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High frequency human genetic oscillators?
The most well studied genetic oscillators in human genomes are involved in regulating the circadian clock (which operates on an approximately 24-hour cycle) and cell cycle activity (with single cycles usually lasting several hours to many days). Are there any known genetic oscillators in humans (or other mammals) that operate on shorter timescales?

Many mammalian cells (or cell lines) have cell cycle period < 24hours. What timescale are you interested in. Usually it takes few hours for proteins to achieve steady states.

I'm looking for an example where oscillations occur within hours and are not coupled to the cell cycle. Thanks!

Natural or synthetic ?

Natural, and the simpler (fewer parts) the better. I'm looking for an endogenous oscillator that can be coupled to synthetic circuits.

Here are some examples:

electric oscillators:

neural activity
cardiac automatism (0.8 ... 1 Hz)

mechanical oscillators (as a result of neural activity):

heart beats
breathing (0.2 ... 0.3 Hz)
intestinal peristaltic waves
vocal chords activity (up to a few kHz)
muscular spasm (pathological)

chemical oscillators:

insulin variation in concordance with glucose intake
endocrine oscillations
menstruation
feedback enabled metabolic pathways

See this Wikipedia page too: http://en.wikipedia.org/wiki/Oscillation#Human
When it comes to genetic oscillators, some of them follow circadian rhythm.

A typical proliferating human cell divides on average every 24 h. This division timing allows cells to synchronize with other physiological processes and with the environment. The circadian clock, which orchestrates daily rhythms, directly regulates the cell division cycle and is a major synchronizing factor [5].

Immune system:

In every single cell an oscillator goes ticking through a molecular clock operated by transcriptional/translational feedback loops driven by the rhythmic expression of circadian genes. This clock gene machinery steers daily oscillations in the regulation of immune cell activity, driving the periodicity in immune system function [1].

Glucose homeostasis:

The master circadian clock, localized in suprachiasmatic nucleus (SCN), regulates multiple metabolic pathways, while feeding behavior and metabolite availability can in turn regulate the circadian clock [2].

Retina:

... the retina itself possesses intrinsic circadian oscillations, exemplified by diurnal fluctuations in visual sensitivity, neurotransmitter levels, and outer segment turnover rates. Recently, it has been noted that both central and peripheral oscillators share a molecular clock consisting of an endogenous, circadian-driven, transcription-translation feedback loop that cycles with a periodicity of approximately 24 hours [3].

But there are others which don't.

Genetic oscillators are ubiquitous regulatory motifs in the molecular control circuits of living cells. Prominent examples include the cell cycle and cellular signaling [4].

The frequency is much lower in some human cells [6]:

Cell Type      Process    Time
______________ __________ ______________________
fly embryo     mitosis    8 minutes
bacteria       mitosis    20 minutes
yeast          mitosis    2 hours
human skin     mitosis    20 - 24 hours
human sperm    meiosis    about 64 days
human liver    mitosis    1 year or more
human egg      meiosis    up to 40 years or more
human nerve    mitosis    never, once mature

References:

Vinciguerra M, Borghesan M, Pazienza V, Piepoli A, Palmieri O, Tarquini R, Tevy MF, De Cata A, Mazzoccoli G. The transcriptional regulators, the immune system and the the circadian clock. J. Biol. Regul. Homeost. Agents. 2013;27(1):9-22. PubMed PMID: 23489683.
Chrościcki P, Usarek M, Bryla J. [The role of biological clock in glucose homeostasis]. Postepy Hig Med Dosw (Online). 2013 Jun 20;67:569-83. doi: 10.5604/17322693.1053906. PubMed PMID: 23799401.
Ramsey DJ, Ramsey KM, Vavvas DG. Genetic advances in ophthalmology: the role of melanopsin-expressing, intrinsically photosensitive retinal ganglion cells in the circadian organization of the visual system. Semin Ophthalmol. 2013 Sep 6;28(5-6):406-21. doi: 10.3109/08820538.2013.825294. PubMed PMID: 24010846.
Davit A. Potoyan and Peter G. Wolynes. On the dephasing of genetic oscillators. PNAS 2014 ; published ahead of print January 27, 2014, doi:10.1073/pnas.1323433111
Samuel Bernard and Hanspeter Herzel. Why Do Cells Cycle with a 24 Hour Period? Genome Informatics 17(1): 72{79 (2006).
wiseGEEK.org. How Long Does it Take for Cells to Divide? (accessed 21.07.2014)

Great list! Thanks! Sorry, I was too vague in my question. I've edited it to refer specifically to 'genetic' oscillation. Do you have an example of a 'feedback enabled metabolic pathway' where high frequency oscillations depend on RNA/protein expression and degradation? Sorry for the confusion.

Thanks! This is a solid answer. Reference 4 is especially helpful.


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Would it be possible to force the pineal gland to release dimethyltryptamine on command?
To my knowledge, the pineal gland is responsible for the release of dimethyltryptamine (DMT) upon death.  Would it be possible to force the pineal gland to release this DMT while still living?

According to this page the release of DMT upon death is speculative and its presence has so far been confirmed in rodents brain and human melanoma cell line SK-Mel-147. DMT is also produced in humans; however, its production and purpose in the brain has yet to be proven or understood (http://en.wikipedia.org/wiki/Dimethyltryptamine). Hence from what I have gathered on the matter DMT has not yet been proven to get secreted from human pineal gland and its command based secretion is yet to be discovered.

Personal research on 4chan has revealed a group of people who believe that DMT is a molecule responsible for spirituality and that the pineal gland has some sort of supernatural/psychic function. They also believe that fluoridation of water is a government conspiracy to calcify the populations' pineal glands and cut off that supernatural function. Just thought I should warn you where these questions come from in case we get more.

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What are the atmospheric requirements for large dinosaurs?
What are the atmospheric requirements for large dinosaurs? and are the atmospheric constituents for supporting large dinosaurs any different from the atmosphere today?

nice question! worth looking at the atmospheric composition of earth at that time but whether that was the optimal atmosphere for large dinosaurs is much harder to tell I would imagine!

@caseyr547 good point! but it would still be interesting to know about the atmospheric composition of earth at that time and whether that was in anyway more suitable to species back then compared to now if they switched environments. I suppose species back then either had to adapt or die based on the particular atmospheric conditions they were in although it is more likely that they evolved slowly over time as with any other evolutionary processes. I agree with you but thought provoking still.

In general large animals would need more oxygen. This would be especially true for animals with less efficient oxygen transport, such as insects. There was more oxygen in the atmosphere in the distant past due to an imbalance in cellulose creation and digestion. This is also where coal comes from. It's explained in more detail in some episode of Cosmos ( the new one ). If I find more details I'll come back with an answer.

Thanks for this info! From that data, I wonder if something besides oxygen levels may have been involved 350,000 years ago. Isn't the real issue the partial pressure of oxygen and not just the amount of it? Is there any reason to believe that partial pressures of oxygen varied? Can that be detected in the rock record?

Oxygen levels have changed greatly throughout Earths's history starting with very little atmospheric oxygen and gradually increasing as photosynthetic activity appeared until all the oxygen sinks such as minerals had been filled, then taking off, reaching as high as 35% of the atmosphere during the carboniferous period 3. The reasons behind this sudden increase in O₂ has to do with the development of bark covered wooden plants, a feature made possible by the molecule lignin, which strengthens the trunks of trees and makes tall plants possible. However, lignin was hard for microbes to digest, and the dead trees built up, never returning their carbon to the atmosphere as CO₂. So the oxygen they had made while alive stayed in the air 4.

The plot shows the upper (red) and lower (green) estimates for O₂ concentration over time. The data for this plot was taken from a review of analysis of sulfur, carbon, iron, and manganese deposits 2. If you're interested in how isotopic analysis can give information about atmospheric oxygen, read that paper, it's detailed.
That spike in the plot is the carboniferous. This period in history is interesting because of the appearance of large invertebrates, such as 3 foot wide dragonflies and 6 foot long centipedes 5. Since these animals move oxygen through a series of tubes called trachea, where air just moves through by diffusion, it was speculated that the higher concentration of oxygen allowed this growth. Recent research indicates that insects can force air through their trachea, and that competition between predators and prey could have explained most of the size 6.
So how does this affect dinosaurs? The carboniferous period was about 350-300 million years ago, which corresponds with the spike on the graph. Dinosaurs appeared in the Triassic, which was about 250-200 million years ago, but oxygen levels were at 16% of the atmosphere at the time 7 ( current O₂ levels are about 20% ) If we move into the Jurassic, about 200-150 million years ago, oxygen levels rise to about 26% 8. In the Cretaceous, about 150-65 million years ago, O₂ was at about 30% 9. The O₂ percentages are taken from the infoboxes on the right side of the wikipedia articles, which in turn take the number from a plot very similar to the plot I posted here, despite being in German 10.
I compiled lists of heaviest and lightest dinosaurs by going through the wikipedia article on dinosaur size 11 and going to the article on each dinosaur and checking if it was Triassic, Jurassic, or Cretaceous.
If we look at the heaviest dinosaurs, most of them appeared during the Cretaceous:
Heaviest Dinosaurs
Theropods                           Metric Tons     Period
Spinosaurus aegyptiacus             7-20.9          Cretaceous
Carcharodontosaurus saharicus       6.1-15.1        Cretaceous
Giganotosaurus carolinii            6.1-13.8        Cretaceous
Tyrannosaurus rex                   6-9.5           Cretaceous
Oxalaia quilombensis                5-7             Cretaceous
Acrocanthosaurus atokensis          5.6-6.2         Cretaceous
Tyrannotitan chubutensis            4.9-5.6         Cretaceous
Suchomimus tenerensis               2.7-5.2         Cretaceous
Therizinosaurus cheloniformis       5               Cretaceous
Tarbosaurus bataar                  4-5             Cretaceous

Sauropods                           Metric Tons     Period
Amphicoelias fragillimus            122.4           Jurassic
Argentinosaurus huinculensis        60-90           Cretaceous
Antarctosaurus giganteus            69-80           Cretaceous
Mamenchisaurus sinocanadorum        75              Jurassic
Sauroposeidon proteles              40-60           Cretaceous
Paralititan stromeri                59              Cretaceous
Brachiosaurus altithorax            28.7-56.3       Jurassic
Puertasaurus reuili                 50              Cretaceous
Ruyangosaurus giganteus             50              Cretaceous
Alamosaurus sanjuanensis            50-60           Cretaceous
Futalognkosaurus dukei              38.1-50+        Cretaceous
Turiasaurus riodevensis             40-50.9         Jurassic/Cretaceous
Camarasaurus supremus               47              Jurassic
Diplodocus hallorum                 30-42.5         Jurassic
Supersaurus vivianae                32-40.2         Jurassic
Elaltitan lilloi                    42.9            Cretaceous
Tehuelchesaurus benitezii           41.3            Jurassic
Apatosaurus louisae                 18-41.3         Jurassic

Ornithopods                         Metric Tons     Period
Shantungosaurus giganteus           9.9-22.5        Cretaceous
Iguanodon seeleyi                   15              Cretaceous
Saurolophus angustirostris          6.6-9           Cretaceous
Iguanodon bernissartensis           8.3-8.6         Cretaceous
Edmontosaurus annectens             3.2-7.6         Cretaceous
Brachylophosaurus canadensis        4.5-7           Cretaceous
Saurolophus osborni                 6.6             Cretaceous
Lanzhousaurus magnidens             6               Cretaceous
Parasaurolophus walkeri             3-5.1           Cretaceous
Charonosaurus  jiayinensis          5               Cretaceous
Barsboldia sicinskii                5               Cretaceous

Ceratopsians                        Metric Tons     Period
Triceratops horridus                5-14            Cretaceous
Triceratops prorsus                 6.5-11          Cretaceous
Titanoceratops ouranos              6.5-11          Cretaceous
Eotriceratops xerinsularis          10              Cretaceous
Pentaceratops sternbergii           3-4.8           Cretaceous
Pachyrhinosaurus canadensis         3-4.4           Cretaceous
Styracosaurus albertensis           4.2             Cretaceous
Agujaceratops mariscalensis         2.6             Cretaceous
Centrosaurus apertus                1.1-2.5         Cretaceous
Coronosaurus brinkmani              2               Cretaceous
Rubeosaurus ovatus                  2               Cretaceous
Achelousaurus horneri               2               Cretaceous
Pachyrhinosaurus lakustai           2               Cretaceous
Chasmosaurus belli                  2               Cretaceous

Thyreophorans                       Metric Tons     Period
Dacentrurus armatus                 5-7.4           Jurassic
Ankylosaurus magniventris           1.7-6           Cretaceous
Stegosaurus stenops                 2.6-5.3         Jurassic
Cedarpelta bilbeyhallorum           5               Cretaceous
Hesperosaurus mjosi                 3.5-5           Jurassic
Tuojiangosaurus multispinus         4.8             Jurassic
Wuerhosaurus homheni                4               Cretaceous
Niobrarasaurus coleii               4               Cretaceous
Stegosaurus ungulatus               3.5             Jurassic
Gobisaurus domoculus                3.5             Cretaceous
Nodosaurus textilis                 3.5             Cretaceous
Palaeoscincus costatus              3.5             Cretaceous
Sauropelta edwardsi                 3               Cretaceous
Edmontonia rugosidens               3               Cretaceous
Edmontonia schlessmani              3               Cretaceous
Edmontonia longiceps                2.3-3           Cretaceous
Tuojiangosaurus multispinus         2.8             Jurassic
Euoplocephalus tutus                2-2.7           Cretaceous
Jiangjunosaurus junggarensis        2.5             Jurassic

This isn't exactly a fair way to do it, but I didn't want to calculate average dinosaur mass over time. I know that some groups, such as the ceratopsians didn't appear until the late Jurassic, skewing the results, and I didn't make any attempt to differentiate between late or early periods. However I also noticed that many of the smallest dinosaurs appeared in the Cretaceous as well. Pay attention to the units, even the smallest sauropods are measured in metric tons.
Lightest Dinosaurs
Theropods                           kg              Period
Parvicursor remotus                 0.137           Cretaceous
Epidexipteryx hui                   .164-.391       Jurassic
Compsognathus longipes              0.26            Jurassic
Ceratonykus oculatus                0.3             Cretaceous
Juravenator starki                  0.34-0.41       Jurassic
Ligabueino andesi                   0.35            Cretaceous
Microraptor zhaoianus               0.4             Cretaceous
Sinosauropteryx prima               0.55-0.99       Cretaceous
Rahonavis ostromi                   0.58            Cretaceous
Mahakala omnogovae                  0.76-0.79       Cretaceous
Xiaotingia zhengi                   0.79            Jurassic
Mei long                            0.85            Cretaceous
Microraptor gui                     0.95-1.50       Cretaceous

Sauropods                           Metric Tons     Period
Pleurocoelus nanus                  0.5             Cretaceous
Magyarosaurus dacus                 0.75            Cretaceous
Europasaurus holgeri                0.8-1           Jurassic
Bonatitan reigi                     1               Cretaceous
Lapparentosaurus madagascariensis   1.4             Jurassic
Lessemsaurus sauropoides            1.8             Triassic
Lirainosaurus astibiae              1.8-4           Cretaceous
Shunosaurus lii                     2.2-6.7         Jurassic
Ampelosaurus atacis                 2.5             Cretaceous
Amargasaurus cazaui                 2.6-3.8         Cretaceous
Hypselosaurus priscus               2.7-8           Cretaceous
Euhelopus zdanskyi                  3.4             Cretaceous
Neuquensaurus australis             3.5-6.1         Cretaceous
Rinconsaurus caudamirus             4.1             Cretaceous
Atacamatitan chilensis              4.3             Cretaceous
Dicraeosaurus hansemanni            4.4-5           Jurassic

Ornithopods                         kg              Period
Gasparinisaura cincosaltensis       1-13            Cretaceous
Yueosaurus tiantaiensis             3.9             Cretaceous
Fulgurotherium australe             6               Cretaceous
Notohypsilophodon comodorensis      6               Jurassic
Yandusaurus hongheensis             6.6-7.5         Jurassic
Hypsilophodon foxii                 7-21            Cretaceous
Thescelosaurus sp.                  7.9-86          Cretaceous
Valdosaurus canaliculatus           10              Cretaceous
Haya griva                          11              Cretaceous
Agilisaurus louderbacki             12              Jurassic
Drinker nisti                       20              Jurassic
Changchunsaurus parvus              20              Cretaceous
Qantassaurus intrepidus             20              Cretaceous
Zephyrosaurus schaffi               20              Cretaceous
Oryctodromeus cubicularis           20              Cretaceous
Orodromeus makelai                  20              Cretaceous

Ceratopsians                              kg        Period
Liaoceratops yanzigouensis                2         Cretaceous
Yamaceratops dorngobiensis                2         Cretaceous
Psittacosaurus sinensis                   4.1       Cretaceous
Psittacosaurus lujiatunensis              5         Jurassic
Yinlong downsi                            5.5       Cretaceous
Micropachycephalosaurus hongtuyanensis    5.9       Jurassic
Chaoyangsaurus youngi                     6         Jurassic
Xuanhuaceratops niei                      6         Jurassic
Bagaceratops rozhdestvenskyi              7         Cretaceous
Psittacosaurus meileyingensis             8         Cretaceous
Psittacosaurus neimongoliensis            8-8.4     Cretaceous
Archaeoceratops oshimai                   10        Cretaceous
Psittacosaurus mongoliensis               12.1-20   Cretaceous
Psittacosaurus sibiricus                  15        Cretaceous

Thyreophorans                       kg              Period
Scutellosaurus lawleri              3               Jurassic
Emausaurus ernsti                   50              Jurassic
Scelidosaurus harrisonii            64.5-270        Jurassic
Animantarx ramaljonesi              300             Cretaceous
Struthiosaurus transylvanicus       300             Cretaceous
Struthiosaurus austriacus           300             Cretaceous
Gargoyleosaurus parkpinorum         300             Jurassic
Mymoorapelta maysi                  300             Jurassic
Minmi paravertebra                  300             Cretaceous

So what does this mean for the relationship between oxygen levels and dinosaur size? Higher oxygen levels in the Jurassic and Cretaceous probably allowed for larger animals to exist, however as time went on Dinosaurs became more diverse in general, including size. Many of them evolved to become smaller, despite being allowed to become larger by higher levels of oxygen. We should also note that even though oxygen levels were still lower than they were during the carboniferous, the animals were much larger, most likely due to their more efficient oxygen transport systems (lungs, 3(4?) chambered hearts, sealed circulatory systems, hemoglobin).
If we think about what could drive species to become larger, competition for food and protection from predators comes to mind. Sauropods that could reach the leaves in taller trees had distinct advantages over those who could not. Prey animals stood a better chance at fighting off predators if they were bigger. Likewise, predators could kill larger prey if they became larger too. Oxygen didn't drive them to become larger, it simply allowed them to.
To actually answer the question, could the modern atmosphere support animals as large as dinosaurs? It probably could. The heaviest living animal today is the blue whale, at an average mass of 110 metric tons, is heavier than all but 1 of the sauropods on the list I compiled. The heaviest land animal living today is the African Elephant, with average mass of 4.9 metric tons and as high as 10 metric tons, would be a respectable competitor with many of the dinosaur groups I listed 12.
Another interesting question is not how oxygen affected the size of organisms, but how it affects it their metabolism. Cold blooded animals don't need as much oxygen because they don't spend as much energy. Warm blooded animals must constantly expend energy to maintain body heat, and this requires greater consumption of oxygen. Obviously being large and warm blooded would force you to need even greater levels of oxygen than 1 or the other. It may be that the advantages of being warm blooded outweighed the advantages of large size, but I don't want to dig into that question right now.

How can I make those lists look better? I wrote them in a spreadsheet, and I'd like to make them look like a spreadsheet here too. I know how to make a table in HTML, but I don't want to write that much HTML by hand.

Tables are cleaned up, citations are inlined, and added some information about how the % O2 was determined, with a link to an article with much more detail than I could post here.

I'm not so sure that larger land animals require that much more oxygen.  The problem is metabolism's waste heat.
Anyone remember the square-cube law?  All other things being equal, double an object's size, and its area quadruples, while its volume octuples.
Broadly speaking, an object loses heat in proportion to surface area, while an animal produces heat in proportion to volume.  For our double-sized creature, heat production per unit area would double.
Other things being equal, to reduce overheating, metabolic rates would have to go down, thus reducing the oxygen demand.
Conversely, consider the opposite: a creature half the size of the original.  It now produces half the heat per unit area.  If it needs to maintain a minimum body temperature, then (other things being equal) its metabolic rate will need to go up.  This will certainly be easier if the oxygen concentration is higher.
Of course, other things are never equal, so this is only one piece of the puzzle.  But it seems that, for land animals that are already large, increased oxygen levels alone should push size downward.
Or am I missing something?

Also, why would land animals necessarily require more oxygen than aquatic ones?  The largest whales today weigh more than the largest known dinosaurs, and they do perfectly well on the current atmosphere.

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Has it been confirmed yet that the DNA found in dinosaurs was really DNA?
I hear different sources claiming different things, bbc said they did, wikipedia says it hasn't which is it?

I have never read from any reputable source that DNA was extracted from some dinosaur bone. They did manage to sequence a few partial proteins like collagen through mass spectrometry a few years back..

Which source says that DNA has been found? I am not aware that any discoveries have been made.

Apparently it wasn't. According to Wikipedia, A study that reported Dinosaur DNA was,

mitochondrial cytochrome b sequences that had apparently been
  extracted from dinosaur bones dating to over 80 million years ago
  (reference).

However, contamination was found in the reported study (reference). Don't expect too much because this is a close to impossible task (reference 1). Most researchers pinned their hopes on DNA surviving trapped in amber resin but even that is not possible (reference).
If interested in cloning a dinosaur, quickly go through this article (or not).

Could an approximation of dinosaur DNA be made by analyzing the genomes of modern birds and trying to come up with a closest common ancestor? If it worked at all, it would probably be closest to DNA for an Archeopteryix, not a Tyranosaur.

@user137 That would be hard or next to impossible I would say. There has obviously been many many mutations  before when an Archeopteryix evolved into the birds of today. Going back means estimating these mutations as well as estimating what genes might have been present or not. There is a limit to these estimations and it would never be accurate enough.


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Pharmacokinetics: why do certain drugs follow zero-order kinetics?
I understand that alcohol and phenytoin are two examples of drugs that follow zero-order kinetics. Why do these two particular drugs follow zero-order kinetics as opposed to first-order kinetics?

Hi and welcome to Biology.SE! We encourage making a decent attempt to answer questions before we make new posts - could you let us know some of your thinking that led to this question, and what part of it you couldn't find easily by searching the web?

Zero-order kinetics is linear, and the rate of metabolism of a particular drug is constant despite the amount of drug present. I was curious to know if there were any biochemical processes involved that would cause alcohol and phenytoin to follow zero-order kinetics.

You would observe zeroth order kinetics when the metabolism is dependent on a catalyst (enzyme) that is limiting. Very low $K_m$ and low enzyme concentration compared to substrate would show this kind of effect.

Basically any compound in concentrations sufficient to saturate its metabolization machinery will show zero-order pharmacokinetics. This reflects the fact that metabolization is taking place at full speed while facing a comparatively enormous amount of substrate (just as @WYSIWYG pointed out). This effect can also be shown in vitro with pure substrate/enzyme solutions.
But the above is a rather simplistic model, valid only in specific situations.
Most of the time in humans, zero-order kinetics stem from the fact that liver enzymes are saturated. However, for most drugs the redistribution phase is much more important than metabolization/elimination in defining the duration of effect. A good example of that would be sodium thiopental. As a single iv bolus dose, it will induce loss of consciousness for a short time due to redistribution. However, continued infusion will allow blood and tissue concentrations to equilibrate, and then the metabolization/elimination rate will become much more prominent in defining the duration of effect. And as sodium thiopental happens to have zero-order metabolization kinetics in continued infusion, it will take you a loooooooooong time to wake up! This is why in human pharmacology, we use context sensitive half-life to better represent drug kinetics.

Alcohol is a drug that is cleared by an enzyme. This interaction is what follows zero-order behavior. However, initially alcohol follows first order behavior because the ability of the enzyme to clear the alcohol exceeds the concentration of alcohol. That means clearance is constant and does not depend on the alcohol concentration.
Now what makes alcohol zero order is that the desired effect of alcohol (the therapeutic effect) occurs when the dose is greater than that enzymes ability to clear the alcohol. Once the alcohol concentration is greater than a certain point the body begins to struggle to clear the alcohol (roughly near the Km of the clearance enzyme) because of a physical limitation on the quantity or quality of the enzyme. So now when you increase the concentration of alcohol, the rate of clearance is not able to account for that increase proportionally because it is saturated. Therefore the alcohol you consume after a certain point (Km of the clearance enzyme) has a greater toxic effect. One drink too many is a very real thing.


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What is the purpose of Y-shaped adapters in Illumina sequencing?
Y adapters different sequences to be annealed to the 5' and 3' ends of each molecule in a library.
The arms of the Y are unique, and the middle part, connected to the DNA fragment, is complementary.
What are the advantages of this?
My take of this over having fully-complementary adapters (ADAPTER1 - - - - - ADAPTER1) is that:
-Upon primer annealing, the primer in turn would bind to the start AND end of the DNA fragment, and thus not allow synthesis to continue to until the end. Therefore, the next primer would not have a template to bind at the start of the fragment...
Y-shaped adapters also allow for paired-end sequencing. Fragments have a unique sequence on either end, which allows for the first "run" to sequence one side of all molecules, then synthesize the reverse and sequence that.
Am I on the right track?

This looks like a nice explanation.

Normally, when you need two unique adapters, say A & B, on either end of unknown insert sequences, cohesive-end ligation is difficult because the insert sequences are "unknown". So you have to do blunt-end adapter ligation, in a reaction containing Unknown Inserts + adapter A + adapter B. This can result in 3 possible versions of insert-ligated product: A-insert-A, B-insert-B and A-insert-B, among which only A-insert-B is the only desired product.
1) Ligation of A-tailed inserts with Y-adapters gives you 100% A-insert-B.
2) Lets now assign a directionality to the insert - say from base 1 to base 400. Following Y-adapter ligation, you will have 2 kinds of insert-ligated products per insert: A-Insert (1-->400)-B and A-Insert(400-->1)-B, both of which are very useful. Each will create a separate clonal cluster and you will get sequence information starting at both base 1 and base 400 of the insert, since in single-read sequencing, the instrument always sequences from Adapter A. However, to know that both these sequences belong to the same insert, one will need to do paired-end sequencing.


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Primer design and BLAST E value stringency
When searching for misprimings I have been told that an e value that is higher than 0.01 is ok and will produce no significant amounts of mispriming. Yet I searched some and it would seem that the e value threshold limit is dependent upon the "amount of information" in the database.  Indeed I found that some papers cite as values lower than 0.07 to be significant already.
What are the criteria you use at times to judge this issue, and how do I know when to lower or increase my stringency when running a routine BLAST for the purposes of designing primers?

I never used BLAST for primer design, but often for finding out where a sequence came from.
From the FAQ of the NCBI:
http://www.ncbi.nlm.nih.gov/blast/Blast.cgi?CMD=Web&PAGE_TYPE=BlastDocs&DOC_TYPE=FAQ
"The lower the E-value, or the closer it is to zero, the more "significant" the match is. However, keep in mind that virtually identical short alignments have relatively high E values. This is because the calculation of the E value takes into account the length of the query sequence. These high E values make sense because shorter sequences have a higher probability of occurring in the database purely by chance. For more details please see the calculations in the BLAST Course.".
What they say in the papers is true, the size of your database matters in deciding how significant the match is. I can imagine that for primer design you want to be more careful with the E-values, as they often fall under: "because shorter sequences have a higher probability of occurring in the database purely by chance".
I hope this helps to make your decision for deciding your threshold, otherwise please give more information.

This NCBI page offers a primer design tool which appears to incorporate a specificity check run via BLAST. However it seems to base stringency upon degree of mismatch rather than an e value.


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Photosynthesis regulation
I read about the regulation of Calvin cycle by thioredoxin which activates key enzymes essentially by converting disulphide linkages on inactive enzymes into sulfhydryls. Another regulatory mechanism is the pH control. The enzymes work at a slightly alkaline pH which is established as soon as the proton gradient is set up by the light reactions. But aren't these two mechanisms contradictory: at alkaline pH, the sulfhydryls $-SH$ groups, being acidic, will dissociate by giving up a proton and will be more stable in the dissociated form.
In general I fail to understand how pH will decide which bio-compounds will dissociate into proton or hydroxyl.

Your question conflates two separable events, a redox process and an acid-base dissociation.
The interconversion between disulfides and free sulfhydryls is a redox reaction, governed by the redox potential of the surroundings. The importance of redox potential to the -S-S- <> -SH equilibrium is illustrated by the difference between the cytosol and the lumen of the endoplasmic reticulum (ER). The cytosol is reducing and so free thiols are prevalent (there are usually no disulfide bonds in cytosolic proteins) whereas the ER lumen is oxidising, and the formation of disulfides in secreted proteins is promoted. The redox potentials of the two compartments is set primarily by the ratio between oxidised glutathione and reduced glutathione.
The thiol group in cysteine residues of proteins typically has a pKa of around 7, so it will indeed have some acidic character at slightly alkaline pH, dissociating to form a thiolate group. This doesn't however promote the reformation of disulfides, and in any case if it is important for a protein to have an undissociated thiol, then the environment of the specific cysteine residue can be adapted to raise its pKa. Note however that it is also possible that the thiolate form may be compatible with (or even required for) the function of the enzyme.


text:
Can I simply take the trend of heart rate amplitude to get breathing rate in an ECG?
I processed an ECG signal using findpeaks in Octave. Then, I plotted the amplitude of the "peaks" found by that function and got the followinge result (original unprocessed ECG signal on top, simple plot of "peaks" on bottom).

If I analyze the "peaks" signal, I get a frequency of about .07 Hz, which translates to about 14 events per minute. This correlates nicely with breathing rate. Is that really the breathing rate that I found, or am I jumping the gun? I've heard this may be referring to a "DC Drift"?


text:
What are evolutionary implications of contraception and reduced childhood mortality rates worldwide?
I've heard the following idea this morning: Before the introduction of contraception, humans conceived quite a lot of babies (there was little to do to avoid that), but the population was kept in check by very high childhood mortality rates. This mortality rate ensured that only the fittest survived.
The idea seems common sense, but I decided to investigate if this is really true. I know that for evolution, even 2000 years should be an instant.
I did some research, for example the worst childhood mortality rate currently in the world is around 17.5%, which is still about half of what it was in "developed" countries during the 1700s, according to the table below. But looking at the wikipedia map of childhood mortality, it seems that a baby nowadays has only around 1-3% chance of dying before adulthood, because even the weakest baby can be kept on life support long enough for the danger to pass.
What are the implications of reducing childhood mortality rates worldwide on human evolution? Maybe evolution is a wrong term to use here. Would it be fitness as species? I'm particularly interested in how this relates to developmental defects and genetic disorders. Is there any evidence that people who lived in a world without contraception and with high childhood mortality rate were more physically or mentally fit?
Here's an paper that deals with the subject and the table is from the paper below:
IS CHILD DEATH THE CRUCIBLE OF HUMAN
EVOLUTION?

I think that technically, there's no such thing as natural selection reducing fitness (except due to random chance). What we're doing is changing the environment to which humans are adapted. This means that we may see an increase in traits that reduce infant robustness against disease and injury, but that increase fitness or reproductive success in adults. Of course, we'll also probably see an increase in traits that decrease infant robustness with no compensatory benefits, but that's because we've created an environment where those don't reduce fitness.

Before the introduction of contraception, humans conceived quite a lot of babies (there was little to do to avoid that), but the population was kept in check by very high childhood mortality rates. This mortality rate ensured that only the fittest survived.

Woh! Let me stop you there. No, high rates of childhood mortality do not ensure that whom Natural Selection is acting upon are the "most fit." That title is given to individuals who are able to survive long enough to breed.
Many, many conditions that affect humans do not interfere with a person's growth or ability to perform physical or intellectual feats - but can definitely reduce or completely eradicate a person's ability to reproduce. These individuals are evolutionary dead-ends, and thus - while they survive in the environment - are not "fit" in the context of this topic.

What are the implications of reducing childhood mortality rates worldwide on human evolution? Maybe evolution is a wrong term to use here. Would it be fitness as species?

What it means is that populations will rise. As populations rise and intermingle, alleles get spread around. Perhaps rarer alleles become more common, or more common alleles become rarer. We're talking about Hardy-Weinberg equilibriums in the allele frequencies. However, with populations large enough true equilibriums are impractical to reach.
The more pragmatic explanation is that more mutations will arise, they'll be passed around, rare mutations will see more exposure, and humanity - in a very general sense - becomes more diverse genetically until a Selective Pressure is applied. Until there's a detriment to having a particular gene, there isn't a need to eliminate it from the population.
Your example is children who are too weak at birth to live outside of an NICU for their first few months - well, because we're capable of providing such care, until that care goes away it's not negatively affecting us. If it comes with an additional cost - say that, for whatever reason, premies can't digest mother's milk until the 8-month mark, then Natural Selection would pressure humans to evolve so that only 8+ month or older babies are born.
There's no evidence of significant pressures in human populations at this time, though. At least not in politically stable and technologically apt countries, although in areas undergoing long-time drought or other dangers it is seen. Sickle-Cell Anemia is though to be an adaptation to rising Malaria rates - which was quite fatal until medication was devised to treat it in the last 50 years or so (not even a blip in evolutionary terms).

Is there any evidence that people who lived in a world without contraception and with high childhood mortality rate were more physically or mentally fit?

Not that I can think of or find easily. While there are detriments associated with being born prematurely, and some evidence that women waiting until they're late 30's and men until they're 60 or older can negatively affect their gametes and consequently the development of any children born from them - it's been such a short time since the introduction of hormonal contraception and modern medicine that we may not see results tangible results for hundreds of years. Although condoms have been around for several hundred years, and there's been no associations with condom use that I can think of.
In the short term, what it has done is affect the ethnic diversity of countries. For the first time ever, Hispanic births have outnumbered Caucasian births in 2012 in the United States. Other countries, mostly European countries, are seeing declines in birth rates - which means their populations will decline with age or be compensated for by immigration. Higher birth rates, however, are associated with lower income brackets or very religious communities - both of which are associated with ethnic Minorities, at least in the United States. So while minority populations have more kids, they do so on fewer resources which may negatively affect their children in the long-term, whereas higher-earning segments of the population might have fewer children later in their lives, but can provide a much more stable environment and opportunities to continue that success.
One thing that hormone-centered birth control has done, however, is eliminate rape as a viable form of passing on one's genes. As gruesome as it might be to consider, pregnancies as a result of rape can produce "fit" offspring. It is a legitimate reproductive strategy in nature, and is in humans... unless the woman is using contraception. In the long-term this will probably show some interesting results (nominally an enhanced "Female Choice" effect - which is already evident in human evolution), but nothing right now.
It's also worth considering the ability for humans' increasing abilities to manipulate our own genome. At this point, we're nearly able to remove detrimental genes at-will and replace them with more effective versions. Because of this bio-engineering ability, the generations after ours might never be susceptible to inherited diseases - or they might all hop on the trendy "genes" and end up completely identical to each other. That's part of the fun of being human, though; we're very messy when it comes to Evolution. We tend to muck things but up good. :)

Thanks for an informative answer! It seems that common sense is not always true when evolution is concerned. Where do I sign up for trendy genes? ;)

@AlexStone I wouldn't say Evolution goes against common sense, per se. A lot of people simply haven't had a thorough education concerning Evolution via Natural Selection, so it's easy to come to misunderstandings. As for Trendy Genes, I'd say give it about 20 years and a celebrity endorsement!

Well , Ime sorry but sometimes a question have to be rephrased in order to reach the ''elefant in the room''  : The important question is if the existence of contraceptives in itself wil change the direction  of human evolution . After the invention of contraceptives the meaning of ''survival of the fittest'' is something very different , from now on the RESISTANCE to the effect of contraceptives becomes the dominant factor in determining fitness for suvival .
 This resistance can be compared to the resistance develped by a population of insects being subjected to a targeted poison :  before or later the population will develop some kind of resistance , even in cases where this can only be achieved by a complicated and indirect mecanism .
  Humans can achieve such resistance in several ways easy to imagine , and probably also in others very hard to imagine .
 The most obvious is by cultural adabtion , by developing a culture that prevents the efects of contraceptives . This can already be seen in the demografic growth of several population groups dominated by strict compliance with a beliefsystem damning contraceptives... . Many would argue that this has nothing to do with genetics , but actually a very strong case can be made for the opposite position .
 A less obvious way to devellop resistance is selection for a maternal or parental instinct , operating seperately from the sexual drive which has been ''poisoned'' .  In any population , even with an extemely low birthrate , there will always be a few individuals who will have lots of children , no matter what .  Given time enough ,and especially in a low-bithrate population , this behavour will be selected again and again until the underlying genetic mecanism  will cause it to be come  truely hereditary .  Such is the lessons of  selective breeding towards a derirable quality in  everything from horses to tomatoes , and there are  no reason to believe  humans to be different .  The million dollar question is how many generations this proces wil take ....

This is highly speculative and doesn't answer the question.

It also seems to muddle up genetic evolution evolution and cultural evolution, let alone the complexities of gene-culture co-evolution.


text:
Do egg-whites dry as right-handed helices?
Do egg-whites dried at cool temperatures form mostly right-handed helices, and if so is there an explanation for this? Because there is so much (mostly crystal-related) research a quick search did not turn up anything. Below is an image at low magnification (400x).

Maybe the coiling reflects aggregate properties of proteins that make up the albumin? If someone has a cite that would be welcome.
Edit: different spiral from same batch. This one apparently left-handed.

It could be something unrelated to biology - like rotation of the Earth.

@RogerVadim: In that case Australians should see left-handed helices...maybe so.

Forgive my pedantry, but isn't this a left-hand spiral? (Growing from the center that is). Related paper gravity.

@ARogueAnt::  that's a good question. it appears to me that that spiral travels toward the slide (away from the viewer). if that is true we have to begin at the closer end and follow it away (clockwise). if we begin at the center and assume it's going away from us then yes, it's left-hand. the visual evidence--(1) the larger coils are closer and (2) they cover some of the smaller ones. but i am not certain.

instead of anonymous downvotes, maybe let me know how i can improve the question?

@daniel I tried fighting against downvoting and particularly anonymous downvoting. Here is my highest downvoted metapost on the subject ;)

@RogerVadim: Wow. Nicely downvoted! I was thinking of posting on meta- but you have expressed my opinion for me.

@RogerVadim: The one virtue of anonymous downvoting is that it gets one used to the real world, in which reputations are made and unmade in secret meetings.

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


text:
Preservation of citrus fruit
A decade ago [1] the possibility of using Cas9 systems to impart desirable properties to oranges seemed within reach [1]. Antifungals like Imazalil can increase shelf life of citrus but are known to disrupt hormones and are perhaps carcinogenic [2]. A more recent article suggests that Cas9 is in fact being used to overcome "biotic stresses"[3]. Problems like citrus greening, black spot, and penicillium cost growers a lot and GM seems preferable to the chemicals mentioned in [2].
Does anyone actually know how citrus is currently preserved in the U.S.? Are both fungicides or GM at work? Neither? Both?
[1] A Jia H, Wang N. Targeted Genome Editing of Sweet Orange Using Cas9/sgRNA. Prasad M, editor. PLoS ONE. 2014 [accessed 2023 Jun 6];9(4):e93806. https://dx.plos.org/10.1371/journal.pone.0093806. doi:10.1371/journal.pone.0093806
[2] Temkin et al., Hormone-disrupting fungicides found on most citrus fruit samples tested by EWG, found online in Shoppeer's Guide to Pesticides on Produce, March 2023, https://www.ewg.org/foodnews/citrus.php.
[3] Tanwir, S.E., Soares, J.M., Welker, S., Grosser, J.W., Dutt, M. (2021). Genetically Modified Citrus: Current Status, Prospects, and Future Challenges. In: Kavi Kishor, P.B., Rajam, M.V., Pullaiah, T. (eds) Genetically Modified Crops. Springer, Singapore. https://doi.org/10.1007/978-981-15-5932-7_7

For example, I put a ripe store-bought orange out in mild, humid weather 10 days ago. Untreated, this orange would be coated with aspergillus and/or penicillium. it is completely zombified--hopefully in a good way...

I had a look through some web pages and came across one on shipping of oranges that indicates the storage conditions and treatments that may be applied to oranges.
This isn't necessarily about oranges in the USA, but ones from California are mentioned. It seems that there are a number of methods of maintaining shelf-life and that oranges are usually washed to remove dirt and contaminating fungal spores and then sprayed with a wax to inhibit loss of water as washing removes the natural surface waxes. To quote the article (emphasis is mine):

Quality / Duration of storage
Experience has shown that it is the care taken with preparation of the fruit for shipping which very largely determines whether individual batches withstand the rigors of transport. Such preparation for shipping is carried out in packing houses. These include:

Post-ripening of green or unsatisfactorily colored fruit to achieve a salable peel color in ripening rooms.
Removal of dirt, sooty mold, spraying residues and scale insects in washers.
Finishing of oranges which do not develop the typical orange color, but instead remain pale gold, green or with green spots, in a dye bath at temperatures of 45 – 50°C. Fruit treated in this way must be marked accordingly with a stamp (color added).
Coating with a layer of wax and treatment with preservatives and marking accordingly.
Grading of the fruits by size (gaging), color and other external features.
Counting, weighing and packing. Marking each package with details of number of fruit, quality class, variety and origin.
Storage until shipment in cold stores.

Waxing to prevent loss of aroma and weight is required because the washing process removes the natural wax layer. The film of wax sprayed onto the peel only partially seals the pores so that the fruits are still able to respire.

I suspect that the wax also helps prevent fungal growth through physical inhibition of spores getting to the fruit. In addition, storage conditions play a big role here - if you don't have any other fruit around your single orange, then it might not mature further (no ethylene) and it will have adequate ventilation to prevent rotting from too much CO2:

Care of the cargo during the voyage must be aimed at controlling respiration processes (release of CO2, water vapor, ethylene and heat) in such a way that the cargo is at the desired stage of ripeness on reaching its destination. Inadequate ventilation may result in fermentation and rotting of the cargo as a result of increased CO2 levels and inadequate supply of atmospheric oxygen (see Ventilation).

Fungicides are used in parts of the world, and I would be very surprised if they weren't in use in the USA:

Fungicides are diphenyl, orthophenylphenol (OPP) and thiabendazole (TBZ). Diphenyl can be recognized from its naphthalene-like odor. The fungicides primarily prevent blue and green molds, but they do impair flavor and indication of their use is mandatory.

As far as processing for juice, Pectinases are used to extract more juice from the pulp. GM from Aspergillus niger or Penicillium spp.
For citrus fruit with any bitterness, naringinase is used to destroy naringin.
Technically the pectinases are:
pectin methyl esterases,
pectin lyases,
and polygalacturonases
Info from page 141, Industrial Microbiology - An Introduction.

This seems like it should be a comment. The question is about preserving oranges, not extracting juice.

Perhaps change “processed” to “preserved” in the question.

I will do so. Didn't realize it was unclear.


text:
How much does donating blood affect the amount of oxygen in your blood stream at high altitude?
I am a regular blood donor and I am also a skydiver.  We normally go to around 13,000 feet AGL (above ground level).  Depending on how high above sea level the ground is, altitudes could be as high as 15,000 MSL (mean sea level) before a jumper is required to use supplemental oxygen.
At those altitudes hemoglobin is less effective at carrying oxygen, which is why hypoxia is a risk.
The following chart taken from this article about aviation and the body shows how oxygen levels decrease as altitude increases:

What I would like to know is if there is any research into the effect blood donation has on the blood stream's oxygen capacity?  Is it possible to say that x days after a donation, due to reduced hemoglobin levels, operating at 15,000 MSL would be equivalent to operating at 15,000 + x MSL without donation?

The American Red Cross (http://www.redcrossblood.org/donating-blood/donation-faqs) says it takes 4-6 weeks to restore hemoglobin levels.

Right but how much are hemoglobin levels reduced and what does that reduction do to the overall oxygen levels in the blood?  If you lose x% of hemoglobin after donation then being at sea level would be equivalent to being at.... 5,000 feet MSL?  Basically my question is: how much earlier will altitude affect the body after blood donation than without?

The oxygen-carrying capacity of the blood is:

amount of haemoglobin * % saturation

The average blood donation is approximately 10% of total blood volume. . Since the donation will have no effect on the % saturation, the oxygen-carrying capacity at each altitude will go down by 10%.
By inspection of the graph in the question, the % saturation goes down by 10% at 10,000 feet. So I conclude that donating 10% of blood volume is equivalent to ascending to 10,000 feet in terms of the effect upon the blood's oxygen-carring capacity.
Response to OP comments:
1) Anyone living at 5,000 feet will have adapted to that altitude in two ways. First of all the erythrocyte levels of 2,3 bisphosphoglycerate will be elevated to maintain unloading of oxygen from haemoglobin in the tissues. Secondly, the number of red cells per mL of blood will have increased, to restore oxygen delivery. Incidentally this increases blood viscosity which is deleterious in the long term. Tibetans living in the Himalaya have adapted genetically to prevent this effect on their blood viscosity.
2) The effect of air pressure is already included in the graph, since it shows the actual degree of saturation of the blood.

I'm not sure that is right.  If you lived in Denver which is 5,000 MSL then donating blood would be the equivalent of being at 15,000 MSL.  At 15,000 MSL the time of useful consciousness can be as low as 30 minutes or worse depending on things like smoking or general health?

Also the graph shows that the degradation of oxygen saturation isn't linear.  In the linked article it noted that oxygen saturation is also tied to air pressure, so it's probably a more complex formula.

I have responded by editing my answer.


text:
Does embryonic development mimic (partly at least) the evolution of organisms on earth?
What do we know about the forces/mechanisms which lead to this seemingly "fast forward" evolution stages of the embryo? What are the theories dealing with this idea?

You might want to read up upon the recapitulation theory, and reword your question, to be more specific.

Can you provide some kind of evidence for your claim? In the meantime, I'm voting to close.

@canadianer he is talking about the recapitulation theory by Haeckel. Ontogeny recapitulates phylogeny The developmental history of the organism recapitulates the developmental history of the species.

I vote too close because the question asks to review a theory, which is too broad to my opinion.

seems like OP received an answer from @RoverEye already

@RoverEye Thanks. That's what I was looking for.

Voted to reopen, but still feel that the OP should give more background, e.g. by pointing to cases where recapitulation/fast-forward seems to be a good explanation. Why do you think that "embryonic development [should] mimic [...] the evolution of organisms"? What made you ask this particular question?

@RoverEye Yes I saw your first comment. I'm not familiar with the theory but Wikipedia describes it as a "largely discredited hypothesis". If that's true, it is not evidence for the claim that embryonic development mimics evolution.

@canadianer Indeed it has. This paper gives the latest (I think) view on whats going on. Irie, Naoki, and Shigeru Kuratani. "Comparative transcriptome analysis reveals vertebrate phylotypic period during organogenesis." Nature communications 2 (2011): 248.

@fileunderwater Essentially the hinted wikipedia article says it all: the vague impression is/was there and I was happy to learn how this idea developed and influenced other areas and got debunked... or not.

@pointernil I'm familiar with the theory, and my comment was meant to make the question more complete and self-contained. At the moment, the question is probably very unclear for readers that are unaware of the ontogeny-recapitulates-phylogeny theory.

You only need to read Stephen Jay Gould's entire book on this topic, I believe it is called "Ontogeny and Phylogeny." He argues persuasively that there is no support for Haeckel's ancient theory.


text:
Brain + ethanol experiment suggestions needed
I need to demonstrate the effects of ethanol on a human brain (or other brain with developed telencephalon) in vitro; ideally the effects on vigilance and/or memory.
Could you please suggest such an experiment?
What method would you suggest to demonstrate the effects of ethanol on NMDA receptors or membrane penetration by ethanol?
Edit in respose to the first comment by @MadScientist:
The point is to empirically demonstrate how ethanol affects the cognitive performance of brain (specifically vigilance and memory) and explain the biochemical nature of such an effect on an observable real example (not using computer simulations). It is aimed at mature layman audience.
The experiment has to be in vitro due to ethical and environmental limitations (well, I am not permitted to intoxicate mature students nor animals).
Demonstrating the effect of ethanol in the role of an NMDAR antagonist would be satisfactory as the chain of implications would be illustrated on a theoretical basis.
I have access to standard laboratory equipment on a university level, but the simpler it is, the better. As to the material, the same is true while a fresh brain slice will hopefully be available as well.

In vivo experiments are much easier to perform for this topic ;-). You'll have to specify what exactly you want to achieve, there's a huge difference between "effect on the brain" and "effect on the NMDS receptor". You'll also have to give us a rough idea on what kind of equipment and material you have access to.

@MadScientist I have edited my question to give additional details.

Can you patch? Do calcium imaging maybe?

@nico I have not done it before. Could you perhaps suggest an exact methodology, please?

@Harrold Cavendish: if you haven't done it before, forget about patching, it would be very technically challenging. I will try to write an answer later today, now I'm late for work!!! :D

@HarroldCavendish: Can you explain more about what this experiment is for? Are you trying to do a PSA about the dangers of alcohol? What sort of experimental background do you have?

The main problem with what you are asking is that you want to show effects on vigilance and memory in vitro. That is just not possible: if you want vigilance and memory you need a live animal, there is no way around it.
Next point: you have an audience of non scientists, so you can lose them very quickly if you start speaking about NMDA, LTP or similar things without a clear explanation, so start with that: get a nice review (Pubmed is a good start, as always), and give a simple theoretical explanation of one of the mechanisms involved. It is then important to clearly explain the experiment you will perform, and what you are expecting to see in case there is an effect.
Unfortunately the best way to see effects on NMDA receptors would be electrophysiology. This is not trivial and, if you have never done it, I would not suggest going that way. However, if you have access to an electrophysiology setup you will most likely have access to someone who uses it, and that could make the experiment for you.
I am not an expert on this topic, but a quick research on Pubmed seems to indicate that alcohol can, for instance, reduce LTP in hippocampal neuron.
Maybe what you could do is having someone patch hippocampal neurons and show how an LTP protocol is used. You don't necessary have to show them the whole thing (I doubt anyone in a right state of mind would bare to stay until the whole experiment is performed in control condition first, and alcohol later...).
Also, the results of these experiments are often non obvious to analyse, so you should have some data prepared and analysed earlier and quickly show how analysis is performed, before showing the final results.
Calcium imaging experiments could also be used and would probably give results that are easier to understand for a laymen audience.
See for instance Fig. 1 or Fig. 5 of this paper (just the first one I found, there surely are other):
Ethanol alters calcium signaling in axonal growth cones.

+100 for noting the requirement of a live animal and how non-trivial the proposed experiments are


text:
Will the "frog in boiling water not jumping out" work on warm blooded animals
There is the famous saying about a frog that is put in water that are slowly boiling will not jump out until it's too late. I realize it happens because of the frog's cold blood that adjusts to the temperature change until it's too late.
Will this work as well on an animal with warm blood, or will the animal jump out ones it gets hot, but not hot enough to cause permanent damage?
Edit due to comments:
Cold blooded animals, like the frog, can adjust easier to their surrounding when the surrounding changes temperature gradually as their body temperature adjusts with the surroundings. Will the same happen to a warm bodied creature, and will it find it easier to adjust to the surrounding if the change is gradual.
For example, I don't like saunas, when I get in them I have problem breathing and I can't stand the heat, which means that I can be in a sauna for a very short time until I have had enough and get out. Will putting me in a sauna at room temperature and then turning it on to gradually begin to heat until its destination temperature will allow me to fill more comfortable and stay longer inside once it's at the normal sauna temperature?

"There is the famous saying"... which holds the answer to your question! :)

The frog part is true. According to Wikipedia:"An 1872 experiment by Heinzmann demonstrated that a normal frog would not attempt to escape if the water was heated slowly enough" and later it states that if water are heated at a rate of 1.1 C degrees per minute or faster frogs will jump out, which infers that if heated slower they will not jump. references are given in the Wikipedia article (http://en.wikipedia.org/wiki/Boiling_frog)

You should also read Poincaré's La Science et l'Hypothèse. If I remember correctly, he does mention such an experiment when discussing the fact that sensible perception is not continuous, but discrete: I can't make a difference between a 1kg and 1.1kg weight, but I sure can tell between a 1kg and a 2kg weight.

Concerning that wikipedia article, it seems to me you're cherry-picking your "evidence". I could post an answer copy-pasting parts of that article, but that'd be too easy.

My question regards the affect of gradual temperature change on warm blooded animals. The frog adjusts fairly easily (at start) to the temperature change fairly easy and can adjust its body temperature to that of the water so that it'll fill comfortable.
Warm blooded animals can't change the temperature of their body, but have other mechanisms of coping with temperature difference. So will a worm bodied animal will sit in the water and adjust it self with the gradual change, or will it just say at one point or will it get more and more uncomfortable until it'll get out?

One could make a joke about us not noticing global warming

Sorry to disappoint, but the "boiled frog" phenomenon is an "old folk warning". This essentially negates your original question altogether. Neither a cold-blooded animal (such as a frog) or warm-blooded animal will boil to death under the conditions implied by the warning (i.e. escape is permitted and water is heated very gradually).
1897 research by German scientist E. W. Scripture, upon which the fable may have first been based, has been deemed flawed by scientists:

From Scripture's research: “. . . a live frog can actually be boiled without a
movement if the water is heated slowly enough; in one experiment, the
temperature was raised at the rate of 0.002 degrees Celsius per
second, and the frog was found dead at the end of 2.5 hours without
having moved."
According to Dr. Karl S. Kruszelnicki (Australian scientist): "[T]he numbers just don’t seem right. If the water comes to a boil,
that means a final temperature of 100 degrees Celsius. In that case,
the frog would have to have been put into the water at 82 degrees
Celsius. Surely, the frog would have died immediately."
According to Dr. Victor H. Hutchinson (Herpetologist and Zoology Professor at University of Oklahoma):
"The legend is entirely incorrect! The 'critical thermal maxima' of many species of frogs have been
determined by several investigators. In this procedure, the water in
which a frog is submerged is heated gradually at about 2 degrees
Fahrenheit per minute.  As the temperature of the water is gradually
increased, the frog will eventually become more and more active in
attempts to escape the heated water.  If the container size and
opening allow the frog to jump out, it will do so."

Whit Gibbons (University of Georgia) says that there is an important message behind the false legend:

So where does that leave us with the boiling frog as a metaphor for
the human response to economic change or environmental degradation?
Well, it's not true that you can induce a frog to willingly remain in
boiling water by starting it off in cold water. But that does not
diminish the truth of the message that the accumulation of
imperceptible changes can have a significant effect on the economy and
the environment. We need to be aware of what changes are occurring and
to respond to them in a timely fashion. The metaphor lies in the
frog's ability to escape from the container: if there's no way out,
then the frog's fate is a foregone conclusion.

Actually, it is already on Skeptics: http://skeptics.stackexchange.com/questions/5402/can-a-frog-be-slowly-boiled-alive-without-it-noticing


text:
Do effects of caffeine on human body change with habitual use?
I've been reading about homeostatic nature of a lot of neurobiological processes - the brain is trying to maintain a balance by desensitizing receptors, re-uptaking and breaking down neurotransmitters.
With this in mind, I'm interested in what happens to the receptors in the brain with chronic use of caffeinated beverages.  Let's say an occasional caffeine drinker likes the cognitive boost of caffeine and starts to consume it habitually/chronically - every day. Will the caffeine drinker experience the same effects day after day, or will the effect change over time?
If there is a change in how the body responds to caffeine, are there any time frames that can be used to estimate when the change takes place - is it X days/weeks of habitual use?
Thank you for your input!

Related CogSci question: http://cogsci.stackexchange.com/questions/111/does-caffeine-improve-performance-for-habituated-consumers


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How is human biological clock modelled in modern science?
Im an engineer by education and i program a lot, so the question sounds weird to people from other disciplines.
Im trying to better understand the human biological clock. Yet i do not really know what it is. I read about clock genes, endogenous cycles, and other observed phenomena that is time sensitive or cyclical in nature. But is there a centralized model of what the circadian rhythm is or how itis exhibited within the human body?
For example an electrical clock can be modelled with feedback loops or electrical flip flops that control the timing. Ive seen the heart modelled as Van Der Pol oscillator.
Does modern science have some notion of how the "master" clock within the human body work? Is there a feedback or an oscillator model of the master clock?
Thank you for any articles or keywords that ican use to research this question!

Lacking references, this is only a comment instead of an answer. But the central point of any answer will be: biological clocks also use feedback loops (which form oscillators), albeit (sometimes vastly!) more complex ones than mechanical clocks. There are some fascinating studies which have identified specific gene regulatory feedback loops which control the cyclical expression of specific phenotypes.

I'm looking at this link that was posted around here earlier: http://www.ncbi.nlm.nih.gov/pubmed/21811695 The first image in this link, would that count as a model of the "master" clock?

I’m not sure. The image surely shows a feedback control due to the overall self-inhibitory function. But I cannot comment on whether it’s self-sufficient in maintaining a consistent oscillation frequency or whether it needs external input (the existence of the “clock/npas2” gene seems to imply that).

The situation is quite complex, and there are certain things that we do not fully understand, but I will try to give you an explanation.
First of all, at the cellular level, you have the genetic components of the circadian clock, the clock genes and their protein products.
You can divide clock proteins into positive and negative regulators: the positive regulators modulate transcription of clock-controlled genes and are inhibited by the negative regulators in a loop that lasts approximately 24 hours (in Latin: circa = around and dies = day).
For instance the Clock and Bmal1 nuclear proteins, when present in sufficiently large amount, will dimerize and act as transcription factors on a series of genes that contain a region in their promoter element called E-box. Amongst these are the Period (Per) genes.
Per is then synthesised, and exported to the cytoplasm. Here, if in a sufficiently large amount, it can heterodimerize with the Cryptocrome (Cry) proteins: the dimer will then enter the nucleus and inhibit the transcription actions of the Clock/Bmal couple. This will in turn, block the transcription of Per, that will therefore not be able to dimerize with Cry and stop the inhibition of Clock/Bmal and so on. All of this takes approximately 24 hours.
This basic loop (and some more) is nicely schematised in this review by Reppert and Weaver
Coordination of circadian timing in mammals. - Reppert and Weaver, Nature. 2002 Aug 29;418(6901):935-41.

I report here the legend of the figure:

The clock mechanism comprises interactive positive (green) and negative (red) feedback loops. CLOCK (C, oval) and BMAL1 (B, oval) form heterodimers and activate transcription of the Per, Cry and Rev-Erbalpha genes through E-box enhancers. As the levels of PER proteins increase (P, blue circle), they complex with CRY proteins (C, diamond) and CKIε/CKIδ (ε/δ, circle), and are phosphorylated (p). In the nucleus, the CRY–PER–CKIε/CKIδ complexes associate with CLOCK–BMAL1 heterodimers to shut down transcription while the heterodimer remains bound to DNA, forming the negative feedback loop. For the positive feedback loop, increasing REV-ERBα levels (R, circle) act through Rev-Erb/ROR response elements in the Bmal1 promoter to repress (-) Bmal1 transcription. CRY-mediated inhibition of CLOCK–BMAL1-mediated transcription de-represses (activates) Bmal1 transcription, because REV-ERBα-mediated repression is inhibited. An activator (A, circle) may positively regulate Bmal1 transcription (?) alone or by interacting with mPER2. There are probably kinases (?) other than CKIε and CKIδ that participate in phosphorylation of clock proteins.

The clock machinery, however, is even more complex than this and different tissues need to integrate different signals (e.g. light, hormonal concentrations and so on).
However, as nice as this may be, our bodies are not constituted by one single cell... if we "zoom out" a little bit and we go to the tissue or the whole body level, we see that circadian rhytms are present in all sorts of tissues and involve all sorts of different physiological processes. A very interesting question is then: how do cells from different organs coordinate each other so that the interrelation of different circadian processes is always the same? For instance, the release of cortisol peaks in the morning, our body temperature has a peak in the late afternoon and a trough in the early hours of the morning, and our heart rate is higher during the daytime.
In 1972, an article by Moore and Eichler was published, showing that lesioning the suprachiasmatic nucleus (SCN) of the hypothalamus (a region at the base of the brain) resulted in the "breakage" of the circadian rhythm of corticosterone (the stress hormone).
Loss of a circadian adrenal corticosterone rhythm following suprachiasmatic lesions in the rat. - Moore and Eichler, Brain Res. 1972 Jul 13;42(1):201-6
The fact that lesioning a bit of the brain resulted in loss of circadian rhythm in the adrenal gland was obviously a very big deal: the central circadian clock of the organism had been discovered.
I will not going too much into that but, since 1972 many advances have been made and nowadays we know that, although the role of the SCN is very important, it is not the only clock in the body. Several peripheral clock exist, in organs such as the pituitary gland, the liver or the pancreas. How all these clocks communicate between each other and what is their contribution to the generation of non-circadian rhythms (ultradian and infradian) are questions that still have to be solved.
A few interesting papers on the matter:
A riot of rhythms: neuronal and glial circadian oscillators in the mediobasal hypothalamus. - Guilding et al., Mol Brain. 2009 Aug 27;2:28.
A clockwork web: circadian timing in brain and periphery, in health and disease. - Hastings et al., Nat Rev Neurosci. 2003 Aug;4(8):649-61.
Peripheral circadian oscillators in mammals: time and food. - Schibler et al., J Biol Rhythms. 2003 Jun;18(3):250-60.

A fantastic answer! This is the second time I'm seeing a diagram of PER and CRY, and still, I cannot understand it. What I read is that DNA is involved. Does the clock involve the DNA, or is it an "external" protein structure that only touches the DNA?

@AlexStone: well, DNA is used to code for mRNA which in turn generates protein. So, for instance, you will have a Cry gene, which will generate a Cry mRNA which will give the CRY protein. The passage DNA->RNA is due to the fact that certain proteins, called transcription factors, bind to the DNA and allow the initiation of transcription (through another protein, called RNA polymerase). Transcription factors, being proteins, have also been derived from the translation of some mRNA, which was derived from the transcription of some DNA. CRY, PER and the likes are, in fact transcription factors.

@AlexStone: so, in essence you have some transcription factors that control the transcription of each other through their corresponding proteins. Because there is a delay for the cellular machinery to transcribe, translate etc. and the concentration of the proteins need to be sufficiently high, this is not immediate, but takes ~24h. Note that circadian clock proteins do not just regulate their own transcription, that would be useless. They can act as transcription factors for many other genes. Hope it is clearer now, you may have a look at http://en.wikipedia.org/wiki/Crick%27s_central_dogma

I've stumbled upon a detailed explanation of the Biological clock. This one is broken into multiple steps and helped me better understand what PER and CRY are. I cannot vouch for the scientific accuracy of the diagrams, but they make sense when combined with text.


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Is it essential to add cholesterol to agar or liquid culture for C. elegans?
In preparing agar plates with NGM, and also liquid cultures for growing c elegans, how essential is the addition of cholesterol and heavy metals? I have prepared both. I can't notice any obvious difference and I hate having to add all these supplements.
I'm using yeast extract and peptone as the primary components of the base.
Isn't this just supposed to be a moist semi-soft substrate for them to crawl around, their nutrients come from the bacteria they eat.

C. elegans needs cholesterol, but can't make it. Since bacteria don't make cholesterol either, the food bacteria aren't a source. As explained in the linked paper,  lack of cholesterol affects normal development.

And without supplementing there is enough in the peptone and yeast extract to already. I wonder if this stuff is only essential for   cholesterol biosynthesis studies?

Just FYI @alan Boyd's I upvoted and would like to keep open for a few days to see what else out there but this is prob best foreseeable response

No, it's not just for sterol biosynthesis studies. You don't need to add the metals to NGM. There are enough in the peptone, yeast extract, and agar. But they will be visibly abnormal (although alive) if you don't add cholesterol. Believe me, I have done it :-/


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Why is Homo sapiens not categorized as an invasive species?
According to Invasive Species Advisory Committee (ISAC), the definition of the invasive species is “a species that is non-native to the ecosystem under consideration and whose introduction causes or is likely to cause economic or environmental harm or harm to human health.”
But considering the following facts, why is this species not categorized as an invasive species?
Homo sapiens:

is non-native to the most of the ecosystem which it is inhabiting, since it originated from a certain area of Africa and spread quite recently.
has often caused environmental problems by decreasing the local species after its introduction, as it is known that the number of species in the planet is drastically decreasing ever since the advent of Homo sapiens.
is likely to cause the same problem after introduced to new environment where homo sapiens hasn't inhabited yet.

http://www.invasivespeciesinfo.gov/docs/council/isacdef.pdf

Well I bet the answer is as easy as: "Because we just wanted to ignore that Homo sapiens is an invasive species!". Following a strict definition of invasive species (although current definitions are not that strict!) we should add Homo sapiens in the list. Adding Homo sapiens would not change anything to the way conservation actions are performed, we will always consider Homo sapiens very differently than the other species. Do you feel concerned about this issue? Do you think it would change anything adding Homo sapiens to this list?

Because we are not invasive ones, we expansive ones...

Thanks. I didn't know that the definition isn't so strict. Yes, there's actually no special reason for us to call human as an invasive species. Only thing in the real world which it matters with is probably my final grade for the third quarter. If human is an invasive species, I could get A instead of A-.

Haha.. because we are the ones who are setting up the organizations, making categories and writing books.

I'm voting to close this question as off-topic because it does not concern biological classification but classification by governmental or inter-governmental bodies for purposes of husbandry. The question is framed to appear "clever". It isn't.

I'm voting to close this question as off-topic because this list is concerned with biology, not policy decisions of civil authorities. This appears to be political posturing rather than a genuine request for information.

Ignoring for the moment the question of politics, let's consider the various definitions of the term "invasive species" that are in use. Colautti and MacIsaac write in their discussion of invasive species terminology (1):

The greatest confusion [among the discussed ecological terms]
  surrounds the common term ‘invasive’ and its various derivatives
  (Richardson et al., 2000a). Explicit or implicit definitions for
  ‘invasive’ include: (1) a synonym for ‘nonindigenous’ (e.g. Goodwin et
  al., 1999; Radford &Cousens, 2000); (2) an adjective for native or
  nonindigenous species (NIS) that have colonized natural areas (e.g.
  Burke & Grime, 1996); (3) discrimination of NIS established in
  cultivated habitats (as ‘noninvasive’) from those established in
  natural habitats (e.g. Reichard & Hamilton, 1997); (4) NIS that are
  widespread (e.g. van Clef & Stiles, 2001); or (5) widespread NIS that
  have adverse effects on the invaded habitat (e.g. Davis & Thompson,
  2000; Mack et al., 2000).

Note that except for #2, all the definitions require that the species is a nonindigenous (non-native) species in the area under consideration. Therefore, while humans may be considered to have been an invasive species for much of our species history, under most definitions of the term we no longer qualify because except in a few places (mainly the arctic, antarctic and marine environments, where human presence is minimal) we are now a native species.
See also http://www.smithsonianmag.com/science-nature/are-humans-an-invasive-species-42999965/?no-ist

This argument seems to hinge on the pretty arbitrary decision of the point at which an invasive species can be considered indigenous...

Well, yes. How can it be any other way?

That's not what the term native species means, don't confuse the legal term native with the biological term.

I don't think there is a good answer.

Many people and organisations do not even consider Homo sapiens when making such lists.  Why? Because we have been for millennia a narcissistic species (think about religious narrative). This is similar to non-scientifically talking about animals. Homo sapiens is usually implicitly excluded from considerations.
Although Homo sapiens is present on all continents apart from Antarctica, Homo as a genus has been present for millions of years in Eurasia. Homo erectus has been there particularly long. Homo sapiens has outcompeted these species.
Ecosystems do change. Whether or not Homo sapiens is sufficiently long to be a native species is not a well posed question. Any answer would depend on arbitrary cutoffs. For instance if the first migration of Homo sapiens to Americas happened 14k years ago and it took 20 years per generation, then Americas are populated only for 700 generations. Is it a lot or is it little?
However, there are places in the world (mostly islands) where Homo sapiens settled very recently. Mauritius was first settled in 1638. And it is clear that since then many bird species (not only the famous dodo) went extinct and most of the area was converted from forests to sugar cane fields and towns. So yes, in this case there is no doubt the migration was recent and that it drastically changed the ecosystem, therefore it fulfils the definition.
Pragmatism. Probably the most important of it. We define invasive species for a reason: to give them a negative connotation and possibly plan a future removal. Doing these actions against humans are completely different from the legal point.

To sum up: a external observer would classify humans as an invasive species in at least some regions (Mauritius) and not in other (Africa south of Sahara). But people don't classify themselves as such because of political, moral, legal and pragmatic reasons.


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Why is the 4.4 kb band barely visible in this HindIII digest of lambda DNA?
Why is the 4.4 kb band barely visible?
Also, what is the mass (ng) of DNA in band X if lane S contains 250 ng of digested lambda phage DNA?

This question is literally impossible to answer with the information given. What samples are run in each lane? How were they prepared? I assume the left lane is a ladder. What ladder is it? What sample are you adding the HindIII-restricted phage DNA to?

First of all, the 4.4 kb HindIII band is derived from the right end of λ DNA, so during storage it anneals to the 23.1 kb left arm fragment via λ's 12 bp cohesive ends. You can solve this problem by preheating the markers to 65°C for a few minutes then cooling rapidly (i.e. on ice).
In a stained gel the intensity of a band is proportional to the amount of DNA in that band. This is why the heavier bands are more intense. The fragment X in lane 2 is similar in intensity to the 0.5 kb λ fragment so DNA content of the two bands is similar.
The amount of DNA in the 0.5 kb band is 250 ng *(0.5/48.5) where 48.5 is the size of wild-type λ DNA. I'll leave it for you to complete the calculation.


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DNA and gene activation
As far as the genetic content of each cell is concerned I have read to my satisfaction that all cells of a person's body except the red blood cells (with no nucleus and so no genetic message) and the gametes ( with just half the genetic copy or 23 of the 46 chromosomes) have the same DNA copy and so all the 60,000-80,000 estimated genes. The only difference is that which genes are active and which are dormant. For example the gene for insulin would be present in all cells but would be active and functional only in the cells of pancreas assigned the function of insulin production.
My question is:-

What is the factor or process or molecule or information that
  tells a cell or helps it to activate the genes necessary for its own
  growth and more importantly its designated function?

this assumption is not really correct - its now well understood that epigenetic factors including rearrangement of the chromosomes in the nucleus will affect the expression of genes in different cell lines.  I guess you could say that the genome is not different in this case, though it behaves quite differently, but even then, in some cell lines the telomeres shorten when the cells divide, so even the sequence is not uniform in all cells in the human body.

As i understand, you mean why all cell have the same gene, but they can know what they do. It's because gene like a computer programming language. They are programmed to be converted from stem cell into different type of cells in different environment. There must be a series reaction that cause the environment different for cells itself know what they need to do. And i think this question related to how to convert stem cell into different type of cell. Scientist using different environment to do it.

By the way, lymphocytes do not have all the genes as they undergo recombination for creating antibodies.

Humans have about 20000 genes. But see also this http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898077/:

Your question refers to differential gene expression and methods of Eukaryotic gene regulation. This is a very broad question for there are a lot of methods to control gene expression. They can function as transcription control, mRNA processing control, translational control, post-translational control and so on in eukaryotes. In prokaryotes, the methods include the operon model etc, which is much simpler than eukaryotes and multicellualr organisms but still quite complicated when studied in its entirety. Here and Here are few places where you can study differential gene expression. As an introductory text,  chapter 19 of Life:The science of Biology by Purves, Sadava, Orions and Heller(the link is to a supplementary-material site and not to the book itself), Otherwise, to elucidate all mechanisms here would become too long and in any case uncomprehensive.


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Why do cells vary in shape and function when they have the same genome and the same organelles?
Why do cells vary in shape and function when they have the same genome and the same organelles. For example: why do all cells have nuclei but red blood cell's don't; why can't the cells of a eye perform the function of the tongue; and the list goes on and on. If you say it is because of gene regulation, so then how does the RNA know to transcribe the specific genes that are necessary to that particular cell?

The shared genome also produces the different sexes, this and the multipurpose genome (or which is present in many different cell and tissues in an individual) leads to a conflict over gene optimization

There is a lot of literature available on this subject - Search for gene expression in multicellular organisms, enhancers, control elements etc.

Remember that not all cells (in the same organism) have the same DNA and organelles - most notably being red blood cells in mammals which are anuclear, have no DNA, and also lack many organelles.

Because cells are not only characterized by by their genetic material and other interior components, but also by the genes they express. Cells have to fulfill multiple different functions to be able to build complex multicellular organisms. Differently expressed genes lead to different proteins made in the cell, which leads to different morphology, shape or function. For example melanocytes in the skin are highly specialized cells which mostly make the pigment melanin. Plasma cells on the other are highly specialised for making antibodies.
It is all about regulation of genes. The RNA doesn't know or transcribe anything -
the DNA is trancribed into the mRNA (which is then further processed) and finally translated into proteins. Cells develop from precursors which proliferate and finally differentiate into highly specific cells. This progress is controlled and activated by specific transcription factors and growth factors. For example: pigment cells only develop, when a specific transcription factor is present. When this factor cannot be expressed, these cells do not develop at all.
This developmental process is shown schematically in the figure below (the figure is from the NIH website on stem cells):

Could be absolutely perfect with some sources and link for further readings imho.

@A.Bourgoin I'll look into it tomorrow.

The easy answer is: Each cell is living in its own environment and getting different signals that they act on. (Environmental cue --> Cell signal --> Cell turns on or off different genes based on these signals)
Recognizing that all cells have the same DNA is a good place to start. Imagine a single celled zygote formed from the union of one sperm and one egg...Early on, each of cell is capable of reacting in the same way to the same signals. And as the early embryo's cells begin proliferating, but before it implants in the womb, each cell is pretty much the same. And each cell has the possibility of becoming any of the myriad of cell types in the body. In fact, you can even split these early embryos apart and generate twins - two bodies (or more) instead of one.
However, soon, the embryo comes to rest against the wall of the womb and implant there. From this point on, not every cell gets the same signals. One cell is resting against the wall of the womb, another is several cell-widths away from the wall. A bit of randomness acts as the start of differentiation. The two cells start reacting to the signals in their slightly different environment and progress towards different fates. As development proceeds, these small differences become more pronounced and cells begin to commit to distinct lineages. No longer are they 'pluripotent' and able to become any given cell. The possibilities are more restricted as the environment of each cell gets more and more different. Cells 'commit' to their decisions and can't go back.
One good book you can pick up that will walk you through this idea is Neil Shubin's 'Your Inner Fish.' The overall story is about evolution of the first land quadrapeds, but he pursues a lot of different lines of evidence, and several of them involve molecular biology and cell differentiation.

Despite of the fact that all cells have the same genome, not all the genes contained in the cell nuclei are functional. During embryonic development, cells are subjected constantly to division and differentiation processes; this means that in the earliest stages of embryonic development, each cell of the embryo can form, by itself, a new complete body. However, these cells loose their ability of "all-forming" as the embryonic development progresses and they become able to form only certain group of tissues. Lately, they would be only able to form just one type of tissue.
All these cells have, obviously, the same genes, but what makes a cell of early stages of embryo development (stem cell) different from another of the body if they have the same genes? The answer is that although they have identical genes, differentiated cells use less genes than a stem cells would use. For this reason, only a certain number of genes of the total that a differentiated cell contains, are in use. A neuron, for example, wouldn't need a gene that produces hair protein because simply, its function isn't that, so neurons inactivate the gene of hair-producing.
There is much more to investigate and to research in this field because many questions still remain without answer such as how cells acquire certain shapes and not other or how do they form perfect 3D organized shapes (tissues and organs) and much more question in this way.