text:
Can ants learn things?
I have an ant nest in a jar. Whenever I want to observe them, I have to remove the cover and therefore put them in light - that scares them. They also can see shadow cast by myself.
I often throw in some food when I'm uncovering the jar.
I was curious if ants will ever remember that I'm not dangerous and that light means food.
If not, are there other things they can learn? Do they teach each other to hunt? Can queen learn things ants can not (queen has shown a lot of individuality compared to ants)?

I was wondering the same with insects in general.

Ants can usually learn patterns, colors and sequences. Species that do not use pheromone trails rely heavily on landmarks for navigation, that is they perform learning walks during which they look backward and circle around the nest to learn what the landscape looks like so they can easily return to the nest after foraging.

Harris, R. A., de Ibarra, N. H., Graham, P., & Collett, T. S. (2005).
  Ant navigation: Priming of visual route memories. Nature, 438(7066),
  302.
Chameron, S., Schatz, B., Pastergue-Ruiz, I., Beugnon, G., & Collett,
  T. S. (1998). The learning of a sequence of visual patterns by the ant
  Cataglyphis cursor. Proceedings of the Royal Society of London. Series
  B: Biological Sciences, 265(1412), 2309-2313.

This is usually the case in large ants that tend to rely less on pheromones and more on visual cues to navigate. Studies commonly focus on species such as Gigantiops destructor or Myrmecia spp.

Macquart, D., Latil, G., & Beugnon, G. (2008). Sensorimotor sequence
  learning in the ant Gigantiops destructor. Animal Behaviour, 75(5),
  1693-1701.
Jayatilaka, P., Murray, T., Narendra, A., & Zeil, J. (2018). The
  choreography of learning walks in the Australian jack jumper ant
  Myrmecia croslandi. Journal of Experimental Biology, 221(20),
  jeb185306.

The type of learning you are referring to may be termed habituation, and habituation has been shown in ants, for example some ants tend to be less aggressive to other colonies that they encounter frequently.

Langen, T. A., Tripet, F., & Nonacs, P. (2000). The red and the black:
  habituation and the dear-enemy phenomenon in two desert Pheidole ants.
  Behavioral Ecology and Sociobiology, 48(4), 285-292.


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What is an effective method for putting on blue rubber butyl stoppers?
They look like this.

We have to do a lot of gas sampling and these are really difficult to assemble. I've been scouring the internet for advice but there are none. Do you have experience with these? Have you found a good way to put them on that doesn't destroy hands, hearts, and dreams?

To clarify, the hard part is putting the blue stoppers in the tubes in the first place. Once they go thoroughly in, we can crimp them with our hand crimping tool. Since the time I posted this, I find a (little) better luck using a piece of cloth / putting the cap and the glass vial between a vice. With too much pressure, I actually broke a vial and glass shattered everywhere. The best way to put them in is with a twist, but that usually comes with an expense of bruised hands after extensive use.
Wish I had a camera on me, but they look somewhat like this:

does application of some lubricating agent to the tops help or would that interfere with/contaminate with your gas mixture in the bottles?

Alternatively you can try heating the blue top perhaps in warm/hot water and see if that helps!

Well these will be gas samples, so I'm not sure, but we are trying to stay away from too much contaminates. Thanks for the idea though! It should make more sense to heat up the bottles first, and we may give that a shot.

From what I can tell from this machine (https://www.youtube.com/watch?v=TwRtsAG5Oy4), the blue caps are put on the bottles first, then a loose version of the aluminium neck seals are put around the top of the capsule, which is then pressed in the machine to seal the lid hence if you use many gas sampling techniques, it might worth investing in purchasing a similar machine/technology to seal your samples, which would be the most efficient in the long run.
EDIT: as pointed by @user137 there are also hand crimping tools, which you can use, which are considerably cheaper, which as @user137 pointed out, can be found here

That looks expensive, you might be able to get away with a hand crimping tool. This site has a wide variety : http://vialcrimpers.com/

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are sperms considered living
recently i got into a debate with this question on hinduism.se ,
as the link given above shows, are sperms considered as living or non-living
as far as my knowledge is concerned, sperms undergo locomotion, senescence, more over the best thing to say they are living is they contain genome, i.e. haploid sets of chromosomes
so in short are sperms living or non-living

Given that there is no definition of life that even comes close to being commonly accepted, any question that asks "Is X considered alive?" has a high chance to generate highly opinionated answers and is thus unfit for the SE format.

The question of what is living is nothing but a matter of definition. We can only tell you what are the standard definitions of what is a living thing but no absolute truth exist behind these definitions. Therefore, I am afraid that all discussions here will bring anything new to your ethic or religion related discussion.
I want to argue that the @user137's answer is very misleading for two reasons. First, he based his discussion exclusively on the "reproduction ability" definition of life. Second because his definition of reproduction might be misleading as well.
Reproduction is not only cell division obviously. Following this same definition one would not consider a human to be a living things but only to be a collection of living (and non-living) things. It is important to understand that a spermatozoid is just one phase of a life-cycle. This phase yield to the next phase. That's it. It seems weird to say that a kid is not alive just because he cannot reproduce. It seems weird to say that a grandmother is not alive because it cannot reproduce. You can say however that a kid is a living thing that cannot reproduce and at another moment of its life cycle it will be able to reproduce (assuming it will survive to this age). One should not think of spermatozoids as something totally detached from the human phase as we know it. These things just form a cycle and it seems to me miseleading to say that a part of this cycle is not alive. Saying such thing would yield someone to think that two living things create non-living things that by fusion will become alive. That seems weird. But again, it is nothing but a matter of definition. I cannot say that user137 is wrong, I cannot only say that his definition seem neither useful, intuitive nor common among biologists.
You may want to have a look to life-cycle and to understand what are the haplontic and diplontic phases with a bunch of wikipedia readings.
Other concepts such as the ability to synthesize its own components, having a boundary between interior and exterior and ability to response to environmental stimulis are often used in order to define what is a living thing and what is not.

Damn.. this is getting into a huge debate.
There are different levels of life. What we mean by living when we say living is generally an Organism.
This is highly debatable. If you say viruses are nonliving because they need a host then almost every hetertroph is nonliving because they need the support of autotrophs.
An organ is living as long as it remains inside the body; similarly a cell in a multicellular organism can be considered alive only if it remains associated with the multicellular whole.
So is a single man alive?? Well he can eat, carry out metabolism, form a habitat but he cannot reproduce. Man as an organism is alive as he can sustain cell division and metabolism within himself but in that restricted zone human population is dying. He is living because he has the potential to reproduce. It is same as a lone enzyme- it can carry out its metabolism but will one day degrade unless it is re-formed.
Sperm on the other hand is just a vehicle- it doesn't have the potential to sustain itself; its sole aim is to deliver the potential to the egg so that life can be created.
To conclude- the question of what is "life" is purely philosophical. A more scientific question would be - "What is a stable, self-sustaining and dynamic biological system"

exactly, this was what I had in mind when we had that debate with OP. A sperm is nothing more than a cell which very predefined function. It's not able to live a life of it's own.

Sperm are unquestionably alive, according to all or most sensible definitions of life (They move around, they have goals, they eat things, they die). They are not, however, a human or animal life.
Vineet Menon has a shaky grasp of species definitions, and I'd like to correct some misunderstandings. Chromosome number is not that useful in distinguishing different species. There are a large number of genetic disorders that alter your chromosomal count without making you not a human being. (Klinefelter, Turner, Edward, Down, etc.) It's also worth noting that all mosses are haploid except during the sporophyte stage of their life cycle, when they're diploid. I doubt Vineet Menon intends to categorically declare mosses 'not alive'.
Your blood is alive, and your feces is also thriving with bacteria. Some yogurt is alive, most cheese is alive. All fermented beverages are alive, or were once. Bread dough is alive. The argument you linked to is debating whether or not they are alive enough to qualify as a macroscopic living thing for ethical purposes, which is an entirely different question. A chicken definitely qualifies, single-celled algae like spirulina, mushrooms, and yeast do not. Eggs, fertilized or not, seem to be somewhere in the middle. It is a continuous spectrum with people and cats and chickens and things at one end, and viruses and tuberculosis and dirt at the other. Eggs and sperm and mushrooms I would put somewhere in the middle.
So whether the answer to the question 'Are gametes alive?' is unquestionably yes;
The answer to the question of whether or not that makes them 'a life' is up to you.

I don't think that because something has life in it, it can be considered alive. Would you consider a rock alive if it was covered in bacteria? Similarly, you cannot consider yoghurt, cheese, etc as alive.

The rock is just a big pile of silica(probably). The lichen on the rock is definitely alive. As a composite object, I'd go with 'sure, that rock is alive'. (some) Yogurt is definitely alive. I wouldn't give it civil rights, but there's a big difference between rocks and yogurt. There's also a big difference between yogurt and a cat, though, so I see your point of view. The phrase of the day is 'it's a spectrum'. The important part here(for me) is there is such a thing as 'dead yogurt'. If it can be killed, surely it is alive?

So a dead human is actually alive because there are bacteria in it? Your answer seems more philosophical than biological.

The human is dead. The body is alive, sort of. The gut is definitely still alive.

Sperm, in my opinion can't truly be considered "alive"...but they are living. Bear with me before you skip my answer.
A cell can be considered a "living" thing since It has RNA/DNA, it imbibes nutrition, it grows and is destroyed, we cannot say however that it is alive. It has a specific set of instructions coded into the RNA which it follows till its death (which is also protein,and hence RNA, mediated). Alive is a term reserved for organisms and not single haploid somatic cells. On the other hand...sperms have spiral mitochondria hence they contain RNA.
In short..yes..they can be considered living

i think you too follow hinduism so what views do you have in regards to my question on hinduism.se, let us continue on hinduism.se

Your best chance of actually reaching an answer for yourself (*) to this is by parallel.
Do you consider independetly-living single-celled organisms alive? This includes bacteria, amoeba, bacteria, some parasites such as plasmodium (the malaria germ), and more.
Sperms are not quite independently-living single-celled organisms. They have many things in common with the ones mentioned above: they move, metabolise, communicate and sense, and most importantly they can cease to do all those things, i.e. they do what we commonly call, "die".
The main difference is, they don't reproduce themselves, they are the reproduction vessel for a larger organism.
There is absolutely no objective way to decide whether that difference is sufficient to decide that all those single-celled creatures are alive and sperms aren't, it's a question of definition. You might even decide that you don't consider bacteria or anything that exists commonly as single cells "alive", and thus this whole approach is pointless. In any case, it's not a biological question and thus should be discussed somewhere else.
(*) For yourself because there is no false or correct answer as long as nobody can get more than two people to agree on a definition of life.

One requirement most biologists have to consider something living is the ability to reproduce. This is why viruses are generally not considered alive. They contain proteins and DNA or RNA, but require infecting a host cell and hijacking its replication machinery to reproduce itself.
Fully differentiated sperm cells cannot divide and therefore can't reproduce. Their only role is delivering DNA cargo to an oocyte and creating an embryo. An individual sperm cell is just as alive as an individual neuron or muscle cell. These require nutrients and energy, carry out metabolism, perform functions, contain DNA, but a plate of neurons won't grow into a human.

By this definition anyone who is infertile is non-living, which seems absurd to me!

@AlanBoyd I believe user137 was referring to groups, rather than individuals. People in general can reproduce on their own.

there are sterile individuals too in the living populations which cannot reproduce by any means, so are'nt they alive?

@J.Musser is correct. The definition applies to groups. The average human is fertile and can reproduce, and is considered alive. Infertile humans are still humans and still alive. But no individual human cell can just grow into another human. The cells are parts of the organism, not organisms in themselves.

@user137 so you mean life comes non-living stuffs??

@agharehanabbas It's a problematic definition, but it seems to be well accepted. Wikipedia has more detail at http://en.wikipedia.org/wiki/Definition_of_life#Definitions But this definition of life always bugged me because it should be possible to build a machine that takes materials and energy from its environment, and builds a copy of itself. It would fit all parts of that definition, but would it be a living organism or just a fancy computer?

@J.Musser thanks, I hadn't previously thought of this distinction. However it still creates some problems. Imagine a species going to extinction, with two males and one female left. There are three living organisms in this species. Then the female dies: the males are no longer living organisms. As far as I can see the only counter to this is to say that the 'group'  has to be large to meet the definition of living, but this is even more problematical.

@AlanBoyd That isn't correct. There need to be both male and female humans in a population, therefore two males do not equal a proper population, they are alive, but disabled.

@AlanBoyd It is like spaying a cat, then calling it dead, because it cannot reproduce. That isn't it's natural state, just like two male humans isn't a natural state for the global human population.

Based on this definition a lot of cells in the human body, which are not dividing, would be called dead.

Using this definition, flawed as it is, to declare sperm unalive is... problematic? They are, on a fundamental level, the only cells to 'reproduce' on a population scale in the male body. Declaring humans alive because of their reproductive potential but sperm unalive is crazy.

@Chris The individual cells are alive, as together they form a living organism. Now, a single-celled organism that cannot reproduce I wouldn't define as living. It always helps me to have something concrete, and you have to draw the line somewhere.

But in the same logic sperm cells are living (you can treat them in a way that they are not able to fulfill their function) as a part of a bigger organism.

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What are the benefits of statins in terms of prolonging life?
Recently the UK government suggested that all adults over the age of 50, without exception, would benefit from taking statins.
I have an elderly female relative who may, or may not have had a minor cardiac event (the diagnosis is still out) and low blood pressure. It has been suggested to them that they would benefit from statins and have asked me (a former biologist) to find out more.
I've had a look at the mechanisms of action, which seem clear. But the clinical data is somewhat confusing.
It seems we can state with certainty that a small but significant number of users report relatively minor side effects, and a very tiny minority have serious ones.
In term of the benefits, however, the picture is much less clear. I have found a variety of statistics about how they reduce cardiac events but what this translates to in terms of length of life and quality of life is not stated.
One article I looked at suggested that on average, someone at high risk of heart disease taking statins for 30 years would only live an extra 9 months.
The author of that site has a book to sell, and may have an axe to grind. But there are several other articles out there - such as this, and this and this - which make worrying claims about statins being both more unsafe and less beneficial than clinical trials suggest. In particular there seems very limited evidence of any benefits to women.
I am inclined to treat these as alarmist nonsense - they have that sense of hysteria about them. But given that the authors look legitimate, that clinical trials data do not appear to agree with one another (widely varying in the percentage of users reporting side effects, for example), and that this is a relative, I wanted to get a second opinion.
So - can someone please crunch the numbers and tell me what the benefits of statin use are in terms of life years and quality of life? Is there any benefit for women with or without heart disease? And is there any basis to some of the alarmism around their use?

I suspect I won't be crunching as much numbers as you'd want me to, however here are some basic points:

Statins have shown a clear ability to improve the blood llipid profile.
Their use in primary/secondary prevention for cardiac events is justified by the belief that less blood lipid will leave less lipids to clog the arteries with. This is an old paradigm, and it is debated, even if we nowadays indeed give statins to all (potential) cardiac patients. There is evidence for a positive effect of those drugs, but it is not undisputable.
An enormous amount of money is made from statins, and the pharma pushes very hard for their use.
They do have undesirable effects, but those appear mostly early, so patients are usually well monitored for them and they mostly pose no real threat.

On the subject of women: women before menopause are protected from cardiac events by their hormone profile, and would therefore likely benefit very little from statins at that time. After menopause, women present the same cardiac risk as men do. I do not know if studies have shown a difference in outcome for statins in postmenopausal women. If you want to know more, I advise you to go searching for it on Pubmed
DISCLAIMER: The above does not represent professional medical advice, and is subject to debate.

Wouldn't this paper be helpful?https://www.tandfonline.com/doi/full/10.1080/17512433.2018.1519391


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How does strength of a pulse related to EKG(ECG)?
There are variabilities in the heart rate as well as strength of heartbeats. I want to know if one can predict which heartbeat will be strong or weak based on the corresponding EKG/ECG signal. I am interested in the displacement of brain due to the heartbeat, which probably correlates with the peak pressure, and total volume caused by the beat.
If there is such a correlation, which part of EKG would be related? The interval between P and R? The amplitude of QRS?
Human or primate information is preferred.

image from wikipedia

Predict? I have no idea. I know V-tach and A-tach can be reasonably predicted by increasingly chaotic signals on an EKG, but I don't think the equipment would have the granularity to predict "strong" and "weak" beats.

Are you referring to stroke volume, pulse pressure, or something else?

@louism Thanks for the interest. I suspect volume would be the best, but pressure or delay could also be useful. Any reference is welcome!

@MCM to me it's not a matter of granularity, but fundamental plausibility. I can always improve signal-to-noise ratio, and do signal processing to improve the readings. But is there any signal related to beat strength at all?

Is it plausible to estimate stroke volume from EKG (with significant measurement error)? Perhaps. Is it likely that you will achieve reasonable results without several months of research and access to large databases of patients who had both an EKG and a cardiac echo (gold standard for SV) in order to validate your results? Probably not. That said, if you did find a way, you would probably become incredibly rich.

Higher QRS complexes particularly in the lateral leads would suggest hypertrophy of the left ventricle. This in turn would suggest a stronger pressure is in place, although it is not known whether this is because it is required (incompetent valves) or a physiological response to exercise (where the volume is likely to actually be bigger).
Alternatively, if it really is just displacement of the brain you're interested in, why not use an EEG taken with an ECG and measure if there is a variation with each heartbeat. Then you can tease apart whether this is due to pressure or oxygenation or many other things.
Otherwise you could place something overlying the carotid which will loosely, but perhaps more accurately, reflect the pressure and one could potentially calculate the volume this way once enough other factors are known.

Thanks for the response. Hypertrophy would be a long term effect, right? I am interested in beat-to-beat variability. Do you have a reference for this by any chance? We are sure that it is the displacement of brain due to the heartbeat, and the displacement varies from beat-to-beat. We wish to control it as much as possible, but just wondering if there are better features in ECG that can be used to do so.

It is unclear from your question what exactly "beat-to-beat variability" means from a physiological perspective. It would help if you could provide more information on the application you are working on and what kind of sensors you have access to.
If you wanted to measure the force of the arterial pulse, you would need to measure pulse pressure (which is the systolic blood pressure minus the diastolic blood pressure). However, these pressures do not only depend on the heart's action, but also on blood vessel compliance - which is influenced by ageaing, disease processes, and changes in the concentration of vasoactive substances in the blood. The EKG signal does not provide any of these latter parameters, and therefore it is highly unlikely that you would be able to estimate pulse pressure from an EKG. That being said, you could very easily measure pulse pressure with an arterial line, which would be the gold standard for such a task.
If you wanted to measure the force of the heartbeat, you could look at ejection fraction, which is a measure of how much blood is ejected from the ventricle in one heartbeat. Again, this is not related purely to the electrical activity of the heart (contractility and heart rate), but also to extra-cardiac parameters (preload and afterload). The EKG, which only looks at the intrinsic electrical activity of the heart, does not provide information on these extra-cardiac factors.
You could settle and look purely at cardiac contractility, which measures how much force the heart generates during a heartbeat. Keep in mind that this does not reflect how "well" the heart is working - you could have very good contractility, but a poor ejection fraction for other reasons. This is also not necessarily related to how "strongly" a person will feel his/her heart beating. I'm aware of
 one paper on how to measure cardiac contractility from EKG tracings.

Thank you for the detailed response! We have a setup where surface of cortex is imaged at high speed, and the image is contaminated by the displacement of the brain. This displacement significantly varies per beat, and we want to remove the effects. EKG and the video are pretty much all we are measuring.

The paper you shared could be very useful. Thank you again.

The displacement of the brain would be related to pulse pressure. I doubt you can measure this from an EKG signal. Again, the paper I shared shows a correlation between EKG signal and contractility, but moving from contractility to pulse pressure requires more information.

If you want a likely predictor candidate for the pulse wave amplitude (which seems to be what you are looking for), you will need to take into account some factors:

is the heart normal or pathologic?
are the vessels normal or pathologic?

Now from your question, I assume that you want your model to represent a sane vascular system. In this case, the best predictor of a strong heart beat would most likely be the area under the curve (AUC) of the QRS complex. However, you seem interested exclusively  in the arterial pulse wave of the great circulation. If that is the case, Maybe it would be better to reduce your sampling to the QR waves AUC in an attempt to restrict your signal to the left ventricle contraction.
In short, you are trying to predict the beat-to-beat cardiac output from ECG. Some have already investigated that sort of thing. You could try looking at this device for a start, and then look up the list of supporting reference for additional information.
good luck!

Great suggestions. Yes, we are interested in the normal heart. I'll test with your suggestions. Thank you.

@Memming BTW it seems that your question is just geared towards correction of other measurments. Can you give us a sample image or video of what your cortex camera is recording? Because it could be far better to try to adjust these images using fixed image features and compensating for the movements in code than trying to derive that from ECG...


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DpnI over-digestion
We have a long protocol that we are optimizing that includes DpnI digestion of a PCR product (to remove any of the template DNA if it's methylated, and while we're not certain in the blind tests, likely relevant DNA will be methylated).
I'm wondering if we can extend the DpnI incubation/reaction time to 4-5 hours.  This will make concurrent steps in the screen easier to manage.  Has anyone extended DpnI digestions?  How "leaky" or nonspecific of a process can it be?
Thanks.

We used DpnI a lot for eliminating "old" plasmids after PCR based site directed mutagenesis. The incubation time varied between 1-5 hours (depending on what else needed to be done) and I never had problems with getting clones from these reactions - and never had trouble with false positives due to incomplete digestion.

If you take your DpnI digest tubes out of the 37oC water-bath after the instructed time (for me its after 5 minutes for PCR based site-directed mutagenesis) and either put at RT or preferably on ice, then you should be fine since the enzyme will not be functioning at those temperatures!

@Bez I'm trying to avoid having the person travel back to the room where the PCR machine is (from an animal facility), thus my question is more in line with Chris's response (I want to know if leaving it longer will be an issue).

According to this instruction (http://www.chem.agilent.com/library/usermanuals/Public/200521.pdf) it can be done for 1 hour but this is for large plasmids. I agree with Chris that it should not be of a problem. Alternatively you can setup your 37oC DpnI incubation step in a PCR machine and after however long that is recommended, you can set the PCR machine to cool to 10oC automatically, that way you can leave it there for as long as you want.

@bez good point.  While I hate to keep PCR machines at low temps for extended periods of time (causes more stress on the machine), dropping it to 4C after an hour is probably the best bet.  Make it answer and I'll accept.

@AtlLED Cooling is less a stress problem (this is done with Peltier elements) but this process produces heat on the other side of the Peltier element which needs to be removed. This is usually done with fans which makes the whole thing pretty loud. Additionally it takes a lot of energy (for example when compared with a fridge).

I regularly do DpnI digestion at room temperature overnight. Can't vouch for 37oC overnight, but certainly didnt notice any off-target activity in my case.

According to this instruction it can be done for 1 hour but this is for large plasmids. I agree with Chris that it should not be of a problem. Alternatively you can setup your 37°C DpnI incubation step in a PCR machine and after however long that is recommended, you can set the PCR machine to cool to 4°C automatically, that way you can leave it there for as long as you want.

My mentor taught me that we can do DpnI digestion for minimum 4 hours and maximum 12 hours. I have ever left the reaction until around 16 hours (?) but the result was okay. My mentor recommended to put at 4oC after 12 hours, if we cannot continue the work immediately.

can you add any references to your answer? also, can you check your answer for typos - is "ever" supposed to be "never"?

In the lab I'm training in, we generally add small quantities of enzyme and keep it for overnight digestion at 37 deg. So the amount of time you want to keep it for depends on the amount of enzyme you're adding. Check the units of the enzyme and add accordingly to the amount of your DNA.
We did a DpnI digestion for mutagenesis too, we added 100 ng of our plasmid with 1uL enzyme and it worked decently. We had another set with 2uL DpnI but that doesn't seem to have worked out since we had zero colonies.
Probably the excess enzyme caused a loss of specificity or some sort of negative feedback inhibition.

Sharing lab practice is great, but preferably add your sources (links, books, papers,reference works (Maniatis?)) so that folks can background-read on your topic.


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What regulates the timing of the motion of molecular machines during DNA Replication?
This question is about this video I found on Youtube. I just want to know what is the mechanism which regulates the timing of motion of the parts of these molecular machines.
I know that those big molecules moves using mechanical energy from ATP molecules and take advantage of the electric forces specially the hydrogen bonds, they also take advantage of the Brownian motion of water molecules around them.
From what is see, the green floating molecule triggers the whole process by attaching the purple one, then some electric equilibrium is disturbed so the {purple+green} molecule is attracted by the horizontal cyan molecule...etc.
But the problem is: does the green molecule attaches to this group in a periodic timing ? or in other words does the Okazaki fragments have the same lenght evertytime ?
Thank you in advance !

http://www.singlemolecule.nl/publications/vanOijen_AnnuRevBiophys_2010.pdf

That's a pretty neat video, I'll just give you some background information first. It's an illustration of the "trombone model" of DNA replication. The darker blue molecule is helicase, it unwinds the DNA and facilitates translocation (this is an ATP dependent process). The dark purple molecules are DNA polymerase, they catalyze DNA strand synthesis (an NTP dependent process) using an ssDNA template and 3'-OH primer (the primer:template junction). The green circular molecules are sliding clamps, they increase the processivity of DNA polymerase. The light purple molecule is the sliding clamp loader, unsurprisingly it loads the sliding clamp onto the DNA (ATP dependent). The light blue molecule is a flexible linker that connects everything together. The other green molecule (the one that contacts helicase) is primase, it synthesizes RNA primers (which contains the 3'-OH initially used by DNA polymerase).
Certainly intermolecular forces play a significant role in this (and every) biochemical process, but I'm not really sure what you're talking about when you're describing electric forces and Brownian motion.

Anyways, the answer to your question is no, Okazaki fragments do not have a fixed length. DNA synthesis, as mentioned above, occurs only by adding NTPs to a 3'-OH primer. Thus the length of Okazaki fragments is dependent on the spacing between primers on the lagging strand. This is dependent on when primase binds which in turn is dependent on primase concentration as well as its binding affinity with DNA and other replication fork proteins (especially helicase). High concentration and/or high affinity leads to a higher binding frequency and therefore shorter Okazaki fragments. The opposite is true for low concentration and/or low affinity. Note that most (or all?) primases have some degree of sequence specificity which means that specific DNA motifs will increase binding affinity. For example, Escherichia coli primase (DnaG) recognizes the trimer GTA.
This process also requires some degree of coordination between leading and lagging strand synthesis. Primer synthesis and DNA polymerase recycling on the lagging strand is much slower than the continuous synthesis on the leading strand. It has been suggested that primase acts as a "molecular brake" by halting the replication fork during primer synthesis to prevent the leading strand polymerase from rapidly outpacing those on the lagging strand (Lee JB, Hite RK, Hamdan SM, Xie XS, Richardson CC, van Oijen AM. 2006. DNA primase actas as a molecular brake in DNA replication. Nature. 439(7076):621-624.).

Thanks !! That makes sense. I mean by electric forces the forces between molecules because molecules contain electrons and protons. This is interseting because if you know the electric structure of a protein very well you can know how its shape will change after a protein or even an electron attaches to it. I mean by the Brownian motion, the motion of water molecules which constantly collide with the protein, I think it plays a role in the stability of the movement of molecular motors. Thank you again !!


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Periodic Muscular Growth in Humans
If a healthy human is at a certain muscle state and then experiences muscular atrophy solely due to disuse/lack of exercise, is it easier to gain that muscle back than if the human had never reached that certain muscle state. If so, is there a name for this effect. The reason I'm wondering is because it seems like muscle mass was definitely periodic in ancient times when food would become scarce during the winter, and that an increased ability to put back on muscle might have developed evolutionary-wise. I thought that this would fit best in biology, let me know if this isn't the case.

What are we assuming caused the atrophy?  Because the correct answer would be "depends," which isn't very satisfactory.  From your example, do you mean in the case of malnutrition?  You also have injury, illness, senescence, lack of exercise, or parasites--though they can be put under the others.

Good point see edit

Muscle memory specifically in the effects of hypertrophy. There is also muscle memory for skills which shares some factors but mostly differs.
When muscle hypertrophies or "gets bigger" extra nuclei are recruited to make more sarcomeres or proteins involved in muscle action. Once these nuclei have been recruited and essentially activated once, they're much more easily activated again.
Above is an answer based on my knowledge, but you can wait for Atl LED if you need references.

Disuse and lack of exercise are actually exceedingly new problems when considered on an evolutionary scale.  The bigger evolutionary pressure for the last few million years has been not starving to death, therefore not maintaining expensive muscle fibers unless they were absolutely necessary.
I haven't found any evidence of previous musculature effecting growth, but I'm going to look into it more (only some quick pubmed searches), and edit this answer.  If someone else knows more immediately, please feel free to answer.


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What is the biding site code recognized by the parts of the spliceosome
Another question about another Youtube video. At 0:50, the splicing process begins to remove the non-coding section of the DNA (intron), so the different parts of the spliceosome attach to the borders on the intron.
My question is, what is the code found in the borders of the intron which is recognized by the parts of the spliceosome, so they attach to it ?
For example, in the transcription of the DNA, the process begins after the transcription factor "TBP" recognizes the code "TATA" in the DNA string, then attaches to it. This triggers a whole process described by this video.

Did you try googling "splice site recognition sequences"?
In general, the first two letters of the intron must be GT, the next three are often ARG.
The last three letters of the acceptor site of the intron are virtually always YAG

Thanks !! Do some section inside the intron play a role in this process ?

Well the GT-AG motif is inside the intron (the actual consensus sequences for humans are 5'-(C/A)G|GU(A/G)AGU ... NCAG|G-3', | denotes the intron/exon boundary). Additionally, there is a branchpoint site near the 3' end of the intron which has consensus sequence YNYURAY followed by poly-Y. The A is highly conserved and its 2'-OH is used to join the 5' end of the intron, creating the lariat. Also, note that because splicing requires high precision (an indel of 1 nucleotide means a frame-shift mutation), the spliceosome has additional mechanisms to ensure the splice site is selected accurately.


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A Genetic linkage problem
I have recently switched from electronics to computational biology. So having some hard time with my homeworks. Can someone guide me on this problem?

Consider 6 genes A,  B, C, D, E, F, G. Some recombination rates are
  given between these genes AB = 0.2, BC = 0.1, AC = 0.25, AD = 0.5, BD
  = 0.5, DE = .1, AE = 0.5 ,EF = 0.1 ,DF = 0.15.
a) Find the number of linkage groups? b) Construct possible genetic
  map showing relative positions of these genes?

http://hos.ufl.edu/sites/default/files/courses/pmb5056/2012_16_Linkage%20paper%20to%20post.pdf

Please show the efforts that you put into solving the question.

@TheLastWord : OK I did it alone. (ABC and DEF in different chromosomes, certainly distance matters)


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Assembly reconciliation
We have some bacterial genomes that were assembled using Spades, they were sequenced with and IonTorrent PGM.
There are many assemblers and they give different results. I was interested in a tool that can merge the results from different assemblers but there are not many. I found only 2 : GARM and GAM-NGS.
Are there other tools to do merges? Does this improves the genome seq quality?

I think, you might lose quality they have their own error system which is only partially considered.

do the different assemblers five very different results with similar parameters ?

This is an old question but it seems relevant to answer now given current state of art. See also this related thread on biostars.
There are now many tools that perform this function, which is somewhat routine. A partial list:

quickmerge
metassembler (older)
MAC
RagTag (successor of RagOO)
CAMSA

I don't know which is best. Quickmerge is the one that I remember seeing the most. I believe that it is more common with eukaryotic genomes than microbial, as microbial genomes are now often getting closed with long reads.
In general we should expect that the regions that are agreed-upon by the assemblers will be fairly trustworthy, e.g. "improved" potentially. Artifacts are more likely to be found by using this kind of comparison as well.
The strategies used in each case will depend upon which tool you use. I haven't used them enough to say for sure.

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


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Can a bacteriophage be used to treat bacterial diseases?
Some bacteriophages reproduce using the lytic cycle which ends with the destruction of the host bacterial cell. I was wondering if theoretically this could be used therapeutically to treat bacterial diseases.

Yes: http://en.wikipedia.org/wiki/Phage_therapy

Yes, this is possible and is researched as an alternative to antibiotics. It has been used experimentally before antibiotics became widely available. Research was abandoned when antibiotics became widely available. See for example here and here for reports on this.
Today bacteriophages are researched for the treatment of bacteria which have a lot of resistances against antibiotics like Mycobacterium tuberculosis, Enterococcus faecalis, Staphylococcus aureus, Acinetobacter baumannii and Pseudomonas aeruginosa. See the references for more details (the first article also contains a nice historic overview of the field):

Bacteriophage Therapy
Bacteriophages: an appraisal of their role in the treatment of
bacterial infections
New ways to treat bacterial infections

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


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Can a plate with incompletely filled LB agar be used?
I am falling short of LB agar plates and I have a plate with less LB agar poured. I meant, the plate is not fully filled with the agar (it was the last plate I poured the medium into). Some part of plate is empty. Does this cause any contamination problems or moisture retention? Is it okay if I use this to streak a 5 cm line?

It won't be a problem other than that the surface would be uneven. Seal the plate with parafilm when not using to avoid moisture from accumulating inside. When you pour plates then swirl the plate gently so that the molten agar distributes evenly throughout the plate. The agar will be thin though, and you would have to streak gently so as not to cut the agar; you can add 0.5 % of normal agar-agar to make it a little dense.
Or else use  smaller plates (2 inch) if you have them in your lab.


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What does this Barbary Macaque facial expression mean?
A girl pretended having a piece of food in her hand and pointed it to a Barbary Macaque in Gibraltar. As a response he made this facial expression to her. What does this mean?

What was the sound that it made?  Macaque vocalizations are also well studied, and it looks like it was vocalizing.

@Atl LED The macaque didn't make any sound, its lips were maybe more like this: http://upload.wikimedia.org/wikipedia/commons/e/e1/Expression_of_the_Emotions_Figure_18.png and its eyes wide open

It looks like it is trying too threat.

Source:
Individual differences in scanpaths correspond with serotonin transporter genotype and behavioral phenotype in rhesus monkeys (Macaca mulatta)

That is a threat face.  Barbary macaque threat faces often appear with a brow raise, lowered head, and an o-shaped mouth, sometimes with and sometimes without a vocalization.  Given the context you described it is not surprising the girl received a threat.  *Based on personal research experience

It would be fantastic if you provided some references.


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Do fishes die from old age?
I was watching sea birds eating fishes and wondered whether any fishes died from old age or whether they are all eaten before this can happen?
I imagine that some big predator fishes must be able to live long enough to die from their age. However, do any fishes that are lower in the food chain reach an age such that they die naturally, or are they all destined to end their lives as food for a bird or another fish?

Salmon are famous for their spectacular natural/intrinsic death after spawning.

Yes, at least some fishes have intrinsic lifespans and deaths that are related to their own life-history and not to external forces such as predation or disease.

Fishes show three types of senescence. Lampreys, eels and pacific
  salmon exhibit rapid senescence and sudden death at first spawning.
  The guppy, red panchax, medaka, platyfish, Indian murrel and many
  other teleosts undergo gradual senescence, as observed in most of the
  vertebrates. A number of fishes (e.g. sturgeons, paddlefish, female
  plaice, flatfish, rockfish) show indeterminate growth, the occurrence
  of senescence in them is supposed to be very slow or negligible.

Patnaik BK, N Mahapatro, and BS Jena. 1994. 'Ageing in fishes' Gerontology 40:113-32

Fish do not die from old age, nor do any other animals. Rather, the older the animal gets the weaker it becomes which means that it is an easier target for predators or can easily succumb to disease.

Any citations for this?

interesting way of looking at it but I am not buying it.

@Oreotrephes  I agree with Humza Zaidi that aging itself is not a disease, but an accumulation of biological damage that makes an organism susceptible to eventually lethal diseases. This is discussed in this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4037311/


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What is the point of having evolved two nostrils?
How would having two nostrils be advantageous to your sense of smell or your ability to breath? I already hypothesized that either one of the nostrils could act as a back up for when another gets congested, but even then you can still breath through your mouth and at least for me I almost always have either both nostrils congested or neither at all.

I doubt it's so much that two nostrils are that much more beneficial than one as much as that most complex organisms follow bilateral symmetry for their body design. That said, your body will clog one and keep the other clear during fevers, allergies, or when it's cold to prevent it from drying out completely.

There are two aspects to your question.
First, organisms have some kind of symmetry. The field of evolutionary developmental biology has some theories on why our anatomy is the way that it is.  So, we have two eyes, two halves of our nose and two nostrils, one "tube" that becomes the path from our mouth to anus, etc. Our nostrils are just part of that symmetry. It may be evolutionary advantageous to keep two nostrils so that an animal can tell what direction a smell is coming from.
Second, we see that evolution has provided a path to having just one nostril.  Blowholes in toothed whales are just one nostril.  The other nostril does not have an opening to the outside of the whale.  It would be interesting to explore the split between baleen (two nostrils) and toothed whales (one nostril).  This evolutionary divergence may have been caused by differences in communication styles or the different blowholes may have caused a difference in communications http://www.whoi.edu/science/B/people/kamaral/marinemammalacoustics.html .

It's important to recognize that toothed whales with a single blowhole have two nostrils as embryos, as clearly seen in this image (middle of lower panel). http://www.evolutionevidence.org/wp-content/uploads/2013/08/beardolphembnose.jpg

We have two nostrils for the same reason we have 2 ears and 2 eyes. Having 2 nostrils means an odor molecule coming from one direction will have higher concentration in one nostril than the other, so we can determine what direction the smell is coming from, and allows us to find food or avoid predators more effectively. While humans no longer rely on smell very much, our distant ancestors and relatives did. Moles provide an excellent example and recent research displays their "stereo smell" ability, http://news.nationalgeographic.com/news/2013/02/130205-moles-smell-stereo-animals-weird-science/
And nostrils aren't the only example of smelling in directions, insects have 2 antenna, which are their scent organs. Moths can follow a pheromone trail using their antenna with great accuracy.
So why do humans still have two nostrils despite not needing to smell in stereo? There just hasn't been any evolutionary pressure to move towards 1 nostril. In fact, there would probably be pressure against it, because a human with 1 big hole in the middle of his face probably won't get a lot of dates.
Also, not all cetaceans have a single blowhole. Gray whales have 2 nostrils, and sperm whales have a vestigial second nostril that doesn't reach the surface. http://en.wikipedia.org/wiki/Blowhole_%28anatomy%29
The position of the blowhole is interesting because it's on the top of the head, above the eyes. Rarely, other animals will be born with a disorder called cyclopia, where they have 1 eye in the middle of the face. They usually don't live very long at all, but their nose doesn't develop right either, if it develops at all it shows up above the eye, and is often a proboscis instead of a nose.http://en.wikipedia.org/wiki/Cyclopia
Whales must have developed a way to keep the nose above the eyes while not messing anything else up.

I remember something from the anatomy lecture saying that one nostril picks up one, the other other kinds of molecules depending of the molecule's size and other attributes.
Meaning speed is important: if you breathe in through the nose right now, you'll probably feel the air coming in faster from one side than the other.
And still if i remember correctly this blocking of one side is achieved by blood vessels getting bigger.
The choice which one of the airways is blocked more comes from daily rhythms similar to sleep cycles.

Can you add some references to your answer?


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DNA extraction from agarose gel
Because DNA is soluble in water, is it possible to extract PCR product by dissolving excised gel containing the DNA band of desired length in water, mashing the gel piece with a pestle, centrifuging it and then pipetting out the supernatant ?

If you mash it with a pestle, you'll likely break the DNA. You can use a low melting point gel and mild heating followed by centrifugation to extract DNA.

why not use this? (http://www.qiagen.com/products/catalog/sample-technologies/dna-sample-technologies/dna-cleanup/qiaquick-gel-extraction-kit) or a similar product? I have used it many many times and it can be done very easily!

@Bez - Well, that would cost around 1-2$ per sample, correct ?

@AnuragMishra indeed, however, there might be delivery charges but some times institutes bulk buy and sell it in their own stores and their prices are less and sometimes there are institute based purchase pages which sell the products at the discounted price. ps I'm not promoting any brand or products here and I just put it up as a point of reference.

Yes, this is possible (and I have done it uncounted number of times) - the method is called "Freeze and squeeze". What you basically do is to run the gel, cut out the band of interest (be careful with the UV light, it causes damage to your DNA and also sunburns, so wear appropriate shielding for your face), dissolve it in a buffer, then freeze it in liquid nitrogen (or the -70°C, doesn't matter) and centrifuge it at room temperature for 10 minutes. During this time the ice melts and the agarose pellets at the bottom. Take the supernatant, do a ethanol precipitation (with glycogen when you only have little DNA) and you have nice and clean DNA. No need for expensive kits and is done approximately in 2 hours.
You can find a very nice and detailed protocol here: "Elution of DNA from Agarose Gels" (The rest of the handbook is also very useful).

Yes, we used to call this method 'freeze-squeeze'.

Right, I added this. Useful method and always amazed our new masters students. "What, no columns?" :-)

But, how will Qiagen make money if people know how to do this?

I have just put a comment about the Qiagen product. I guess ease of use of kits has made me very dependent. Its always great to find alternative methods to use. Many thanks for the method Chris.

@Chris instead of ethidium bromide use for DNA detection with UV, you can use SafeView Nucleic Acid Stain by NBS Biologicals, which uses fluorescence excitation maxima at approx 290-320nm, emitting at 515nm so its non-UV detection and it is very sensitive in my experience and safe too!

@Bez: Excitation 290-320 means that it needs to be excited in UV-B (which can cause DNA damage). The only difference is the emission wavelength which is green not orange/red. And that they claim that they are safer than EtBr.

@MattDMo I don't think that companies like Qiagen are in danger of going bancrupt any time in the near future. :-) Besides that, I started to use this, when we had problems of isolating short DNA pieces from the gel with columns. Subsequently I dropped columns for this work.

Extracting from PA gels is more pain. In such cases electroelution is also an option

PA gels are not dissolving when they are subjected to heat. But we rarely use them.

Ethanol precipitation is a overnight step, right ?

@AnuragMishra No not necessarily. Have a look at this and this article here at stackexchange. They go into detail. In short: Overnight brings no advantage.

The centrifugation after keeping the buffer+gel slices at -70C should be at how many RPM ?

@AnuragMishra At maximum speed, 14.000 or whatever your benchtop centrifuge can do.

Sorry to dig up an old post, but how does this method compare to the qiagen spin columns? When using spin columns I always have terrible 260/230 (< 0.1), suggesting that significant agarose is carried over. My yield also seems poor, but this could be related to the amount of DNA used in the gel. I usually do gel purification on PCR products and get <500 ng of DNA, but I can't calculate a percent yield because I don't know how much PCR product was there. But other people in the lab use the columns to gel purify 100 ug of digested DNA and get 50% yield, but don't tell me the 260/230.

@user137 Ihave never compared this systematically with spin columns. And I have mostly used this technique with digested DNA which was subsequently cloned (so mostly digested PCR fragments or pieces of DNA), so I generally had not much material in the beginning. Recovery was ok and cloning with this purified DNA was also not a problem.


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Where can I find the pMON7124 plasmid sequence?
I need the map of the pMON7124 plasmid. As this is not easy to find, I welcome any hints.

perhaps contact these people (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC237841/pdf/jvirol00029-0122.pdf) as these seems to be one of the original papers working with the plasmid.

Addgene is a good site to find plasmids

It seems that no good map of this plasmid is around. Life technology uses it in some of its bacterial strains, the quote:

E. coli also contain the helper plasmid, pMON7124 (13.2 kb), which
  encodes the transposase and confers resistance to tetracycline. The
  helper plasmid provides the Tn7 transposition function in trans.

They link to the original publication, but the image quality in there is pretty bad:

They give some information in the text, so I would recommend reading the paper (if you have no access, let me know, I can help here):

A broad-host-range shuttle system for gene insertion into the
chromosomes of gram-negative bacteria.

If this is not enough, you could still try to get a better version from the author Gerard F. Berry (you can find his Monsanto email adress by googling for it).


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Using RNA-seq to compare gene expression across patients instead of between Control and Experimental conditions
I am working with RNA-seq data from the Cancer Genome Atlas TCGA and I have been reading about how people have compared gene expression levels measured by RNA-seq. Many of the papers I have read talk about "differential expression" for comparing each gene's expression levels in the Experimental and Control conditions.
In TCGA data, I typically have a patient cohort who have had the mRNA in their tumors sequenced just once so there is no Experimental-vs-Control dynamic. I am interested in finding which patients' tumors show gene-expression that is significantly higher than the rest of the cohort but I have not had any luck finding literature describing this kind of comparison. I'm thinking maybe I can apply existing differential expression techniques to my situation but that seems cumbersome and not-necessarily appropriate so thought I'd ask the community here if there's a better way of finding which members of a cohort are outliers for specific genes.
Also: all of my RNA-seq data has already been RPKM normalized for me. I have been advised that using RSEM instead would be better for comparing gene expression across multiple samples but, for logistic reasons, I'm probably stuck with my RPKM-normalized expression levels.
Fundamentally, I'm looking for the best way to compare gene expression across samples to determine which samples have outlying high/low gene expression. Intuitively, I figure I could just compute median z-scores for each gene's expression levels within my cohort and consider anyone with a |z-score| greater than 2 to be an "outlier" but I haven't found any literature to support this kind of approach either.
Any suggestions, papers, or advice will be greatly appreciated.

When you say RPKM do you mean crude RPKM or the estimates that you get using expectation maximization methods like cufflinks and eXpress?
It is better if you get your RPKM or FPKM values from one of these programs because you can differentiate between transcript variants.
I have mostly used cufflinks and eXpress. Cufflinks package is better for multiple datasets. You can use cuffquant (which takes SAM/BAM) files to compute FPKM. Cuffquant will also need a reference GTF file. Cuffquant gives a binary .cxb file which you cannot read directly. Once you have generated the .cxb files for all your cohort samples, then pass all these files to cuffnorm. It will normalize the data and give you FPKM values for each gene in each sample in the form of a huge table.
Next point is which genes do you wish to compare. Do you want to compare known oncogenes which show consistent upregulation in all cancers? Actually there is a paper in which they have done this (I'll let you know the reference when I find it. Not able to recollect now).
You can then see how many of these genes show consistent expression in your cohort. Basically you need to identify a set of genes before you go on to study which patient shows anomalous expression.

I've been supplied with the kind of RPKM values you'd get from the Tuxedo suite but I have no insight into the specific pipeline used. I would love to see a paper that compares RNA-seq data between oncogenes across cancers; please post a link when you get a chance. Also: my collaborators have already identified a set of genes to focus on.

I just don't remember which journal it was but I am sure I read one.. Perhaps it is about miRNAs and oncogene interactions in different cancers.

Nonetheless if you want to compare differentially expressed from different cancers then you can get it by doing a principal component analysis on the RNAseq data for different cancers from TCGA

I expect to use PCA later on to see which expression patterns have the greatest impact on clinical data. For the time being though, my focus is comparing a small set of genes across patients who all have the same cancer (I guess I should have included that in my original question). Don't worry about the paper, I never thought to look for papers comparing expression across different cancer types and I've found some useful literature that way.

Seems like you want to have a general approach for comparing gene expression signatures.
A recent paper,Clark et al, takes a geometric approach which is elegant. The idea is to do dimensionality reduction (singular value decomposition) of the expression data, and then calculate the cosine distance between the gene expression signatures in the reduced space.
If you apply this methodology you will be able to group together patients with very similar signatures (small distances) and identify outliers (larger distances). Moreover, based on the loadings from the singular value decomposition, you will be able to identify which genes are driving the differences in the measured distances, and thus identify 'relative differentially expressed genes'.


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Human body control?
What can we consciously control in our bodies besides our muscles and brain (thought, memory, etc.)? Is the notion Bio Feedback related to this matter?
EDIT: I mean I can move my muscles at will but I can't order my liver to "work" since it's not managed consciously by the human mind. I heard about having some sort of control over temperature, heartbeat, sweating, etc. using techniques like breathing in martial arts or what they teach at the military to fool the lie detector. So my question is : What CAN we control?

Can you expand your question? At the moment I am not really sure in which direction you are thinking.

Is it still unclear?

Please define more clearly exactly what you mean with "conscious control". You can e.g. increase your pulse by hyperventilating, but this is quite different from deciding to raise your left arm. Do you consider both to be examples of body functions we can consciously control?


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Spider identification
This red spider has set up a web in my yard, in South Eastern, Texas, United States:

The spider itself is about an inch long (2.5 cm), and is predominantly red to brown in color, with red legs, and a very striking white line straight down the center of her back. The web is quite large—at least 4 feet (1.2 m) in diameter. It seems to be nocturnal, as I haven't seen it during the day, yet I've walked into the web (or nearly walked into its web) twice at night. Unfortunately, due to lighting conditions I wasn't able to capture the color particularly well.
I've searched but haven't found a species that looks like this yet.

After some more searching, I think stumbled across the answer. It appears to be an…
Eriophora ravilla:

Source BugGuide.net.
This species appears to have quite a diverse range of colors, and even thought I haven't found one that quite matches mine, the other similarities (the large abdomen, the stripe down the back, the four 'dimples', and the dark first leg segments) are enough to convince me. However, if anyone else can shed some light on this, I'd appreciate it.

I found the same type of spider on my backyard in Houston TX. Would love to know if it is dangerous.

@DonnaSummers They're harmless. I've found them a couple of times around my house. They tend to build their web each evening and tear it down by morning. After a few days they seem to move on to a different hunting ground.

Eriophora in general seems to be referred to as "tropical orb weavers", distinguished from araneidae (referred to as other kinds of "orb weavers"). Eriophora edax (http://bugguide.net/node/view/300786) is another possibility in your locale, and also look like they can have a stripe and vary greatly in color.

@JasonC That's another close match, but I still think E. ravilla is closer. From those images, E. edax appears to be have more dull, cryptic coloring (though not always) and have more tapered abdomen (though not always). I just noticed that my specimen also appears to have two red bumps near the rear of the abdomen, that is seen in some other individuals. Thanks for your suggestion though, I could be wrong about ravilla, but it's definitely Eriophora.

I found crab spider for mine,  they seem to vary in color and Design. Maybe this is more your spider found in Katy Texas
They have the same butt and dimples it looks like.

Could you explain why you think this specimen would be the one in the question? I'm not an expert in spiders, a tad arachnophobic even, but imho the spider in your image looks as much to the one in the question as  Margaret Thatcher looks like Napoleon Bonaparte.

Looking at the images on BugGuide.net, it seems there's quite a lot of color variation in E. ravilla. This one in particular looks a lot like yours (given relatively poor lighting). In other words, I think your image is of another E. ravilla, not a true crab spider (Thomisidae).


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Why isn't vomit corrosive?
Vomit comes from gastric acid, right? And in gastric acid there is HCl and HCl is corrosive (strong), how come when I vomit, it doesn't destroy things that it (as the vomit) hits (such as floor, table)?

First of all, it is corrosive. People which are bulimic often get problems with their teeth getting damaged by the permanent exposure to the acidic stomach fluids. See the paper for more information:

Bulimia and tooth erosion

Then it is a matter of concentration. According to Wikipedia, the concentration of the acid in the stomach is around 0.5% which is a pretty low concentration. Additionally the acid gets diluted when you eat or drink things. And last but not least not all things are very susceptible to a fast degradation by acids. Thing tend also not to disappear suddenly, if they come in contact with acids.

so, the Hollywood "acid spill = instant shaft" is completely false?

In the way it is usually displayed in films, yes. Take metals for example. A lot of commonly metal will not dissolve (or only slowly). Of course, if you subject Magnesium or pure Aluminium to a strong acid, it will react rather fast. But who uses these metals in this form to build things?

Is the Aluminum/Magnesium used in many laptop/tablet/phone bodies alloyed to be much more corrosion resistant than purer forms of the metal?

Magnesium is usually used as an alloy, since it is otherwise to hard to work with. Both metals form an oxidative cover on the surface which protects them from further oxidation. And in the case of tablets/phones etc. the surfaces are additionally treated to be much more resistant.

@JanDvorak Hollywood lies and exaggerates? Heaven forbid... :)

Link behind paywall.

@Thorbjørn: At least you can still read the abstract without paid access.

@ThorbjørnRavnAndersen Do want to read the paper? Then I will make this possible...

I am mentioning it so others know immediately without having to go and have a look.  I do know about the problem - I just wanted to skim the conclusion.  The only thing you need to do is to mention in a parenthesis after the link how the information is restricted.  I would, however, recommend that if you want people to find your answer helpful, that  you make it possible to actually read the information you link to.

As Chris said it's a matter of a low concentration for a small amount of time. Most people clean up their vomit rather than leave it to sit. Most people who vomit also have recently eaten something which triggers the reflex but also dilutes the acid or may neutralise it.
To further add to Chris' answer. Even heartburn or gastro-oesophageal reflux disease, is particularly corrosive. Damaging cells that line the oesophagus, it causes changes in the cells that make them pre-cancerous (Barret's oesophagus) and can lead to full blown cancer (carcinoma). This is because the cells change type to try to protect themselves.
Even in the stomach a thick layer of mucus is required to prevent the stomach from eating itself. This is not only to protect the lining against its own acid, but the enzymes which are made are seriously dangerous and will digest our body if able, only work in acidic environments. To understand how dangerous they are, when the pancreas which makes these enzymes is blocked releasing these enzymes it can digest nearby structures such as major blood vessels and cause seriously dangerous bleeding.

Chris is right, I just want to extend his answer a little bit more.
The presence of corrosion and the corrosion speed highly depends on the concentration of the acid, which is very low (0.5% according to Chris) in this case (considering that ccHCl is about 35-40%). According to wikipedia the vapour pressure of water is about 2645 kPa while the vapour pressure of HCl is about 4352 kPa on 22°C. The atmospheric pressure is about 1000 kPa, so one part of the (few) HCl will evaporate before the water does, which makes, the concentration even lower. So I highly doubt that it can cause any damage to a regular floor or metal/wood table in an open environment.

so, the Hollywood "acid spill = instant shaft" is completely false? –
  Jan Dvorak

It is possible to do that with much more concentrated acid. E.g. a bottle of hot concentrated sulfuric acid can cause very serious damage to people in a short time...


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Is there any relationship between heartbeat rate and life span of an animal?
Is there any relationship between heartbeat rate and life span of an animal?
Do they belong to a cause-and-effect relationship or are they both caused by some phenomenons or a common cause?

After reading a story of a man who was sentenced to hard labour, climbing the equivalent of a few miles of mountain every day on a victorian treadmill for many years, and the fact that he lived to 87 or 90, i think cardio is still a good idea:)

Interestingly there is a inverse negative correlation between heart rate and life span, meaning the faster your heart rate is, the shorter is your lifespan. See this figure (from the paper 2 cited below):

When the authors plotted the approximately total heartbeats vs. the lifespan, the amount of total heartbeats was in a pretty narrow corridor:

So it seems that at least the hearts in mammals have a maximum number of strokes they could do. The obvious question what causes this phenomenon is not really answered.
Since the metabolism of small animals is (compared to their weight) higher and also their oxygen consumption is higher because of that, it is hypothesized that this causes more reactive oxygen species and related damage which subsequently leads to an earlier death.
See the references for more details:

Rest heart rate and life expectancy.
Heart rate, lifespan, and mortality risk
Oxidative damage to DNA: relation to species metabolic rate and life
span

In the second plot, getting a "narrow corridor" on a log scale is hardly a surprise. Also, I'm pretty sure that either or both plots must have some of the species labels mixed up (and they both consistently misspell "hamster"). Of course, neither of those issues necessarily invalidate the general claim that short-lived species tend to have faster heart rates (which, given that both traits correlate with body size, is hardly surprising either), but those are the kind of mistakes that proper peer review and competent editors ought to catch. Honestly, I expected more from an Elsevier journal.

So they are both effects of a faster / slower rate of oxygen intake, am I correct?

I wonder if this is more of secondary correlation with size? In other words both life expectancy and heart rate correlate with animal size.  The human influence can't be ignored for the domestic animals on the chart (dog in particular).

@AtlLED Thats the other thing which can be correlated, see here.

Just to emphasise the point about the "narrow corridor", the entire variation in lifespan shown is covered by just over 1 log (with man pushing that up to maybe 1.5 log), and the variation in heartbeat by around 2 logs. Thus, even with no correlation at all, the metric heart beats per lifespan would be bounded by around a 3 log range, only just less than is shown on that figure.

@AtlLED Yes it could easily be. Both scale allometrically with body mass: heart rate with a negative quarter power ($R \propto W^{-1/4}$), and lifespan with a positive quarter power ($E \propto M^{1/4}$); their product  ($R \cdot E$) therefore scales with $W^0=1$, ie. is approximately invariant. You could attempt to explain these allometries in different ways that don't causally relate them to each other.

There is a relationship: they are negatively correlated. Shorter-lived animals tend to have faster heartbeats, and longer-lived animals tend to have slower heartbeats. It gets more striking than that, however: they aren't just negatively correlated, they're approximately inversely proportional. A mouse, and an elephant, will both have around 1.5 billion heart beats before they die.
Poetic as this is, the relationship probably isn't causal. It's not that you have a given number of heartbeats, and when you use up your last one your heart dies of exhaustion. That would be silly.
It is illuminating to view the invariance as emerging from how both heart rate and lifespan scale allometrically with body size ($mass=W$).$^1$ Larger animals tend to have slower heart rates, and also tend to live longer; both relationships are in the form of power functions, whose exponents are multiples of $1/4$.

Heart rate ($R$) scales with a negative quarter power exponent: $R \propto W^{-1/4}$
Lifespan ($E$) scales with a positive quarter power exponent: $E \propto W^{1/4}$

"Total number of heartbeats in a lifetime" is just the product of heart rate and lifespan. As such, it should scale as
$R \cdot E \propto W^{-1/4} \cdot W^{1/4}$
$R \cdot E \propto W^{-1/4+1/4}$
$R \cdot E \propto W^0$
$R \cdot E \propto 1$
That is: if $R$ and $E$ scale in these ways - which they do, approximately, within many taxa - then their product $R \cdot E$, the total number of heartbeats in a lifetime, will be approximately invariant.
The question is why they scale in this way; and, beyond that, why the exponents in rate and time allometries are so ubiquitously multiples of $1/4$.

Does lifespan scale with $M^{1/4}$ because (for whatever reason) heart rate scales with $M^{-1/4}$; and your heart dies of exhaustion after a billion beats? (Call this the Heartbeat hypothesis.)
Does heart rate scale with $M^{-1/4}$ because (for whatever reason) lifespan scales with $M^{1/4}$; and, at the pearly gates, if the ledger says your heart beat 1.5 billion times before dying, you get a free t-shirt; and the heart likes t-shirts, but is also economical, beating as fast as necessary but no faster? (Call this the T-Shirt hypothesis; in my opinion it's barely sillier than the Heartbeat hypothesis.)
Does lifespan scale with $M^{1/4}$ because (for whatever reason) something else, like mass-specific metabolic rate, also scales with $M^{-1/4}$; and that something has damaging and life-shortening effects? (This was the once-popular Rate of Living theory.$^2$)
Does lifespan scale with $M^{1/4}$ because longer life causes selection for larger body size, in such a way that gets you the appropriate scaling? (Long-lived animals can afford to sexually mature later; maturing later means they have more time to grow, and will be bigger when they finally do mature. Apparently this can get you $M^{1/4}$ lifespan allometry if you combine it with certain assumptions about growth and fecundity, you model selection as happening in a stationary population, etc. This is sometimes called the Charnov model.$^3$)
Does heart rate scale with $M^{-1/4}$ because mass-specific metabolic rate does? Does mass-specific metabolic rate scale with $M^{-1/4}$ because heart rate does? (I dunno, these sound plausible? A cell's metabolism is fueled by stuff delivered to it by the blood stream, so it'd make sense for them to be proportional, right?)
Does mass-specific metabolic rate scale with $M^{-1/4}$ because that's how the optimum scales for efficient resource delivery through fractally branching networks like the bloodstream? (The proof is too math-y for me. This idea is the current mainstream explanation for why biological times and rates ubiquitously scale with exponents that are multiples of $1/4$, instead of eg. $1/3$ as you might expect if it were just to do with surface area / volume ratios. This is called the West, Brown & Enquist model.$^{1,4,5}$)

tl;dr: There is a striking negative correlation - specifically, an inverse proportionality - between heart rate and lifespan. But there's no particular reason to think it's causal, and both also correlate strikingly with a million other things. A lot of this has to do with how things scale with body size. Such scaling is called allometry; allometries are often power functions; for biological rates and times, the exponents of these power functions are often multiples of $1/4$ (as opposed to eg. $1/3$ or $1$). This quarter-power ubiquity in biology used to be mysterious, but now has been given an explanation (at least for the scaling of metabolic rate, which intuitively could do part of the explaining for other rates) by the West, Brown & Enquist model as being the result of optimally efficient resource delivery in fractally branching transportation networks.$^1$
The Heartbeat hypothesis is silly; presumably the approximate invariance of "1.5 billion heartbeats in a lifetime" comes from the $M^{-1/4}$ and $M^{1/4}$ scaling of heart rate and lifespan, themselves occurring for some other reason. I don't know but I assume the fractally-branching bloodstream explains the heart rate allometry. The lifespan allometry is more mysterious. It was once commonly thought to follow directly from the mass-specific metabolic rate allometry (Rate of Living theory), but that theory has fallen on hard times.$^2$ It has been given other potential explanations, notably the Charnov model which suggests that low mortality rates result in selection for a later age of maturity, giving animals more time to grow large.$^3$

West, G. B. "The Origin of Universal Scaling Laws in Biology". Physica A, 1999.
Austad, S. N. "Cats, 'Rats,' and Bats: The Comparative Biology of Aging in the 21st Century". Integrative and Comparative Biology, 2010.
Charnov, E. L. "Evolution of Life History Variation Among Female Mammals". Proceedings of the National Academy of Sciences, 1991.
West, G. B., Brown, J. H. and Enquist, B. J. "A General Model for the Origin of Allometric Scaling Laws in Biology". Science, 1997.
Dawkins, R. and Wong, Y. "The Cauliflower's Tale" in The Ancestor's Tale, 2004.


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Mitochondria - are they really separate organisms that once merged into eukaryotic cells?
Theoretically, mitochondria are said to be a separate organism that is concerned with its own life and its own processes. In fact, it even duplicates individually. I know a similar question is here but I have something else apart from that to ask.

Is the presence of their own DNA/RNA - like compound justify or prove that the mitochondria was once a separate living organism?
If the mitochondria is indeed a separate living organism, then how is it controlled by the nucleus? Or is it not? Logic would suggest that since mRNA exists in the mitochondria separate from DNA in the nucleus, they have their own control over how they behave.
Often, living organisms working together have to have some sort of payment system. For example, bacteria in the body provide Vitamin K and other breakdown vitamins, and in return the body gives it a suitable home to live in. Is there any such business occurring between the individual cell and the mitochondria? Does it keep some nutrients for itself? If not, what is its mode of nutrition?
In effect, cells did exist before mitochondria joined the party. Is there any way to at least have a feasible hypothesis on why and how the cells bonded with the mitochondria or how the cells even existed in the first place without the presence of and organnelle that can break down food and convert it into energy?
Why do mitochondria have their own membrane? And that too folded? Is that to increase the surface area available for the electron transport chain, or is it for simple compactness?
Why does the mRNA in our bodies always exactly match the mRNA of our mothers and only our mothers? Can any genetic mutation change this fact?
Is it possible, that a mitochondrion can somehow escape the cell and start performing its life otherwise?
mRNA would suggest that mitochondria make their own proteins / at least some basic amino acids. If there are any such proteins, are they utilized for the cell? Or are they used for cellular respiration? Or are they kept by the mitochondria for there own means?

I will appreciate all answers!,
SmallDeveloper (a.k.a SmallScientist :) )
EDIT : Basically, I am asking 3 things:

Were mitochondria really separate organisms once?
If so, how do they get their nutrition?
How did cells exist before mitochondria came along?

Have you read the Wikipedia article on the Endosymbiont theory?

As @Chris pointed out, this is a very broad set of questions on mitochondrial endosymbiosis, and doesn't seem to show much in the way of independent research/effort into the question (not that you necessarily haven't).  After doing some reading on endosymbiosis, come back and ask more specific questions (probably split up your list) on specific elements you are having trouble with.  There are books dedicated to answering 1-8.

Thanks for pointing that out. I have edited the question for a more minimalistic point but have kept the original question for reference. @Chris, yes, but then this does not explain how mitochondria get their nutrition now, neither how cells existed without them. I know its an unknown topic, I just wanted some hypotheses.

Yes. But it is incorrect to call mitochondria an organism now.
Most of their genes were lost and are now encoded in the nuclear genome
It gets most of its metabolites
It is not known. See the other post for details.
Why membrane: I guess you know that. Why folded: you guessed right.
Only ovum donates mitochondria and other cytoplasmic factors. Sperm just provides the haploid genome.
No
Most of them are key respiratory enzymes

Thanks for the answer. Even though I asked I broad question, I didn't expect any broad answers. Really thanks for the prompt answer.

About question 4, isn't endocytosis how mitochondria were adquired by primitive eukaryotes? I think that this notion is supported from the observation that some species today can establish symbiosis by ingesting other cells, such as Paramecium bursaria, which has Zoochlorella algae (another eukaryote) living inside.

@Jagoe Question 4 is more than how organelles were acquired. Endocytosis is the first step.

Then, I cannot provide more details.


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Do human anal glands have any function?
Anal glands in all kinds of animals play a range of diverse functions - providing fat for preening feathers or waterproofing fur, generating distinct scent, even repelling predators.
None of the resources I found about human anal glands ever mention their function. There's info or infections, location, treatment of problems related to them, but never a word about a role they might serve - if any. Are they vestigial organs without any role or do they have some evolutionary purpose?

never heard of a human anal gland

@WYSIWYG: Here.

my anal glands produce a distinct scent...

@MattDMo: uh... comparing to whose? No, wait, scratch that question.

This question may have more to do with a depreciation in the ability to detect anal secretions than with the function of the glands themselves.

They are vital if not incredibly useful in many other mammals but not humans. People have tried to look for a role and seen that they activate in times of stress or anxiety. However this probably only serves to heighten both stress and anxiety as you now also don't smell that great either. There is no identifiable role in humans apart from causing a variety of disorders such as an abcess.
When physically examining a patient with a very painful condition, doing something that greatly provokes symptoms will often cause the anal glands to secrete. As a doctor, I interpret it as a clear warning that the patient is in distress, and that I need to exercise greater caution. I don't know of any science supporting this, but the function seems self-evident.


text:
How much time does it take a human body to replace all of its atoms?
Mikel Vsauce (Vsauce youtube channel) said in his video that it takes about 5 years for the body replace all of its atoms, while in asapscience youtube channel they are claiming that it takes 10 years. I am confused and I can't find anywhere the precise time it takes.
Mikel's video (minute 1:14)
AsapScience video (minute 1:07)

It would have been nice if there were some references/studies for that claim. I'm not sure for example if DNA in neurones in CNS (i.e. brain) get replaced unless its through DNA repair mechanism but still, that claim should be viewed with some amount of scepticism until a study is put forward and the assumptions are clarified!

http://www.quora.com/How-long-does-it-take-for-most-of-the-atoms-in-your-body-to-be-replaced-by-others

I also imagine atoms in the bone mineral that sets in the actual matrix doesn't change too often.

I expect this to have a mathematical model resembling a half life. Bone turnover is significant. Bone remodeling is part of the normal mechanism for responding to physical activity. Bone loss in space is also significant doe to this effect. http://cjasn.asnjournals.org/content/3/Supplement_3/S131.full

I don't think Iron would be totally replaced because we can't excrete it well. The iron in our red blood cells is very efficiently recycled by macrophages, and excess iron is stored in hepatocytes. If you really have too much iron it will accumulate as hemosiderin in hepatocytes, which is almost irreversible. The best way to treat iron overload is through regular blood draws, which is a non-natural way to remove iron, I don't know if men have a natural way to remove excess iron, so if the atoms can't leave, they can't be replaced.

Forever, since some atoms are not ever replaced: https://skeptics.stackexchange.com/q/18427/155

Not all the atoms in the human body are replaced.
Carbon atoms in tooth enamel are not replaced after the enamel is laid down during tooth development. This was demonstrated in the 2005 Nature article "Forensics: Age written in teeth by nuclear tests", where the researchers showed that the amount of carbon-14 in tooth enamel can be used to accurately determine date of birth.

Another good SO answer with more references and details of atomic replacement time for other tissue types is at Are all the atoms in our bodies replaced on a regular basis?

No. Some structures in the body are ever present from birth to death. The first things which come to mind are nerves, the eyes, the auditory hairs in the ears and the list goes on.....

could you please reference this! I tend to agree with you but over time replacement at molecular level is not inconceivable for any structure in the human body hence it would be nice to get some solid references!

Sure but I have not ate today so I am hungry it will be a while

I don't know about this. While it's true that cells in many parts of our body don't divide and have to last our entire lives, the atoms in those cells might be turned over. While the same neuron may last for 80 years, it will have to make some repairs to the membranes, DNA, proteins, etc. Whether or not this happens quickly enough to get total replacement within a human lifetime I can't say.

@Bez i added references...if you would like citations that is possible too.

@user137 no it does not atoms are extremely tiny there are just too many of them.

Autophagy is the mechanism by which cells recycle their own molecules. I'm not aware of any molecule besides DNA which does not get turned over by autophagy. http://en.wikipedia.org/wiki/Autophagy

@caseyr547 many thanks for the references and while I agree that structures such as neurones can not regenerate but they most certainly have turnover at cellular and molecular level such as ribosomes or mitochondria (mitophagy), which is what I think user137 was referring to (although this is not at atomic scale as such), which your references have not addressed but I'm no expert which is why I was looking for evidence to the contrary.

@Bez no its simple visible hair (the part that hits the drum) is virtually dead. the part that is alive does not regrow when damaged. dead things dont fix themselves. its there from birth to death.

there are also other atoms like mercury which in many do not leave the body once they have entered


text:
What happens to bones that do not heal?
I would like to know the steps the body takes to heal a broken bone and what happens if it cannot heal properly.  I am not looking for advice or explanations on resting and not doing activity, I am genuinely interested in understanding the outcome if activity is not stopped
Here is the scenario:
A rock climber develops a pain in the lower part of their middle finger.  The pain is not so bad so the climber continues to climb for four weeks, but the pain has not gone away.  The climber decides to go to the doctor fearing they have an A2 Pulley tear.
To their surprise the Doctors tests show no A2 pulley tear but rather a minor stress fracture of the Proximal Phalanx.  The doctor says stop climbing, however the climber has several trips planned and does not experience any pain while climbing nor a loss of strength or power while climbing.  The only time pain is felt is when the lower part of the middle finger is squeezed.  Because of this the climber decides to continue climbing as they just love it so much.
Question:  What will happen to a stress fracture in the finger if adequate rest is not given?
I understand the first thing the body does is try to stabilize the break and then starts to repair.  What happens if it is continually used and not given the chance to properly heal?  Will the climber just have a sore spot on their finger for the rest of their life or will it progressively get worse and worse?

Fracture healing occurrs in several steps:

haemorrhage: blood and surrounding cells fill the space created by the fracture.
fibrous callus: chondrocytes colonize the fracture space, with neovascularization.
bony callus: osteocytes colonize the fracture space and rearrange in woven bone
remodelling: in long bones, woven bone is remodelled into lamellar bone and creates a new haversian system

If the fracture is not immobilized enough (not enough rest), several things can happen that are mutually exclusive:

normal healing: luckily, the bone is not too much mobilized and is able to heal normally
fracture displacement: the bone heals, but in an incorrect alignment. This gets partially corrected over time, but the correction mechanism is limited, especially in adults.
pseudarthrosis: the worst case. instead of normal healing, cartilage grows to protect the bony extremities that are mobilized and prevents further healing. This causes pain, and will require surgery in most cases.

Exactly the answer I was looking for, well done. Thanks :)

Can non Union or delayed Union occur in such a bone?

@CRags non union of a phalanx? Yes, of course it can happen as in any long bone fracture. However, it is true that my answer refers more to an acute event than to a stress fracture, which would most likely cause more of a periosteal reaction/chronic pain & inflammation than displacement or pseudarthrosis.


text:
Does the fossil record disprove Evolution?
It is said by people opposed to Evolution, that the fossil record contradicts and disproves it. They say all the animals suddenly appeared, exploded everywhere, were fully formed, had no transitions, no gradualism, no change, and no sign of an evolutionary trend by which they could have emerged from an earlier type.
They then use these quotes to back this up from Evolutionists themselves:
"All the larger groups of animals, e.g. fishes, amphibians, reptiles, mammals seem to have appeared suddenly on the earth, spreading themselves, so to speak, in an explosive manner in their various shapes and forms. Nowhere is one able to observe or prove the transition of one species into another, variation only being possible within the species themselves" Evolutionist, Max Westenhofer as quoted in Dewar's More Difficulties, p. 94
"The evidence of Geology today is that species seem to come into existence suddenly and in full perfection, remain substantially unchanged during the terms of their existence, and pass away in full perfection. Other species take their place, apparently by substitution, not by transmutation" Geologist, Joseph Le Conte
"The extreme rarity of transitional forms in the fossil record persists as the trade secret of paleontology (study of fossils). In any local area, a species does not arise gradually by the steady transformation of its ancestors, it appears all at once and fully formed." -- Dr. Stephen J. Gould, Prof of Geology and Paleontology, Harvard University. Mentioned in one of his regular columns in Natural History Magazine (1977) and also in The Panda's Thumb, 1980, p. 181-182
"different species usually appear and disappear from the record without showing the transitions that Darwin postulated -- we are now about 120 years after Darwin and the knowledge of the fossil record has been greatly expanded. We now have a quarter of a million fossil species but the situation hasn't changed much -- We have fewer examples of evolutionary transitions than we had in Darwins' time" Dr. David Raup, a paleontologist at the Field Museum of Natural History in Chicago. Field Museum Natural History Bulletin 50:22- 29
"Evolution requires intermediate forms between species and paleontology does not provide them" Dr. David B. Kitts, Paleontologist
"The known fossil record fails to document a single example of phyletic evolution accomplishing a major morphologic transition" Evolutionist, Dr. Steven M. Stanley
"The record certainly did not reveal gradual transformations of structure in the course of time. On the contrary, it showed that species generally remained constant throughout their history. New types or classes seemed to appear fully formed, with no sign of an evolutionary trend by which they could have emerged from an earlier type." Bowler, 'Evolution: The History of an Idea', 1984, p. 187
"We are still in the dark about the origin of most major groups of organisms. They appear in the fossil record as Athena did from the head of Zeus -- full-blown and raring to go, in contradiction to Darwin's depiction of evolution as resulting from the gradual accumulation of countless infinitesimally minute variations, which, in turn, demands that the fossil record preserve an unbroken chain of transitional forms." Jeffrey H. Schwartz, Sudden Origins: Fossils, Genes, and the Emergence of Species (New York: John Wiley & Sons, 1999)
Is this true? If not, why not? Does the fossil record prove or disprove Evolution?

This related question is relevant: http://biology.stackexchange.com/questions/5138/fossils-of-intermediate-stages?rq=1

It also seems to be pretty directly answered on Skeptics here http://skeptics.stackexchange.com/questions/101/does-the-fossil-record-evidence-sufficiently-support-evolution and here: http://skeptics.stackexchange.com/questions/3481/have-any-transitional-fossils-missing-links-been-found

Questions about creationist arguments are off-topic here. Specific questions about evolution are certainly welcome, creationist talking points not so much.

The fossil record is spotty, very few organisms are ever fossilized upon death, so we see a small sampling of evolution. If you had a digital image of the mona lisa and removed 99% of the pixels, it would hard to recognize, especially if you looked at 1 pixel at a time. Might be doable from far away.

Fossil records are fossil records. The people who use them to attempt to prove or disprove evolution use them to represent their causes in different ways, gleaning sometimes completely contradictory facts from the same bodies of information, sometimes even the same samples.
It is my personal belief that evolution isn't ever entirely phyletic, I like to imagine that once in a while a pup would be born or an egg would crack open and there'd be a malformed creature in there the likes of which the world has never seen, if only because its deformity has made it more adaptable or stronger to its environment, not the opposite which is usually the case with birth defects. And then yes this prototype would survive and find a mate and have offspring with its varied genes dominating, some same, some different, and begin the phyletic process.
But that's not the answer to your question. Your question isn't really answerable. Fossil records only prove that a creature once lived at that time period, and its bone structure and posture can reveal certain things to any observer, but they dont prove or disprove anything. A great deal of the works you quote speak on the topic with great finality, yet they are decades old.

Well, at least the fossil record is completely compatible with the predictions made by evolutionary theory. In so far, it definitely does not disprove evolution.

While I agree with you completely, I try to be as objective as possible. There are people out there who have attempted to use the fossil record to disprove evolution and I know at least a few souls who are proof of their success.