other don't, your fitness is $w_o - c$. If you don't cooperate and the other does cooperate, you fitness is $w_o + b$. If nobody cooperates, your fitness if $w_o$. And by definition , $b>c$. Knowing the frequency of people that cooperate in the population $y$ and knowing and your probability of cooperating is $x$. Then, the level of altruism (frequency of cooperations) increases in the population if and only if
$$R\cdot\frac{dw(x,y)}{dx}>\frac{dw(x,y)}{dy}$$, where $R$ is the coefficient of relatedness which can itself be expressed as a correlation between the variables $x$ and $y$. $w(x,y)$ is the fitness of the the individual being altruistic with probability $x$ in a population where individuals cooperate with probability $y$ and $\frac{dw(x,y)}{dx}$ is the partial derivative of the fitness function with respect to $x$. By definition, $\frac{dw(x,y)}{dx} = B$ and $\frac{dw(x,y)}{dy}=C$ (capital letters).
The mean fitness of the population therefore depends on the frequency of cooperation $y$. Let's assume for simplicity that $y=1$ (equilibrium), then the mean fitness of the population is $w_o + b - c$ (note that the letters, $b$ and $c$ are not capital letter), and the variance in fitness is null. All individuals has a fitness of $w_o + b -c$ as all individuals are altruistic and perform action that has a negative impact on the fitness $-c$ and a positive impact on their fitness $b$.
In short
$b$ and $c$ in your question, correspond to $b$ and $c$ in my answer and not to $B$ and $C$. If you're playing prisoner's dilemna, then by definition, if everybody cooperate (no variance in the population), then everybody has a fitness of $w_o + b - c$ and the mean fitness is $w_0 + b - c$ (as there is no variance). Now the question of whether everybody ends up cooperating depends on $B$, $C$ and $R$.
In your edit, you write $rb$ and $c$ but you get confused about the meaning of $b$ and $c$. If you are playing prisoner's dilemna, when you cooperate with someone that is also cooperating, you inclusive fitness is $b-c + r(b-c)$ and if you cooperate with someone that is not cooperating, your inclusive fitness is $b-c + r(b)$.

What is the quantity $w(x,y)$?

Sorry, it was unclear. See edit. $w(x,y)$ is the fitness of an individual cooperating with probability $x$ in a population that cooperate with probability $y$

You correct me if I am wrong, but your point seems to be that if we formulate Hamilton's rule using PD, my question doesn't arise. The reason seems to be that the derivation of Hamilton's rule via PD only deals with direct fitness. That is, instead of measuring the degree of genetic relatedness, $R$ measures positive assortment (i.e., how likely an altruist will interact with another altruist).

See the "in short" paragraph that I added. I am not sure I am answering your question. You will let me know.

I think I get what you're saying. This is an interesting way of deriving Hamliton's rule. If I understood it correctly, it looks for the conditions in which $dw/dx > 0$. Once we use the chain rule, we get the version of Hamilton's rule you wrote where $R = \beta_{yx} = dy/dx$.


text:
Does the body have a gate control for pain
I understand it is not the most accurate source but I recall a House episode where he claimed the body had a control mechanism for pain in which only the most painful thing was felt. Is that true? and if so how does the body control which injury we feel and could we use this to our advantage?

Speaking from personal experience, no, the body does not just focus on one area of pain, allowing only it to be felt and other injuries not to be. It just means you hurt in more places.

Afaik there is something like that by cold and pain (aka. cryotherapy). http://www.spine-health.com/conditions/chronic-pain/modern-ideas-gate-control-theory-chronic-pain

Pain receptors, more precisely pain signal propagation, can be inhibited in several ways. One is, for example, fine touch receptors (mechanoreceptor in illustration) inhibit propagation of pain signal in spinal cord (a lot of pain processing happens in spinal cord):

That is why humans often rub skin around or nearby injury, whether it is in joints or something more superficial. You should find more information about such control in any textbook on pain. See this page for short primer.
Next, pain propagation is modulated -- still in spinal cord -- by descending pathway from brain and brain stem. See this page for more, or address Kandel's textbook.
Now, I don't know whether or not it is identified how/where brain "selects" to what pain pay attention. My hypothesis is that it happens by competition, e.g. several signals compete by inhibiting each other via some mechanism, probably, related to stress-induced analgesia.

Firstly you have to take into consideration that nociceptors do not adapt to stimulus. This means that a nociceptor will not only fire at the beginning of the stimulus, as seen in mechanoreceptors that have phasic responses, but will fire as long as the stimulus lasts. This type of response is called tonic response (see figure). Figure A shows the tonic response whereas figure B shows the phasic response.

So by this, we can conclude that, peripherally, every noxious stimuli, will induce action potentials as long as that noxious stimulus lasts. During the ascending propagation of the action potentials induced by the noxious stimuli, other neurons will have the "opportunity" to inhibit the response. Some ways that the pain transmission can be inhibited is by the release of endogenous opioids by descending neurons from brain parts in mid-brain and medulla.
The other mechanism is the one explained above by aandreev. And as you mention in your title, this mechanism is called the gate control theory.
Ref: Purves et al (2012).,Neuroscience 5th ed.,Sinauer associates.
http://www.ucl.ac.uk/anaesthesia/StudentsandTrainees/PainPathwaysIntroduction [2015-04-30]


text:
Is cysteine deficiency possible?
Is there such a thing as cysteine deficiency in humans or other mammals?
What effects would such a deficiency have?
As I understand it, most cysteine for humans comes from dietary sources, though it can be biosynthesized in humans.

Cysteine deficiencies are possible, and one cause is the genetic disorder homocystinuria. Cysteine can be produced from methionine through a homocysteine intermediate, and defective genes for the enzymes involved can prevent proper cysteine production and cause a buildup of homocysteine. Patients have to eat a very carefully controlled diet with very low amounts of protein. This prevents homocysteine buildup by avoiding methionine exposure, but also requires that the patient take vitamin B6 and  B12 supplements and betaine. They might need to take cysteine supplements as well. The symptoms affect many organ systems, including the brain, nerves, and blood vessels, with about 25% of patients dying due to blood clots by age 30.


text:
Biostatistics: Pollen dispersal directionality
What Information am I looking for?
Think about a tree that is sending pollen all over the place. Because of wind, most pollen grain will go toward one direction. Imagine, we split the 2D area around the tree where pollen grains fall into two half disks of equal size. We chose the disks so that the number of pollen grains falling into one half-disk is minimized and the quantity of pollen falling in the other half-disk is maximized.
The information I need is what proportion of pollen grain falls into each disk? Is it $\frac{0.5}{0.5}$ (in which case the wind would have no effect) or is it something like $\frac{0.8}{0.2}$?
Where to get the information from?
I was reading this paper about pollen dispersal directionality and was trying to extract the info I need.
On pages 4 and 5 they explain their analysis under the section statistical procedure. More specifically, in the first paragraph of the 5th page, they seem to describe the meaning of the parameters that are trying to estimate. One of them is the so-called directionality parameter $\delta$. I don't understand how to interpret this parameter $\delta$.  This parameter is part of a logistic regression I think (although the authors do not characterize it as such) of "mating success" $y$ against variables $d$ ("distance") and $h$ ("height") and an angular variable $a = \cos(\alpha_0 - \alpha)$.  ($\alpha_0$ is the "presumed prevailing direction of effective pollen dispersal," which apparently is not estimated from these data.)  The corresponding parameters of the model are $\beta$, $\gamma$, and $\delta$, respectively, hence
$$\phi_j = \Pr(y_j = 1) = \frac{\exp\left(\beta d_j + \gamma h_j + \delta a_j\right)}{\sum_{k=1}^r \exp\left(\beta d_k + \gamma h_k + \delta a_k\right)}$$
where the index $j$ ranges over all $r$ "male(s) in the neighborhood."
Their Results
Using maximum likelihood, they found that the directionality parameter, $\hat\delta = 0.56$ (SE = $ 0.15$; bottom of page 6).
Question
How can I relate their finding to the information I need (even if it is just a rough approximation)?
I think I have to understand the so-called directionality paramter $\delta$ Can you help me to interpret the meaning of this parameter $\delta$?

Reference:
Burczyk, Adams, & Shimizu, Mating patterns and pollen dispersal in a natural knobcone pine ... stand.  Heredity 77 (1996) pp 251-260.

Not receiving any answer on Biology.SE, I asked the same question here on Mathematics.SE but sadly, the question doesn't receive any attention!

You might want to have this migrated to math. There are quite a few people their skilled in probability and stastitcs. Also, if we are minimizing and maximizing the two disk, it would seem strange 50/50 has a chance.

@dustin I would say this question is more related to biology as it is asking about the biological meaning of the δ parameter

@CactusWoman in the information I need section, it is a math question.

@dustin, if it is going to be moved, I think statistics might be more appropriate because it is about experimental design. That being said, the question is probably alright in biology.

@dustin Biology involves math, especially population genetics. This question should not be migrated in my opinion and is perfectly relevant for Biology.SE.

@cagliari2005 pretty much every subject out there has some math component but who offers better help in mathematics? Peoples whose only job is mathematics or people who learn math when they need it?

Even before, opening this question on Biology.SE (and therefore before positing the same on Mathematics.SE), I actually posted my question on CrossValidated.SE but it received little attention and I ended up deleting the post (to avoid cross-posting) to open this post on Biology.SE. Thank you guys for your help!

(This isn't an answer, but hopefully it will help get it past the experimental design into just solving the equation.)
Where did you get that α0 was not determined from their data? On p. 10 (256), they state, "The prevailing direction of effective pollen dispersal within neighbourhoods (a0) that gave the best ﬁt of the model was 91 degrees from north (nearly due east)."
The best-fit δ parameter value of 0.56 (which determines the size of the effect of the angle between the male tree and the wind) is also determined by their model (table 1, model 9) based on their sample set.
This math is too much for me to solve, but here is how I would go about getting through the experimental setup to just solving the math equation:
Since you're only looking for the effect of wind/directionality, you would set the tree height and distance between trees to be equal. So βd and γh would remain constant and cancel out when you solve for a.
Then you want to determine what angles would give you the highest and lowest pollen counts. Set a0 to wind direction and aj to the angle between a0 and the half disk. The highest pollen count would happen at aj = a0. The lowest pollen counts would happen at aj = (a0-180) or (a0-π or whatever unit of angle is appropriate. Stupid trig.).
With those settings, it should be possible to determine the values of ϕ where aj = a0 and where aj = a0-180.
Then you can get the proportion of pollen grain falls into each disk by finding the ratio of ϕj(a0-180) / ϕj(a0).
Assumptions:
1) There's a linear correlation between ϕ, "the mating success (i.e. fertility) of each outcross male in the neighbourhood" and the distribution of pollen grain dispersal.
2) That a0 ("The prevailing direction of effective pollen dispersal within neighbourhoods") is entirely due to wind. Here I could see terrain being a factor, which would make the effect of wind xδ, such that x<1. If this were the case, the calculated ratio of high pollen / low pollen would be higher than actual.

The looks great. I'll have to reread that tomorrow morning with a fresher mind! +1 in the meantime. Let me know if you can come up with an actual number for the proportions in the half disks. Thank you so much for your help.


text:
What are the survival limitations of alcohol?
This question was inspired by watching one of the Pirates of the Caribbean movies; particularly where Jack Sparrow allegedly survives on a desert island by finding an unlimited supply of rum. I've heard alcoholic drinks dehydrate you more than hydrate you, so this seems like an unsustainable strategy.
My question is threefold.

How long can a human survive by drinking hard liquor (40%
alcohol by volume) for their sole water intake (ignoring food)?
If it's unsustainable, what will finally take you down?
If the hard-liquor approach isn't viable, what % alcohol can
keep you hydrated (beer, wine, etc.)?

Related:
1. Question on dehydration studies
2. Question on what dehydrates

I would say that the main problem with high percentage alcohol is that it is a cytotoxic substance which will not do good.

There are a lot many things that can happen because of excessive alcohol consumption. First of all the gut will be affected. Excessive drinking can also cause palpitations

One reason this is too broad is there are many ways of drinking alcohol - three tots in a row, spaced out over an hour, etc. - and these things matter when you're dealing with a toxin.  Also, the rum he was drinking was probably greater than 40%, especially if it lasted that long.

I commented above that it will depend heavily on at what pace you drink your rum, but in short, no, no you cannot.  If you do it quickly, you'll die of alcohol poisoning, and if you drink it slowly, you'll probably die of dehydration[1].
io9 summed up some research a few years ago, the majority of which is largely bunk.  One study (ncbi, free pdf) however, from 1996, claimed to find that:

These results suggest that alcohol has a negligible diuretic effect
  when consumed in dilute solution after a moderate level of
  hypohydration induced by exercise in the heat. There appears to be no
  difference in recovery from dehydration whether the rehydration
  beverage is alcohol free or contains up to 2% alcohol, but drinks
  containing 4% alcohol tend to delay the recovery process.

So stick to (American) beer.
Sidenote: In Belgium, they divide their (truly excellent) beer into two categories: special, which are stronger and often bottled, and thirst-quenching, which have a lower alcohol content and are often had with lunch.
[1]: Citation: Personal experience and the story of Johnny Tarr.

Interestingly enough, the mainstay drink in the Middle Ages (medieval times) was "small beer" (cheap low-quality beer with low alcohol content). Back then there was no concept of water purification and treatment - most of the water in a town or city back then would be loaded with pathogens and considered unsafe/unsuitable for drinking. The alcohol in "small beer" was enough to eliminate most of these pathogens while dilute enough to be used almost like water.
However, health problems quickly start as the amount of alcohol increases. As Amory mentioned, 4% alcohol weighs on dehydration recovery. There's no way anyone could survive on a desert island drinking only 40% alcohol hard-liquor or similar.
No matter if the rum is spaced out over time or consumed like water, it's a non-solution. Spacing it out over time and allowing proper detoxification over time will be insufficient to keep up with regular water needs; drinking it like water will quickly cause lethal alcohol poisoning.

Beer contains roughly 5% alcohol. This isn't anywhere near the concentration to kill most of the pathogens possibly present. Beer was interesting, because it is boiled in the process and is thus less likely to be spoiled than pure water at that time. Additionally it would be great if you could add sources to all of your answers.


text:
what is linkage disequilibrium supposed to measure?
During reading about genetics I came across with the term of linkage disequilibrium, and I do not really understand what it supposed to mean. What is linkage disequilibrium? My current understanding that it is "deviation from independent assortment",

@Corvus - you were right, I totally mixed the two things..thx for pointing that out.  This is a good sign that I should go to sleep, I had a long day and its almost midnight.

@poka.nandor I know the feeling! Cheers.

Cagliari -- this is false. The definition of linkage  disequilibrium involves nonrandom association between alleles at different loci. One cause of linkage disequilibrium is physical linkage like you describe, but linkage disequilibrium can exist without physical linkage, Eg due to natural selection.

Linkage disequilibrium refers to a situation whereby two or more alleles, from different loci, segregate non-randomly. Therefore we have a statistical association between this two alleles.
The linkage disequilibrium can be used in gene mapping, because we assume that these loci are in the same region on the chromosome. The more often they appear together, the more they segregate non-randomly, the closer they should be on the chromosome.
http://www.researchgate.net/post/What_is_the_difference_between_Linkage_Equilibrium_and_Linkage_Disequilibrium


text:
Mammal vs Placental Mammal
So for Google Earth Day's quiz I ended up being a "Pangolin." Turns out I had no idea what it was so I looked into it and honestly it reminded me a lot of an Armadillo. So I decided to find out the difference between the two, and I stumbled across this site.
It was all making sense until I got to the "bullet points" at the bottom where I saw this

Pangolin is a mammal while armadillo is a placental mammal.

And I'm now very confused. I thought placental mammal was just a subset of mammals. And I look up Pangolin's taxonomy and now I'm seeing all kinds of stuff I have no idea how to interpret. Back in my day, it was "Kings Play Cards On Fat Green Stools" for "Kingdom Phylum Class Order Family Genus Species". And now I'm seeing things like clade, infraclass, subcohort, superorder and all kinds of things I just don't get.
So I guess I have many questions, but I'm going to boil it down to "If the Pangolin isn't considered a placental mammal, then what kind of mammal is it, and where does it diverge in taxonomy from the Armadillo?"
Oh, and if someone could point me to a primer on the changes to taxonomy in the last 20 years, that'd be cool too.

Both are placental mammals.

Although the Kingdom Phylum Class Order Family Genus Species version of taxonomy is still being taught, it's mostly for convenience's sake. The truth is all higher named clades (like Genera or Orders) are chosen somewhat arbitrarily. So, if people want to talk about a clade that, say contains all of the organisms of several genera but not all of the organisms in the family, they might talk about it as being a subfamily. In short, I would say don't waste your time worrying about the difference between an infraclass and superorder and focus more on comparisons between clades

From the Tree of Life page for Mammalia:

All of these groups of animals are mammals, including extinct triconodonts and multituberculates. Among living mammals are monotremes (most notably the platypus), marsupials (kangaroos and opossums), and eutherians. Eutherians are placental mammals, so all eutherians are placental mammals, but not all mammals are eutherians.
Both armadillos and pangolins are eutherian mammals, so both are mammals and both are placentals. "Difference Between" is quite incorrect.