text:
Why is compensatory negative supercoiling generated in a positively supercoiling ccDNA?
I was reading DNA replication in E.coli in Lehninger Principles of Biochemistry 6th Ed. and stumbled upon the following --

The tight right handed wrapping of DNA around DnaA oligomeric complex induces an effective positive supercoil. The associated strain in the nearby DNA leads to denaturation of AT rich DUE region.

Edit:
Yet again I have come across the following in  in Indian Molecular Biology books which certainly contradict Lehninger.
Binding of DnaA protein to oriC initiates unwinding of the DUE by introduction of negative superhelical turns.
I've done a little more research and found this paper, which clarifies the problem I previously had:

As a right-handed ATP-DnaA spiral would be expected to
  wrap DNA into a positive supercoil, adjacent DNA regions would be
  subjected to compensatory negative writhe (Fig. 6d, left). Although
  any superhelical strain generated by DnaA-mediated wrapping would
  be expected to spread throughout the topological domain that con-
  tains the origin, it may preferentially affect the nearby DUE, which is
  unstable and prone to spontaneous unwinding (Fig. 6d, top arrow).

Changed question: Why is this negative supercoiling generated in a positively supercoiling ccDNA?

Not my area of expertise, but can you further explain the inconsistency/contradiction? I'm not seeing it.

@BryanKrause Expecting that you are aware of DNA replication and supercoiling in general I put the issue in my words,one book says that DnaA protein forms an oligomeric complex and the DNA wraps around it in right handed fashion creating positive supercoils that denatures the weak A=T rich regions and that's where the rep. bubble is formed. The other book says that the DNA wraps around in left handed fashion underwinding the DUE(region rich in AT), not breaking them(remember) by producing negative supercoils.

Again, not my area of expertise, but I think what is happening is that DNA is wrapping "more tightly than normal" around the oligomeric complex - this causes it to be wrapped "less tightly than normal" at the DUE region. The two books are describing the same process from two perspectives - one is the perspective of the protein, the other is the perspective of the DNA where transcription is taking place.

For a piece of topologically constrained DNA, Lk is constant. Since Lk = Wr + Tw, if you increase Wr in one area, it can be compensated by decreased Wr or Tw in an adjacent area. You may ask why the unwinding is concentrated in the adjacent region and not spread throughout. This is explained in the paper you link to:

Although any superhelical strain generated by DnaA-mediated wrapping would be expected to spread throughout the topological domain that contains the origin, it may preferentially affect the nearby DUE, which is unstable and prone to spontaneous unwinding.

The DNA unwinding element (DUE) is unstable because it is AT rich:

…the opening of individual AT/TA base pairs in the three DUEs investigated differs from that of GC/CG base pairs in at least two respects. First, the opening of AT/TA base pairs is significantly more favorable, kinetically and energetically, than that of GC/CG base pairs. Second, the opening of AT/TA base pairs is affected by long range effects of the DNA base sequences, whereas the opening of GC/CG is insensitive to the base sequence beyond that of nearest neighbors. The first difference confirms the earlier proposal that the high content of AT and TA base pairs is necessary to lower the stability and enhance the dynamics of the three DUE sites. The second difference suggests that the sequences of these AT and TA base pairs have been selected by evolution as a means to modulate the energetic stability of the three DUE sites according to their location and function in the origin of DNA replication.


text:
What does it mean to protect RNA polymerase?
From this paper

However, based on the strong interaction between NusA and RNAP, we propose that the chaperone activity of NusA could provide more direct and concentrated protection for RNAP under stress, i.e., NusA could simultaneously act as a latent protector of RNAP during transcription elongation and termination.

By "protection" the authors mean that in the presence of NusA, some proteins are less prone to aggregation after heat shock. "Protection", in general, could also refer to stabilization i.e. reduction in the degradation rates of the protein.

To detect the influence of NusA on heat-induced aggregation, we used
lactate dehydrogenase (LDH). LDH was incubated at 48°C in the absence
or presence of NusA. As shown in Fig. 2b, LDH slowly aggregated at
48°C without the protection of NusA. However, when this experiment was
performed in the presence of NusA, aggregation was visibly reduced.
These results suggest that NusA also protects unfolded proteins from
irreversible aggregation during thermal stress.
...
...
In E. coli, RpoA and RpoB, the major components of RNAP, are prone to
aggregation under heat stress in vivo. They were reported to interact
with GroEL and DnaK, mainly for the protection from aggregation or
refolding into a nonnative state48,49. However, based on the strong
interaction between NusA and RNAP, we propose that the chaperone
activity of NusA could provide more direct and concentrated protection
for RNAP under stress, i.e., NusA could simultaneously act as a latent
protector of RNAP during transcription elongation and termination.

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Can assimilated energy be simply lost from a trophic level?
I was reading Environmental Studies By B. S. Chauhan and there a diagram of a model of transfer of energy.

NU = Not used energy has been shown, energy that was neither stored or exported to the next level.
I wonder what physiological process causes this loss of energy at all trophic levels?

In this diagram, since this is the only loss between trophic levels (along with  respiration and NA within each trophic level), NU represents dead organic matter, that is not transferred along the food chain. In other words, this represents dead leaves that are not eaten by herbivores, hares that die of old age and not predation, and foxes that are killed by falling rocks. So NU is the amount of energy that goes directly into the  decomposer community (another flow to decomposers is coming from matter that is excreted by herbivores and predators), since this diagram only includes primary producers, herbivores and predators.
NA, on the other hand, represents energy that is consumed by the next trophic level but not assimilated (Not Aassimilated). So this represents faeces etc.

fileunderwater I just had some thoughts I wanted to know what you have to say, I couldn't ping you in Biosphere so I would just address you here.
I was wondering do food chain end with a trophic level where the energy content is 0?  I think it is possibly never happening (because if an organism feeds on some food it is sure to consume some sugar/fat/protein if the food is not entirely minerals and vitamins) so it is never zero. Besides though food chain theoretically ends with a greater carnivore but there's no terminal organism at the end to eat-to-be-eaten cycle (the food web). .cont..

So in an aquatic ecosystem where a hawk is supposed to have a very low A it is actually supported by different other food chains, raising its energy content to a sustainable level?

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Are Nilaparvata nymphs winged?

Source: nbair.res.in
I'm wondering if the first individual on the left is a nymph. Even if not do Nilaparvata sp have wings in nymphal stage?
I'd appreciate any authentic source for reference.

The family-level identification I had given I now see was unnecessary; the Wikipedia site for an economically important member of the genus (there called the Brown planthopper) is here: https://en.wikipedia.org/wiki/Brown_planthopper.  The species covered there has long- and short-winged forms; other members of the genus are probably similar.  All of the individuals in the photograph above are adult.  A late-instar nymph will have wing pads (not yet wings) which are fused to the thoracic segment to which they're attached (a life-cycle diagram with drawings of two nymphal instars -- there are probably more -- is found here: http://www.cpsskerala.in/OPC/pages/ricePestbrownplant.jsp [the eighth slide]).
 So nymphs and short-winged adults won't be flying out of danger -- they'll be hopping away.

So the one on the left's a pre-adult (may be? of short winged form)? Comparing with the wings of short-winged Nilaparvata sp (Photograph-6) it's wings look different, too much gap between them.

The different colors of the animal's body and the wing makes me think that if the left-hand example is still a nymph (I'd have to test that idea on a local species--we're on opposite hemisheres) it reached adulthood within a day or two of the photo being taken (either wing-length form would still be possible).


text:
Approximately how long do bacteria live for?
I would like to know how many days or years do the bacteria live approximately.

I think this depends on species and particular conditions. E.G. An amp resistant strain of bacteria would be fine if you grew it on an amp plate and a non amp resistant one would die. Plus how much room does it have?

room? What you mean?

The amount of space they have to grow.

a human body you mean?

Um, no. I mean where is it growing and how much space does it have to grow - I.e. is it a huge area or are they confined to a Petrie dish? - also, how much food do they have? Are they arobic or anaerobic?

Sure arobic and what about a huge area 1-6 meteres

@Orphee Are you trying to ask how long pathogenic bacteria live for in the human body? Because that's a completely different question

Yes, I mean how long bacteria (pathogenic) live in the human body (aproximatly).

They're effectively immortal, albeit in a Phoenix-rising-from-the-ashes sort of way.
In general, a bacterial cell will divide as soon as it's biochemically able to do so, leaving behind two daughter cells. Neither daughter cell is actually the same as the mother cell, so in one sense the mother cell will have "died". On the other hand, the daughter cells are genetically identical to the mother cell and all of the physical material present in each of the daughter cells at the moment right after they split came from the mother cell.

It should be noted, however, that cell viability relies on a number of different factors.

I love how you describe them as immortals. :-)

related: https://biology.stackexchange.com/questions/21111/do-bacteria-die-of-old-age

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text:
What would happen if most the fat in your body was rapidly converted into energy in 2 minutes?
It all started out as an argument I had with my friend.He said that "it would be the equivalent of catching a fire and burning"
But all I thought would happen is that you would now be very hyper because you have a lot of energy in you body.
Please scientific answers only.
I also happen to be in the 11th grade and I dont do bio, but I knew this would be the best place to post the question.Please dont use scientific concepts I would not understand.
You guys are probably going to ask me to give an example of a way through which it might happen. So here is one way I have come up with:
Lets say the AMPK protein malfunctions and causes all the cells to release all this energy.

I would love to read an "xkcd what if" answer to that question

It depends, but you're going to die.
Specifically, it depends on how fat you are. Even Andreas Munzer is going to die. At only 3% body fat, burning all his fat (9kcal/g) would "only" increase his internal body temperature by 270 degrees C. Factoring in the energy required to boil off his body moisture and adding in body heat leaves Andreas at  ~200 C or so (pretty unevenly distributed) minus whatever heat he could give off through his skin in two minutes. He's definitely dead, but probably not on fire. The flash point of animal fat oil is about 300 C, so most of his body probably isn't going to be hot enough to burn on its own. There will probably be some smoking, though.
The average body fat percentage is more like 22%(for males), and the numbers there are unequivocal. That person is going to catch on fire, as their body temperature is going to go up about ~1800 C after boiling off all the water. That's enough to melt your titanium hip implants.
In short: you'll die pretty quickly, and then you might catch on fire before your two minutes are up, unless you're Andreas Munzer or another professional bodybuilder.


text:
Do all species have asymmetric female meiosis?
In all the examples I can think of, (mostly vertebrate), female meiosis, or oogenesis, only haploid gamete is produced while the other cell divisions result in polar bodies. While male meiosis results in 4 haploid gametes. This difference follows the fundamental definition of female and males being defined as resources committed into reproductive cells.
I want to know if this asymmetrical gamete production is truly universal across all organisms. Are all meiosis in plants or unicellular organisms unequal between male and female?

almost two years later and I'm returning to this question because I found a interesting paper relevant to this question. Turns out gametogenesis is much more variable than I ever knew.   "No universal differences between female and male eukaryotes: anisogamy and asymmetrical female meiosis"  http://onlinelibrary.wiley.com/doi/10.1111/bij.12874/full

Plant meiosis gives rise to four megaspores but usually upto three of them die by apoptosis leaving only one megaspore. But they are symmetric and three of them need not die all the time as it seems [REF].
Plasmodium being a haploid organism undergoes meiosis after fusion of gametocytes. Sexual differentiation is initiated at some point during the merozoite stage (See here and also the cross references).
Chlamydomonas is also haploid during its vegetative phase, and produces four flagellated haploid gametocytes. Sexual differentiation is apparently stochastic.
Perhaps there are more examples of organisms that do not undergo asymmetric division as seen in metazoa. There may be some stochastic asymmetry which leads to differentiation of sexes in the haploid unicellular eukaryotes and apoptosis in plant megaspores; these stochastic events may happen later as well. For plasmodium this is not really known; others I am not sure of.


text:
Books about famous experiments in biology - 'methods of investigation'
I'll explain briefly what I need (hoping to find something) :
I wanted to know if someone knew about a book that in a way or another talked about the greatest experiments in biology (Griffith, Avery-MacLeod-MacCarty, Hershey-Chase) or methods normally used to study  certain phenomena  for example, and explaining or talking about the paradigm used in biology research in such cases.
I know it might sound too vague, but I will have a kind of 'exam' essay, in which in addition to the biologic phenomena asked in terms of "notions" one will also have to suggest a 'method of investigation' to study it.
And my main problem is that in school just the theory is normally taught and not the practical approach to such topics, so I really lack knowledge in this.
So what I'm asking is whether there is a certain book or even a suggested approach that I might start using that might help me in learning what I explained above.
Thank you for your help!

Honestly, someone needs to write this book.

Microbe hunters is an excellent book which will fulfill your requirements. You will get an insight into the working of some of the greatest minds....

The Eighth Day of Creation by Horace Freeland Judson is quite good, in the genre you're looking for. Also, Science as a way of Knowing may fit the bill.

Although it's not stricly about biology, A short history of nearly everything by Bill Bryson, especially chapter 5, is a good start to look for historical experiments.


text:
Is this a bedbug? (with picture)
I had some potentially infested clothing (and shoes) in a bathtub, and just after I bagged them to wash, I spotted this little fellow running away.  I put it in a plastic food container and snapped a photo as close up as my phone could get:

Is this a bed bug?  Its length is about 3 mm, so presumably it would be a nymph if so.  Compared to pictures on the Web, it certainly looks similar.  However, it seems too thin (even for a nymph), and the antennas don't have that outward crook that all of the pictures (even of nymphs) seem to have.  Also, at the time that I took the picture, it could not have fed on blood in the previous 12 hours.  So hopefully it's not a bed bug at all; but maybe there's nothing else that it could be, and the pictures give the wrong impression of what's possible.  Can anyone tell?
This is not a StackExchange that I'm used to, so if this is an inappropriate question, then I apologize, and I'd appreciate any suggestions of where to ask instead.
ETA:  This is in the Midwest/Great Plains region of the USA.
ETA:  Having seen more pictures, the thinner (or really, longer) form seems to be after they have fed.  But as I said, this could not have fed within 12 hours at least (when the clothes it might have been in were removed, plus the people had no apparent bites).  And that doesn't explain the relatively straight antennas.  But it does seem closer now.
ETA:  The picture doesn't seem to match any of the false IDs of bed bugs on this site, nor the related insects at bugguide.net.  (And it compares to the actual bed bugs with the slight differences that I noted already.)

Welcome to Biology.SE!  This appears to be a frequently asked question — have you looked at the related questions e.g.: https://biology.stackexchange.com/questions/56200/insect-identification-is-this-a-bedbug?rq=1?  Also, bugguide.net is probably a better place for this sort of question.

Hi @tyersome and thanks for your reply.  Yes, I did look at related questions, including that one, and I've added a paragraph at the end about why they didn't solve this.  And I did look at bugguide.net (also mentioned in my new last paragraph), but I didn't realize before that they have their own identification service, so I'm going to try that now too.

Not a bedbug. They are laterally expanded, not narrow like this one. I can't tell for sure from the picture, but I would guess that it is either a collembolan or a thrips. You could narrow your image search to these two groups. (Collembola, Thysanoptera).

Thanks, @KarlKjer!  Someone on bugguide.net also suggested a springtail, and it does look rather like the one at https://bugguide.net/node/view/90808

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Are there humans which the brain sends signals to the limbs faster than the average?
I have done some researches on the time taken by the brain to send signals, but I didn't find whether that time is the same amongst all humans or there are some differences, and I have based my question on an article which mentioned that Messi(one of the best players in soccer history)'s brain send signals to the limbs faster than the normal human (https://www.ncbi.nlm.nih.gov/pubmed/27010676), so is this possible to happen.

Hello and welcome to Biology.SE! Take the tour to learn about this site and earn yourself your first badge. You surely did find an amusing paper! Good luck with your question!

Your question would be improved if you explained who "Messi" is.

helpful paper https://www.researchgate.net/figure/Experimentally-determined-conduction-velocity-of-a-nerve-impulse-in-a-mammalian_fig12_321016169

Assuming that the time it takes for a signal to travel from the brain to the limbs follows a normal distribution (which is reasonable), then certainly there are people who fall at the upper and lower ends of the distribution. In fact, it's relatively improbable that someone would fall right at the mean.
Consider the normal distribution below. If the mean for all humans is at the center of the distribution, then almost all fall above or below that mean. Whether Messi falls in the lower tail is a separate question.


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Is there a good explanation for this swarming pattern?
A film clip would be helpful here. A few days ago I noticed a swarm of newly hatched flying bugs about 20 feet away from me with the sun behind them so the shape of swarming (such as it was) was easy to make out. Several times, after creating various spiral shapes or chaotic masses they returned to a sort of 'holding pattern' which I either never noticed or never saw before. To a pretty good approximation the bugs arranged themselves in what seemed like an "oscillating drum head" pattern that is well approximated by a rotated sinc function. The peak at zero is a little exaggerated here but the bugs were more or less dispersed on a shape like:

subject to a light breeze and continuous adjustment. I know that people have studied swarming behavior and made models but are there any that account for this one? It has a lot of significance in ODEs and engineering but I never associated it with swarming behavior.
Thanks!

It is a fascinating phenomenon. There is some research on swarming behaviour, see e.g. Collective motion, and in general some research by Tamas Vicsek and Ian Couzin research groups.

I watched some youtube videos but couldn't find any swarming that looked like rotated sinc function.
The following is nothing but the guesses of someone who doesn't know much about swarming!
One pattern that is often found (through computer simulation and empirical observation) in swarming is a simple 2D rotation.

Let's first consider only the static form of the shape you observed. This shape might be the consequences of multiple rotating layers. Do you remember what kind of dynamic had the individuals within your sinc function?
Oscillation is a pattern that is also sometimes observed in swarming. The oscillating behavior might be the result of inertia. Just like a pendulum, individuals that are far away from the group accelerate continuously in the same direction up to the point they reach the middle of the group. Then they undergo a inverse acceleration up to the point they reach a null speed and then start their cycle again. This inertia depend on the number of neighbors they align their movement on are low. For example, it has been shown in I don't remember which species of birds (I can't find the reference) that each individual align their movement according to only the 6th closest neighbors.
For more information about the 3 basic rules (separation, alignment, cohesion) that allow swarming behavior, have a look to the wiki page
In short, I hypothesize that thanks to the underlying 3 basic rules of swarming, the patterns of rotations and inertia together allow to explain your observations.

Yes, I can't rule out multiple rotating layers. +1


text:
Why don't antiseptic agents kill 100% germs?
I've seen innumerable antiseptic, mouthwash, handwash advertisements that claim to be able to eliminate as much as 99.9% of all germs over a surface...but why not the remaining 0.1% (i.e- why can't they eliminate all germs)?

Clarifications:
What they mean by "germs":
Being a student of Biology, I can tell that the term "germs" is crudely defined. I would prefer to use "pathogens" (less ambiguous), and I suppose the guys that market these products have (roughly) the same idea in mind. Pathogens normally include bacteria (monerans), protozoans, fungi and viruses... so I guess these are the "germs" they're talking about.
What I'm looking for in an answer:
Why is it that these (commercial) products can't eliminate 100% of all pathogens? Is this due to the inability of antiseptics to act on a particular (class of) organisms? If so, what's the problem there? Or is it because, the guys who market stuff like this assume an arbitrary amount (0.1%) of the pathogens present on a surface (say, the human hand) is located in microscopic niches that are inaccessible to the antiseptic solution? (If it isn't possible to provide a blanket statement in this regard, use of Listerine as an example will suffice)
In other words:
Is an antiseptic's inability to eliminate 100% of all germs due to its "chemistry", or is it due to physical factors?
Also,
Do antiseptics/mouthwashes/handwashes even kill 99.9% of all germs in the first place? Or is it (as I strongly suspect) an example of marketing fraud?

I think they leave that 0.1% just so that they can pull their hands away in case of any infections. But your question is too broad, in the sense that you are asking too many qiestions at the same time. You need to narrow it down.

@gerardo why don't you add another answer explaining that part? You'll definitely get upvotes, and it might bring this into hot questions list ;)

In a first year lab I used to teach, the students would determine the zone of inhibition for different antiseptics in an agar diffusion test. Listerine didn't kill anything.

I suspect that 99.9% has more to do with marketing and lawyers than biology. They don't promise to kill all the germs so they can't be sued when they don't. On the other hand, it sounds like a promise to anybody who believes in the 3 second rule.

@mmesser314 -  for non-native English speakers: 3 seconds rule means you can safely eat food dropped on the floor if you pick it in 3 seconds or less. Of course not based on any science.

@petermasiar I thought it is 5 second rule coz thats what I've heard everywhere? Has it been modified? I recently also saw many news reports saying "science proves 5 second rule is true" (didn't read any of them though)

@another'Homosapien' - I am not sure who would finance such research, and why. Urban dictionary in my link does not pretend to be scientific, but is (IMNSHO) great resource for non-native speakers to decode expressions obvious for native speakers, but puzzling for others.

I also found 5 seconds rule which says exactly what 3 seconds rule says. And both are correct! Amazing thing, this science!

This is actually an interesting question! Let me answer both the parts separately, taking the example of Listerine® mouthwash.

Is an antiseptic's inability to eliminate 100% of all germs due to its "chemistry", or is it due to physical factors?

In most of the cases, this is due to the physical factors. Clearly, your mouth is not a flat surface. It has many depressions and elevations. And these irregularities are the perfect hotels for all kinds of pathogens. Also, it is difficult for most chemicals to reach those spots and stay there for long enough so that they can act on the pathogens. Thus, most of these chemicals would be unable to kill 100% pathogens because of their inability to reach all of them. Also, in rare cases, it might also be due to chemical factors(!) Yes, I'm talking about antibiotic resistance. And in that case, it would be practically impossible to kill 100% pathogens, no matter whether they're hidden or exposed.

Do antiseptics/mouthwashes/handwashes even kill 99.9% of all germs in the first place? Or is it (as I strongly suspect) an example of marketing fraud?

For that, lets first see what Listerine® contains. As given on its website, its main ingredients are (I'm simply copying what they write on their page, followed by checking whether its true):

Eucalyptol – with antibacterial properties, this eucalyptus-derived essential oil works as an anti-fungal agent within the mouth.
Methol – this natural oil as germ-killing abilities to help halt the growth of bacteria.
Thymol – this powerful oil is derived from the ajowan herb, and helps decrease the risk of gum disease.
Methyl Salicylate – for minty freshness from morning til night, the flavouring agent in this essential oil is, well… essential!

We just need to know whether these ingredients really work or not (why? We'll talk about this later on) and I'll skip methyl salicylate for this (they don't even claim that it is antimicrobial). Beginning with eucalyptol, it has been shown that oil of Eucalyptus globulus (of which eucalyptol is a component) has antimicrobial properties against Escherichia coli and Staphylococcus aureus (see Bachir et al, 2012). It has also been shown to possess antifungal properties (Safaei-Ghomi et al, 2010). Coming to methol, it has also been shown to have antibacterial properties against various Staphylococcus and Lactobacillus species (Freires et al, 2015). Finally, there have been lots of studies about the antimicrobial properties of thymol. You can check out the Wikipedia page for information.
So, where is the percentage? The point is, the exact percentage depends on a lot of factors. When an enterprise, such as Listerine®, claims that their product has been shown to be 99.9% (or any number) efficient against bacteria, they need to cite the particular study through which they claim this number. But they can not, in any case, be definite that their product will be 99.9% effective everytime. How effective a product is also depends on the conditions under which it is tested. Mostly, these tests are performed on a petri dish in a laboratory, something very different from your mouth. Thus, although they can claim that their product is scientifically proven to be 99.9% effective, they cannot claim it to be 99.9% effective when you use it. Again, they cannot claim 100% effectiveness because this makes them liable (saying our product has been shown to be 100% effective requires them to show that even a single microbe did not survive on the petri dish they used for experiment). Also, this gives them a way to escape in case anybody complaints about their product not being effective (since they caught infection even after using their product). In such situation, they can easily say that their product is not 100% efficient!

I really like this answer! As much as I want to "accept" this, I guess it would be wise to give the question a day for more answers to (hopefully) trickle in. Thanks again! ^_^

@bencrowell agreed, but you can't pasteurize your mouth :P talking about soaps, most of them just help you banish those microbes by flushing them with water (only antibacterial soaps do seem to "kill" them, albeit this is debated too)...

For Listerine, you are missing the main ingredient -- alcohol.  Depending on formulation, Listerine is about 22% to 26.9% alcohol.

Answers to this question point to this paper, which says "alcohols [are] significantly [less effective] at concentrations below 50% and is optimal in the 60 to 90% range". It also points out that alcohol is fungicidal, but not sporadical. As the question asks about "Antiseptic" and not specifically organic antibacterial/antibiotic agents, this seems very pertinent. I had another point I wanted some clarification on, but I can't remember it after brushing my teeth.

Well as a Microbiologist by trade, we use this numbers based  on log reductions on the forming units of the organism being tested. There is a limitation on the testing methods that cannot determine an absolute elimination of the pathogen.
For example, I perform the test and perform serial dilutions of the recovered organism and plate it on agar to be counted. Higher concentrations are hard and nearly impossible to count so we must use dilutions to achieve this and then multiply for the dilution factor to react an "exact number". So when I perform a 100 times dilution and the agar plate comes clean (no organism) growing the recorded number is not 0 but <100 because we cannot be sure about how many organisms should be there. I know this is a bit confusing but it is more like a safeguard to not give false information.

+1 Came here to say this - although the others make some interesting points and speculations about liability etc, this is actually the correct answer. Legally, a chemical must result in a 3-log reduction in titre during the specified contact time to be described as a disinfectant. (Source: I run a high containment pathogen lab and we use similar protocols to validate disinfectants whenever we add a new pathogen, want to test a new chemical, or want to modify our protocol - reduction in contact time, validation at low temperatures, etc.)

You could improve the answer by adding a labelled diagram of a serial dilution or some links, though.

I agree with answer of @another 'Homo sapien' - to 99.9% :-) but there is another angle on it:
From millions of bacteria present, few might be genetically different enough to be able to deal with whatever chemical mechanism it supposed to kill them (have resistance to it), and survive. Evolution at work.

Unlike you, I am just a computer programmer who had a pleasure to work for bioinformatics in academia for a decade. So I prefer to read explanations by experts, instead of pretending to be one. I am just a lurker here. Making my answer longer would add fluff, and I like concise answers.


text:
What are the (correct) terms for these flagella-arrangements?
I came across the following diagrams depicting two kinds of arrangement of flagella over cells.

Now according to my (very unreliable) school textbook, the arrangements are termed as:

A - Cephalotrichous (tuft of flagella on one end)
B - Lophotrichous (tufts of flagella on both ends)

Whereas another (equally unreliable) book states the exact opposite:

A - Lophotrichous (tuft of flagella on one end)
B - Cephalotrichous (tufts of flagella on both ends)

A spot of cursory Googling reflects this sort of confusion online (compare the images and their labels here) as well.
According to Wikipedia that arrangement A is lophotrichous, but it makes no reference to arrangement B though.

I tried to figure it out, going by the smattering of Greek I picked up as a Bio. student ( Cephalos = Something to do with the head ; Lophos = something to do with a peak/protuberance ), I arrived at:

Hmm... so cephalotrichous probably means you find the tuft on one "end" (so arrangement A), and ipso facto lophotrichous is arrangement B.

But I guess, I ended up putting a little too much thought into it...

Cephalotrichous is probably used to indicate you have a tuft on the "head" in addition to another tuft on the "tail" (so arrangement B), and ipso facto lophotrichous is arrangement A.

 At this stage I'm not sure what's more serious: my inability to find an authoritative answer to my question... or my tendency to overthink stuff

I'm in a fix.
Could someone clarify, citing (multiple, if possible) authoritative sources, on the distinction between a "cephalotrichous" and a "lophotrichous" arrangement?

Whup! You're right! My bad :3  ( <--- Flag as obsolete)


text:
What further research can the result of gene variation detection be used for
We do a research on a particular cancer (for e.g. breast cancer). Now, we have a result for the gene variation detection (VCF file). What next steps do we need to do? We don't have a clear picture about this. Can you give us some directions or few papers as an example? (of course it is a huge number but just mention a few). Thanks!


text:
Does physical exercise of a specific part affect muscles in the other parts of the body?
There is a theory among bodybuilders, that is, if you train big muscle groups (e.g. legs, chest), it will increase the overall growth of muscles all over the body; the trained muscle will release signals (what are they?) into the blood stream and in turn, triggers the release of muscle growth/repair hormones (insulin-like growth factor?) which have effects on any (skeleton) muscle cells.

Is this story true?
Will the muscle growth/repair hormones also enhance the smooth muscle or cardiac muscle?

Definitely a question that should be asked on bodybuilding.SE.

@Remi.b, the OP is interested in knowing if the popular notion amongst bodybuilders has some authentic biological basis.

Maybe I am wrong but I would assume that on bodybuilding.SE they care about verifying their claims.

@Remi.b thank you for the link. But I just want to find out whether these popular claims are supported by rigorous study. I looked at some references cited by bodybuilding experts, they are pretty crappy.

http://jap.physiology.org/content/65/6/2406 here is a paper on training and increase in testosterone.

@ChenChao what were the references by the bodybuilding experts?


text:
Equilibrium and Metabolism: Can cells exist at STATIC equilibrium? What about dynamic equilibrium?
I understand that in closed systems, once reactions reach equilibrium, they can no longer be used to power other reactions. If a cell was a closed system (which it is not), being at equilibrium would mean that it's dead, for it needs a continuous input of energy from the environment.
I know that the cells are open systems, and my teacher mentions that cells can never be at equilibrium. But, I am confused because can't cells be at dynamic equilibrium (where rates of reactions = rates of products)? So my next question is: can the cells not exist at static equilibrium? I am not quite understanding the differences between equilibrium, dynamic, and static. And, when something is at dynamic equilibrium, why does this mean that the concentrations of reactants and products are not necessarily equal?

There are some things that should be addressed first.

Chemical-Equilibrium
This is a condition at which the forward reaction rate is equal to the backward reaction rate for a reversible reaction.
$$\ce{A<=>[k_f][k_r]B}$$
In this case, $k_f.A=k_r.B$, at the equilibrium, if the reactions are first-order. If $k_f>k_r$, then the concentration of B would be higher than the concentration of A, at equilibrium point.

Steady-State
It is a state of the system at which the overall concentration of all the components (reactants and products) remain constant with time, or oscillate at a constant amplitude and frequency. Mathematically, the differential equations that denote the system (as mentioned by Dexter) would equate to zero.
If this condition applies only for one or more but not all the components of the system, then it is said to be in a Quasi-Steady-State.
If there are only two species which inter-convert but do not get formed or degraded, then steady state would be same as the chemical equilibrium. However, it is to be noted that chemical-equilibrium is a property of a reversible reaction whereas steady state is the property of the system.

Coming to your main question, I do not know what your teacher really had in mind, but this is my explanation.
According to the above definitions, you cannot say that the cell is in equilibrium because the cell is a system and not a reaction. The usage of the term "equilibrium" varies between different fields of study and physicists do use steady-state and equilibrium interchangeably. However, this is not the practice among chemists and biochemists.
Having said that, I would say that a cell does attain a steady state. I think what your teacher wanted to imply was that a cell constantly responds to the external stimuli (which is randomly changing) and therefore never remains at any given steady state for a long time.

Can the cells not exist at static equilibrium?

No, they don't. In fact the term "static equilibrium" in never used in chemistry because it never really happens. At a static equilibrium all the rates have to be zero, whereas in a dynamic equilibrium the rates have to balance each other out. Static equilibrium usually applies only for macroscopic objects (which do not include molecules).
A note on stochasticity: Chemical reactions follow probabilistic kinetics i.e. the reactions occur with some probabilities, instead of fixed rates (these probabilities can be unequal for different reactions). Chemical systems can be approximated by deterministic models at the thermodynamic-limit which reflects the "average" behaviour of the system.

when something is at dynamic equilibrium, why does this mean that the
concentrations of reactants and products are not necessarily equal?

See the first section. Similar logic applies for steady-state. The steady state concentrations depend on the kinetic parameters.

If a cell was a closed system (which it is not),

Yes, you are right. Cell is not closed system.

my teacher mentions that cells can never be at equilibrium

No. It depends on your definition of equilibrium and which kind of equilibrium. E.g.: Cellular membranes are most of the time in chemical equilibrium to maintain their resting potential.

can't cells be at dynamic equilibrium (where rates of reactions = rates of products)?

Yes. Most of cellular processes are assumed to be in dynamic equilibrium which is correct in most of macroscopic phenomenons. Microscopically, everything is stochastic.
Most of cellular processes are assumed to be in dynamic equilibrium.

I am not quite understanding the differences between equilibrium, dynamic, and static. And, when something is at dynamic equilibrium

Look here!

And, when something is at dynamic equilibrium, why does this mean that the concentrations of reactants and products are not necessarily equal?

Suppose system A -> B -> C -> A, with reaction rates v1, v2 and v3. If you write differential equations for this system,
$$
\frac{dA}{dt} = v3\times C - v1\times A\\
\frac{dB}{dt} = v1\times A - v2\times B\\
\frac{dC}{dt} = v2\times B - v3\times C
$$
Now at equilibrium,
$$
v3\times C = v1\times A = v2\times B
$$
Now you can put your v1,v2 and v3 in such way that concentrations of A, B, C will be different. In this care system can be in dynamic equilibrium even when concentrations of A, B and C are not same.

The condition that you are referring to, is specifically called the steady state in chemical and biochemical texts because chemical equilibrium is a different phenomenon. Physicists, generally use the term "equilibrium" to mean steady state.

This is better than all of our mathematical explanations. !

The video is nice.. But I think there are field specific differences (which are quite subtle).


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How can I measure the curvature of bird's beak on the field?
I'm wondering if there is a standard tool to measure the bird's beak curvature.
It seems that a spherometer wouldn't work because the beaks that I'm measuring are not circular but more parabolic.
I guess something like this:

I feel that this can be a problem if your birds have different beak length.
What do you think?

There are possibly infinite superlinear curves that may denote beak morphology. I think what you can use is the maximum slope of the curve. That would generally tell you how curvy is the beak compared to a linear one.

I was thinking about a tool that I can bring with me on the field. Not something to calculate after with photos or something else. Is this what you propose?

Yes I was suggesting something like that. I am not aware of any tool like that. You can perhaps measure the actual beak length using a measuring tape and divide it by the direct point-to-point length (like displacement) to have an approximation of the curvature. The higher the ratio, the higher would be the curvature. For a semi-circle it would be π/2.

Bird beak morfology is often studied (try Google scholar). Aren't there any papers describing how they measure it?

They usually measure it afterwards on photos : https://www.researchgate.net/publication/40039501_Predatory_Functional_Morphology_in_Raptors_Interdigital_Variation_in_Talon_Size_Is_Related_to_Prey_Restraint_and_Immobilisation_Technique/figures?lo=1

Another good one is this: http://redpath-staff.mcgill.ca/hendry/Foster2007JEB21,263.pdf. But I'm thinking something more practical on the field.


text:
How much mechanical stress can a skeletal muscle bear?
In the movie- Saw, for the last trap Bobby was told to insert metallic hooks into his pectoralis major muscle. In his fake story Bobby has raised himself successfully, but when he was "really" trapped, his muscles were broken under his own weight.
Is it true, that muscles can be broken so easy? When human is pulling up on the bar, aren't these muscles undergo much more tension, because of lever effect made by his arms?
Also, what if Bobby insert hooks under his ribs, would he die immediately due to pneumothorax?
The question is biological, no interest of how it was possible to overcome trap with mechanical means.

Can you edit this to make it more about biology and less about a fictional character in a movie? Are you interested in the tensile strength of vertebrate muscle?

I don't watch the SAW series. But with regard to muscle tear, it depends on a lot of factors like the weight applied (was this Bobby heavy or muscular) and whether he moved around a lot. You might have heard of crocodiles rolling around to tear off flesh of their prey. So if he was thin or was muscular and did not move around much, the muscle should be able to handle the weight.

worth noting SAW uses a lot of handwavium when it comes to biology, like there is no hacksaw no matter how dull that will cut through a leg faster than a link of chain. cutting through a human leg is tough.

The skeletal muscle is not isotropic and therefore the effect of stress would be different from different axes. The strength also depends on the density of fibers and the composition of tendons (aponeurosis) that connect the muscle tissues; these can change (positively) with long term exercise [ref].
In this article the authors show the effect of different mechanical stresses on the skeletal muscle tissue — digitorum longus, from rabbit hindlimbs.

Tests were performed on extensor digitorum longus (EDL) muscles,
  chosen for its regular cross-section and low pennation angle (Lieber
  and Blevins, 1989). To ensure that only muscle tissue was tested,
  aponeuroses were carefully dissected away

Figure from the same article by Morrow et al. (2010)
You can notice that the yielding point to longitudinal extension is somewhere near 180kPa. It can be assumed that a hook into the tissue on pulling would generate longitudinal extension stress (unless the hook pierces through the muscle tissue or has sharp edges that can rip the muscle transversely). The stress in the Bobby situation would be: $$\frac{\text{weight (mass)}\times \text{gravitational acceleration}\ (9.8\ ms^{-2})}{\text{area of the muscle covered by the hook} \times \text{number of hooks}}$$
This is the best I can answer your question based on data; this cannot be directly extrapolated to the Bobby situation because:

The muscle tissue is different
The strength of the tissue depends on how much has Bobby exercised his muscles.
There would be additional mechanical stresses in other directions because of his movement while being suspended from the hook.

Ribs are not very strong bones and attempt to hook something on it may cause punctured lungs, not pneumothorax. Death will depend on the severity of the wound.


text:
Open protocol for Ligase Independent Cloning
Ligase Independent Cloning is a protocol that allow an insert to be integrated into a vector without ligation.  It uses T4 DNA polymerase with only ATP to first chew back from blunt ends to create long sticky ends and then a polymerase treatment with full dNTP compliments to fill in the vector.
While there are several nice articles and resources that describe the procedure, I really would like a protocol with concentrations, temperatures and timing, which I'm having problems finding.  OpenWetWare for instance has only stub pages with no details.  Can anyone point to a full step by step recipe to make this work, once you have designed the primers?

Here is the original article. I'm going to get working on that OWW article. http://www.ncbi.nlm.nih.gov/pubmed/2235490

You can look up Gibson Assembly or Circular Polymerase Extension cloning (CPEC).  For both of these the website for J5 has some good protocols.  Here is the one for CPEC:  http://j5.jbei.org/j5manual/pages/80.html
For CPEC you can look at the 2011 Quan paper: http://www.ncbi.nlm.nih.gov/pubmed/21293463
Hopefully that helps.

thanks for this @Justin, but the protocol link, while complete doesn't make clear to me how this works. Why does the Pfusion polymerase have all the dNTPs? I had thought that to chew back from a blunt end, the polymerase would need an incomplete set of NTPs? Also how is the vector cut?  Is there any decision to be made here or is it just any digestion cut at all?

I think i discovered that part of the answer to this question is that Gibson assembly is patent protected...


text:
Is there a biological explanation for perceived altered cognition whilst on cannabis?
Cannabis has been associated with literature, arts, and culture for centuries. There are a few features of the drugs affect on the human mind that account for this, however it remains illegal in most countries.
In a very tangible way, cannabis causes a few alterations of perception, such as an altered sense of time and this is often exploited by police to see if a potential felon is intoxicated. Other psychoactive alterations that are attributed to a cannabis (AKA marijuana or weed) include a temporary sense of deeper metacognition, depersonalization, & derealization.
Whilst I'm aware that this is probably the result of the active compound THC, it's unclear how is this deeper feeling of cognition achieved from a physiological perspective? What is this process in the brain that changes the perception of reality?
Ideally studies mirroring the recent Cahart-Harris et al., 2016 paper would be ideal (but focused on THC rather than LSD). That paper identified key physiological features that correlated with the feelings of being "high" such as changes in brain blood flow, electrical activity, and network communication patterns.
Note I am not talking about long term IQ alteration, but rather the temporary affect the drug has on the brain's cognition.

I'm not ready to answer a perception-of-reality statement, but endocannabinoids such as anandamide need to be mentioned here.  These escaped notice right up until the 1990s - political motivations led the NIDA to deny permission for mechanistic studies and for a long time preserved the very peculiar notion that cannabis was a psychoactive drug without a specific receptor.  But a search for the terms above will yield much useful biomedical research.

There has only been little research on the neurocognitive and neurophysiological effects of cannabis. There have been introductory neuroimaging studies in mainly non-psychotic populations, which show that cannabis does not affect gross brain anatomy. On the other hand however, it has been proved that cannabis does acutely increase cerebral blood flow (temporarily; in the right hemisphere) on the long run, exposure will cause an overall reduction in cerebral blood flow.
There have been studies with animals where they used an active cannabinol called delta-9-THC to demonstrate enhanced dopaminergic neurotransmission in brain regions which are usually associated and known to be implicated in psychosis.
In humans the delta-9-THC causes psychotic-like states and memory impairments. The effect of a CNS cannabinoid system, on humans is still tested by neuroimaging studies.
The endogenous cannabinoid system is sensitive to contact with exogenous cannabinoids such as the delta-9-THC, which is known to impair memory in humans.
In a further study is was examined what impact chronic cannabis use has on memory-related functions by examination of the subsequent memory effect (SME) of the event-related potential (ERP). The study concluded that comparing the group to the control group that chronic users of cannabis have an altered memory related brain activation in the form of dysfunctional SME production which may also go hand in hand with reduced neural efficiency.
Several investigators studied the acute effects of cannabis specifically on attentional processing. Hart et al. (2001) studied the effects of placebo, light (1.8%), and heavy (3.9%) THC cigarettes in chronic, daily cannabis users and found no significant differences in the accuracy of response to attentional tasks. However, performance on a tracking task, which requires sustained attention, was found to improve significantly after the high dose of THC, relative to the other conditions.
In one study of 37 adults with a history of light cannabis use, acute intoxication with a high dose of THC resulted in significant impairment on a measure of impulsivity (McDonald et al., 2003). Another study (Ramaekers et al., 2006) found similar impairment on a task of inhibition in intoxicated, chronic cannabis users. The results measured where in a timespan from 0-6 hours after consumption.
In another study from 2010, researchers investigated "semantic-priming".

Under the influence of cannabis, users showed increases in both automatic semantic priming and schizotypal symptoms compared with controls. When abstinent, cannabis users exhibited hyper-priming at long SOAs.

References and further reading:

Linszen D, van Amelsvoort T. Cannabis and psychosis: An update on course and biological plausible mechanisms. Curr Opin Psychiatry. 2007;20:116–20
de la Serna E, Mayoral M, Baeza I, Arango C, Andres P, Bombin I, et al. Cognitive functioning in children and adolescents in their first episode of psychosis: Differences between previous cannabis users and nonusers. J Nerv Ment Dis. 2010;198:159–62.
Bossong MG, Niesink RJ. Adolescent brain maturation, the endogenous cannabinoid system and the neurobiology of cannabis-induced schizophrenia. Prog Neurobiol. 2010;92:370–85.
Battisti RA, Roodenrys S, Johnstone SJ, Respondek C, Hermens DF, Solowij N. Chronic use of cannabis and poor neural efficiency in verbal memory ability. Psychopharmacology (Berl) 2010;209:319–30.
Hart CL, van Gorp W, Haney M, Foltin RW, Fischman MW
Neuropsychopharmacology. 2001 Nov; 25(5):757-65.
McDonald J, Schleifer L, Richards JB, de Wit H
Neuropsychopharmacology. 2003 Jul; 28(7):1356-65.
Ramaekers JG, Kauert G, van Ruitenbeek P, Theunissen EL, Schneider E, Moeller MR
Neuropsychopharmacology. 2006 Oct; 31(10):2296-303.
http://druglibrary.org/schaffer/hemp/general/mjeff1.htm


text:
How does paracetamol work?
Hinz et al. 2008 found that COX-2 may be inhibited by paracetamol, and this is attributed to it's analgesic and antipyretic properties. However, there are other more recent claims from Andersson et al., 2011 that a toxic intermediate metabolite, NAPQI, may be acting on TRPA1-receptors in the spinal cord. Whilst I'm vaguely aware that the end goal is to affect prostaglandins, to me at least it remains unclear how that translates to painkilling.
There are also other theories I would imagine.
This exceedingly common drug seems shrouded in mystery. I know very little about pharmacology (evidently!), so some expert insight into the popular theories, and why they're popular, would be greatly appreciated.

What are the most popular theories in a nutshell?

Why are they a popular theory?
Which protein is targeted?
How does that inhibition introduce the analgesic and antipyretic properties?

Is it possible multiple theories are correct?
Why is so little known about paracetamol? Is it exceptionally difficult, or the norm in pharmaceutical research of relatively old effective drugs? If it ain't broken, why fix it!

The modern pharmacology of paracetamol: therapeutic actions,
mechanism of action, metabolism, toxicity and recent
pharmacological findings.--
Supra-spinal FAAH is required for the analgesic action of paracetamol in an inflammatory context.--
TRPA1 mediates the hypothermic action of acetaminophen..--
I think these are some good articles, but they may have paywalls.

@Kendall , not to forget placebo effect of paracetamol like this.

@Dexter Fascinating! I imagined there would be placebo to an extent with the pain. I wonder if there are any inflammation placebo affects from paracetamol.

That's possible. Need to search a bit.

Maybe this is why you can't get a satisfactory answer. "Paracetamol (acetaminophen) works through known mechanisms...Although it is widely used, there are only hints as to how it and other common drugs actually work." -The science myths that will not die: Nature News & Comments

What are the most popular theories in a nutshell?

To date, the mechanism of action of paracetamol is not fully understood. There are some experimental evidences, but it is difficult to put things togheter. It is now clear that  paracetamol acts contemporaneously via at least three pathways:

The inhibition of cyclo-oxigenase (COX)

The main mechanism proposed is the inhibition of COX, it's highly selective for COX-2.
COX are molecules involved in the metabolism of arachidonic acid (aa). It catalyzes the reaction to form prostaglandin H2, a pro-inflammatory compound, from aa.
Paracetamol, as other NSAIDs,  block this step , thus reduce the amount of prostaglandin H2. The reduced amount of prostaglandin H2 in the CNS, lowers the hypothalamic set-point in the thermoregulatory centre.
The exact mechanisms by which COX is inhibited in various circumstances are still a subject of discussion.
Some authors state that paracetamol works by inhibiting the COX-3 isoform—a COX-1 splice variant—of the COX family of enzymes.
This variant is expressed mostly in brain, so it is the one supposed to be involved in the antalgic effect of this compound.
There is another physiopathologic possibility to explain its action, that is: paracetamol would block COX, but in an inflammatory environment where the concentration of peroxides is high, paracetamol itself is oxydated and thus inactive. When it founds a non inflammatory environment, such as CNS, it become reduced and thus active (it reduces temperature, it has anti-dolorific action, etc).

The modulation of the endogenous cannabinoid system, through its metabolite AM404, a compound that inhibits the reuptake of the endogenous cannabinoid/vanilloid anandamide by neurons.

The COX model can explain quite well the action of paracetamol, altought it has been demonstrated an important role of the endocannabinoid system aside of COX. When cannabinoid receptors are blocked with synthetic antagonists, paracetamol's analgesic effects are prevented.  This is tought to be due by an active metabolite of paracetamol, that is called AM404 and inhibits the reuptake of anandamide.
Anandamide reuptake lowers synaptic levels of anandamide. This results in a more activated pain receptor (at least the main one, called TRPV1, or according to an old nomenclature: vanilloid receptor). The high levels of anandamine, due to inhibition of its reuptake, desensitise this receptor in a way similar to the capsaicine.
Furthermore, this active metabolite (AM404) inhibits sodium channels, this chemical behaviour is shared with lidocaine and procaine, two common anesthetic drugs.
These two actions by themselves have been shown to reduce pain, and are a possible explanation of paracetamol's mechanism of action; but one other specific activity of this compound remains unexplained by these two models.

Serotonin receptor agonism.

It has been observed that this compound can reduce the social rejection in humans. This can't be explained with COX or type I endocannabinoid system modulation.
Increase of social behavior in mice dosed with paracetamol, wich models a reduction of social rejection response in humansdoes not appear to be due to cannabinoid receptor type 1 activity. .
In the animal model, it seems a result from  serotonin receptor agonism.

Aside of this main features, some other evidences are in bibliography.

In 2011 a debate started on scientific journals. Some has found  a hint to the analgesic mechanism of paracetamol, being that the metabolites of paracetamol e.g. NAPQI, act on TRPA1-receptors in the spinal cord to suppress the signal transduction from the superficial layers of the dorsal horn, to alleviate pain.
This findings has been contested in a  new hypothesis paper  on how paracetamol might act.
This second study concedes that NAPQI is the active metabolite but that this reactive compound should react not only with the thiol in TRPA1 but also with any other suitably available nucleophile that it happens to encounter. This broad interaction with thiol groups in cysteine proteases, like the ones that process  procytokines, might be the targets giving rise to overall analgesic effects, changing the global cytokyne environment.
Even if there are evidences of drug-body interaction with formation of active metabolites and there are some models of drug action, many things are not fully cleared and the debate is still open.

Why are they a popular theory?

Are popular because are based on experimental and clinical evidence. Also, this theories can model lot of the biological effects of this compound.

Which protein is targeted?

Not any time it can be possible to reduce a pharmacological interaction at this level. For instance, in one theory it inhibits an enzyme, the cyclooxygenase (COX); in one other model entire classes of molecules, the sodium channels, are modulated...
Unfortunately many times, dealing with living organisms, it is not possible  to offer an hard, mechanicistic explanation of things.

How does that inhibition introduce the analgesic and antipyretic properties?

In the COX inhibition model, the analgesic properties can be explained trough an affinity for COX3; and the antipyretic activity can be due to the reduced amount of prostaglandin E2 in the CNS, in the thermoregulatory centre it lowers the hypothalamic set-point. The endocannabinoid model can explain preety well the anti dolorific actions, as well as the serotonin receptor interaction the behavioral one.

Is it possible multiple theories are correct?

Yes, there is a substantial overlap between different regulatory systems, so that is straight to think that the same chemical (or some of its different active metabolites) can modulate different systems.

Why is so little known about paracetamol? Is it exceptionally difficult, or the norm in pharmaceutical research of relatively old effective drugs? If it ain't broken, why fix it!

Is it not that difficult topic! One can say that is as tricky as any clinical pharmacology topic. The problem is that many compound are clinically used as drugs even if their molecular functionig is unknown if they are safe and of proved usefullness. This is true for paracetamol as well as many other drugs, like a lot of anaesthetic agents as Propofol.


text:
How did the endoplasmic reticulum come to be?
Organelles are sub-cellular compartments in cells. However prokaryotes don't use organelles to organise their intracellular space.
Evolutionarily, there is evidence that mitochondria and chloroplasts are ancestors of symbiotic prokaryotes. This theory is called the endosymbiotic theory.
I've tried to find an evolutionary story that explains other organelles, specifically the endoplasmic reticulum. There is plenty of literature about biogenesis of these organelles, but nothing about the history of their evolution. I don't think I have found the right area of literature. What did organelles originate from? I'm happy just to know a few keywords or a citation to look it up myself.

This seems rather broad since there are many organelles and nobody really actually knows how they evolved.

@canadier I wasn't sure how broad this would be. For example is there one core theory or multiple theories for each organelle. I'm only really interested in the ER, so I'll edit that in. The gap in knowledge explains why it seems quite hard to pin down a good source! Thanks.

I'm not sure how broad it is either, it just seems broad. I haven't read this, but the abstract sounds promising: http://link.springer.com/chapter/10.1007%2F978-0-387-74021-8_5

To me, an important observation to make is the resorption of the nuclear envelope into the ER during mitosis, and then it's protein-chromatin-protein interactions that reassemble the nucleus.

Found the following on wikipedia. Seems pretty self explanatory:

The Golgi, ER, and lysosomes are likely to have evolved as a result of
  the plasma membrane going through invagination. An increase in the
  overall volume of a cell would require the plasma membrane to fold in
  order to maintain a constant surface area to volume ratio. These folds
  may have led to the specialization of internal membranes to maintain
  communication with the environment. In the first stages of eukaryotic
  cell life, the membranes may have been interconnected and attached to
  the plasma membrane. Later on, as their functions diverged, the
  membranes may have become separate structures

This is ideal and seems, at least to me, hypothetically plausible. The reference is a bit dated though (1994) and their only evidence is that these organelles use a different membrane transport pathway to the chloroplasts or mitochondria, rather than any sequence analysis. So it is somewhat conjecture... It's a start though! I'll trawl through pubmed to see if anything similar cited this paper.

further support for comes from the fact that the Endoplasmic Reticulum of many living groups are connected directly to the exterior. In red algae for instance the ER is contiguous with the plasmalemma (exterior membrane) .

From (brief) section, Evolution, in Wikipedia's article, Endomembrane system:
The most recent concept suggests that the endomembrane system evolved from outer membrane vesicles the endosymbiotic mitochondrion secreted. This OMV-based model for the origin of the endomembrane system is currently the one that requires the least amount of novel inventions at eukaryote origin and explains the many connections of mitochondria with other compartments of the cell.
The text above includes references to two articles published in journals in 2016.
https://en.wikipedia.org/wiki/Endomembrane_system#Evolution


text:
How does bone marrow acts like a valve?
Wikipedia says:

Furthermore, bone marrow performs a valve-like function to prevent the backflow of lymphatic fluid in the lymphatic system.

How can bone marrow act like a valve eventhough they neither have lymphvesseles nor contracting property?

Could you explain why you think bone marrow should not have a lymphatic system?

@anongoodnurse I really didn't understand how is your question related to my question. My question is how does bone marrow acts like a valve to prevent back flow of lymph even though it does not have any lymph vessels, I know muscles can act like a valve by contracting , but not about bone marrow which neither has ability to contract nor have any lymph vessels. Hope you understand my question, Thanks.

I think your question is predicated on at least one false statement. What if marrow does have a lymphatic system?

Okay then also how can it act like a valve?

Hey, you didn't even react to the preceding comment. Do some reading! Show where you're hung up.

My top priority was to know the mechanism behind it, If we even consider that bone marrow has lymphatics then also it doesn't mean that it can prevent back flow in lymphatics since they don't have any contractile property. Also many sites say that bone marrow doesn't have lymphatics, What I have learned is that bone marrow produces lymphocytes which enter into circulation by diapedesis into sinusoids. So, in this sense it makes bone marrow a lymphoid organ but I still don't understand how direcly(or indirectly ) does it prevent back flow of lymph. Thanks, hope you understand my query.

First of all, though bone marrow is not considered a part of lymphatic system because it is not connected to lymph vessels, yet it is the site of production of both B- and T-lymphocytes and is thus considered as primary lymphoid organ1. So, it is closely related to lymphatic system.
On doing some research, I can conclude that bone marrow itself actually does not perform the role of a valve. It is the lymph vessels itself which perform the valve-like function. See this2:

As lymph capillaries carry lymph away from the tissue spaces, they merge to form larger and larger vessels. These larger lymph vessels resemble veins, but their walls are thinner and they have more one-way valves to prevent lymph from flowing backward. Whereas the cardiovascular system has a pump (the heart) to move fluid (blood) through the system, the lymphatic system does not. It relies on the contraction of muscles to move lymph throughout the body. The larger lymph vessels have a layer of smooth muscle in their walls that contracts rhythmically to "pump" lymph along. The contraction of skeletal muscles, brought about by simple body movement, and the mechanics of breathing also help to move lymph on its way.

So, I'd consider that paragraph as one of the few places where Wikipedia has given incorrect fact.

I highly doubt that it could be wrong fact, anyway thanks for efforts.

As long as they mean bone marrow there, and there are no back ups, and counterexamples already present, I would consider it as incorrect.


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Plant cell question in age 12 science test
Can anyone help me answer the questions in the attachment about plant cells. It was a question in my 12 year olds science exam. I'm baffled as I think he has given a good knowledgable answer but it wasn't awarded a mark.
Kind Regards
Matthew

From a picture like this one cannot actually say whether "part-A" is a mitochondria or chloroplast. That could even be some random vesicles or, to think even crazier, assembling viruses.
The question is really bad and the kid isn't really incorrect. Mitochondria as a guess is pretty reasonable too. However, the second answer is incorrect. I don't know what the kid wants to imply by "to absorb photosynthesis"; it is unclear to me.

Hi You've confirmed what I thought but added even more to my knowledge regarding what part A represents. I'm not qualified in biology/teaching in any way but its disappointing when marks get dropped due to bad questions. Personally I think it deserved 1 mark out of 2. The kid wrote the part in green ink as they went over the questions after the teacher has marked the exam. There are some dodgy question s in this test which I'll be posting over the next few days/weeks and definitely appreciate your help. Before my kid goes back to school I'll review them all with him to reinforce his knowledge.

@MasterSQL  perhaps the kid deserved 1mark but don't get disappointed by such frivolous things. Happens all the time. Worry if this is consistent. I had read the entire cell biology book but I got a C grade because the teacher wanted me to match his way of thinking. I think this community, overall, doesn't appreciate a lot of questions like this. These are not of great use to others and doesn't fit very well with the scope and aim of the site. However, if you think the course content and the exams are not good then you can have a talk with the teacher or the principal or whoever is in charge.

Sorry to confuse here - I'm the dad but the test was done by my 12 year old :) I was hopeless at Biology at school but kids today tend to get a lot more support and do better (if their parents help them even if they don't like it - lol). I won't be going up to challenge the science teacher or anything like that - its partly for my own curiosity and to help my son out really.

@MasterSQL Not a problem. I was the one who got confused. However, I want to emphasize again that in this site we don't appreciate a lot of "is this book/exam assessment correct" sort of questions because they are not generally useful to the general public. You can, however, reword such questions such that it is about a scientific query, supported with some research from your side.


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How do you compare unpaired biological replicates?
I have done proteomics and I have obtained genes with ratios. As an small example you can see my data below
Gene    Control1     Control2   Control3    Treated1    Treated2    Treated3
pps-1   324680000   211350000   356350000   269770000   258080000   292830000
R11A8.7 477490000   610780000   539550000   533590000   530810000   578290000
ugt-21  105080000   103430000   74137000    78915000    42381000    31415000
spp-18  1042800000  615030000   332720000   538340000   448280000   412310000

Now My question is that I have Three controls and Three Treated, Control has two biological replicate and Treated has two biological replicate
I am trying to find the pathways which the list of my genes activate it. I use IPA which is a tool for pathway analysis
How can I calculate the fold change for it? If I use the 6 values, IPA will give me 6 different results and then interpretation will lead me to hell.
I appreciate any help.

Fold change is usually defined as the ratio of the mean values for the two groups. It's pretty trivial to compute in any langauge. I think you're mainly after the R code for doing this on each row of the matrix?  I don't think this question is suitable for Biology SE, but check this page: http://stackoverflow.com/questions/9490485/how-can-i-get-the-average-mean-of-selected-columns  Do that for you two groups and then simply take the ratio.

@Roland I am pretty good at few languages including R. I don't have problem with how to do it, I want to know if I do it in this way is right or not. If I had only one control and one treated, I knew how to calculate the fold change but when I have replicate, I don't know what is best to do

I posted a question here http://stats.stackexchange.com/questions/230484/how-to-calculate-fold-change-when-we-have-replicate

How does your data extraction method work? If it produces compositionally constrained data, then everything is far more complicated.

@Eli Korvigo what do you mean with compositionally constrained datacan you please explain ?

@NikBernou basically it means that if your method samples $n$ observations without replacement from a population of size $N$ (where $n << N$, i.e. there are orders of magnitude more proteins/transcripts than the number you can pick and analyse), then in abstract terms you perform sampling without replacement from an infinite population. Suppose you have $m$ classes of observations ($m$ distinct proteins/transcripts), then $\sum_{i=1}^{m}{{x}{i}} = n$, where ${x}{i}$ is the number of times class ${m}_{i}$ was observed...

... Let $\mathbf{p} = ( {p}{1}, \dots, {p}{m} )$ be the vector of relative abundances of each class in the original population. Since you sample without replacement from an infinite population, you perform multinomial sampling with probabilities $\mathbf{p}$. The counts from a multinomial distribution are negatively correlated and constrained by definition. This means that you can only operate in the space of joint-counts distributions.

Comments are not for extended discussion; this conversation has been moved to chat.

Calculating fold change is pretty straightforward but you cannot do one on one comparison because they (control and treated) are not really paired (same sample). That's why IPA gives you six results (FC for each pair). However, you can calculate fold change between two genes because they are from the same sample. Note that fold changes are quite dangerous and can lead to misinterpretation of data (for example 1/2 would be same as 100/200). You should use them cautiously.
I think, in this case, you can simply apply a t-test. This will tell you if your two groups i.e. treated and control are significantly different from each other. You would not be calculating fold changes here. If you had more number of groups then you can go for one-way ANOVA.
I am not sure what output you really want after the analysis but I think the main goal is to say that control is different from treated.
Since you have multiple genes (variables) you can either go for a multivariate t-test, which will tell you if the control is overall different from treated, or many univariate tests which will tell you how each gene differs between the two groups. There are some methods such as Bonferroni correction which can be used to improve the prediction of multivariate tests.
When you have established that a certain gene is differentially expressed, using t-test, you can report the fold change of the averages.

♦ I agree with gene set enrichment you explained. when you say  you can report the fold change of the averages. do you mean that I should take average of my replicate over control and take average of my replicate over treated? then divide them together ?

@NikBernou You can calculate FC but you'll get 6 because of the different pairs which would not tell you anything meaningful. To work around that you can calculate the average of the replicates and report the FC between them (divide). However, before doing that make sure that this is meaningful by doing the statistical test. For the others that were not different as per t-test, just leave them or report an FC of 1 (since they are there is no significant difference between them). Am I clear?

♦ I am really sorry for asking too many questions. what you try to say is I select the upregulated genes (those that are statistically significantly different from control than treated. Then I discard the rest. Then I take average between group and average between treated and then divide treated to control. Is it what you are telling me?

@NikBernou yes. Take average of control, take average of treated and divide them (only for cases that are statistically significantly different).

♦ I see, what will happen if I do this for all? I think replicate suppose to be more or less the same value but taking into account the environmental changes during measurement, no?

@NikBernou It will be just meaningless. You can do that. As I said fold changes are dangerous and can often be misinterpreted. The statistical test takes into account of the random errors (environmental changes, if that's what you mean) that you may expect.

While I do not have any experience with IPA, I routinely face this problem.
How do you analyse separate biological replicates?
One way to approach the problem is to merge the biological replicates.
There are several methods,
To do this, you can show a pearson or spearman correlation. If you have experience in R, it is a simple task of applying the function cor.
I do not use excel for such tasks, but you can check out this excel tutorial which covers correlation in Excel.
The second and harder method is to show the clustering of the replicates, using one of the many clustering methods out there. For this the easiest way I know is heatmap2 from the gplots package, which uses hclust for hierarchical clustering. This method will produce a heatmap with a dendogram specifying the relation between the replicates. Check the package link for the pdf containing details on the heatmap.2 function and how to use it.
I would go with correlation since it hardly takes 10 minutes. Having shown the correlation between replicates, you can then merge the replicates by taking the average of the replicates.
I do not know if IPA has a way for dealing with replicates

Hi dear, thanks for your comment. Actually you don't need to know IPA. what i want is to be able to calculate FoldChange. is it possible to make an example in R ? you can use random values to generate 6 columns of data ? is it possible ?

Having shown the correlation between replicates, you can then merge the replicates by taking the average of the replicates, what will happen to those that are not highly correlated ? why should I do that ? can you please give me details explanation so that I understand your mythology ?

correlation shows you how well the samples/replicates correlate among themselves, before merging replicates this step is required to show that you are not introducing variations within the merged dataset. If you introduce a bias by merging that will lead to false statistical inference. You do not want to do that, if the replicates correlate well then values corresponding to genes can averaged between replicates.

I got your point , you have one like already thanks for highlighting it !!!! would you mind to give me an example in R?


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What is the difference between vegetable and animal fats?
I often hear from many people saying to waiters - "Please, don't put oil to salad". They probably believe the fat from vegetables has the same impact on the weight as an "animal" fat (meat, eggs, butter).
My questions are -

Are these two types of fat have equal influence considering their converting to fat tissue in humans?
What are the pathways for conversion of vegetable oil fats to adipose tissue storage, in humans?
If one eats $X$ grams of either saturated or unsaturated fats, will they (in equal conditions) gain equal weight ($Y$ grams) in both the cases ?

There is a subtle difference between oils and fats- oils are generally unsaturated (Carbon-Carbon double bonds) whereas fats are saturated (all single bonds).

Are these two types of fat have equal influence considering their converting to fat tissue in humans?

No. There are some kinds of fatty acids that are synthesized only by plants (Essential fatty acids). However, these can be obtained indirectly from animal sources such as fish.
Fats have multiple roles- not just storage. They are also critical for making up the cell membrane.

What are the converting pathways for vegetable oil fats to adipose tissue in humans?

The fatty acids in oils are absorbed in the intestine and esterified (wit glycerol) to form triglycerides. Then, they are incoporated in lipoprotein complexes. There are different types of lipoproteins- VLDL (Very Low Density Lipoprotein), LDL (Low Density Lipoprotein) and HDL (High Density Lipoprotein) which have different sizes and compositions.
When lipoprotein comes in contact with lipoprotein lipase in capillaries, the free fatty acids are liberated from trigycerides, which is taken up by adipose tissue.
The fats stored in adipose tissue depends on diet. This has been studied in rabbit but similar principles may apply to humans too. Fats can also be synthesized in the body. It is always saturated fat and is synthesized by the fatty acid synthase complex. The starting substance is Acetyl-CoA which is produced during catabolism of both carbohydrates and fats.

if one eat Y of 2 meal if saturated and unsaturated fats, he/she (in equal conditions) will gain X gram if they were saturated fat and Z in a case of unsaturated fats?

By principles of mass balance, if both have equal rates of absorption and degradation then there will be equal gain. According to this study, absorption rate of unsaturated fats is higher. In that case if you eat $X$ grams of both types then the absorbed amount should be $Y_{sat}$ < $Y_{unsat}$
I am not sure about the degradation rates but I think it is higher for saturated fats because unsaturated has to be reduced to saturated before metabolizing via $\beta$-oxidation. Determining the exact steady state values will be tricky without a mathematical model.
NOTE: Dont confuse this with body weight gain (in the sense of obesity); it is a complex phenomenon. You have to consider a lot of things when predicting weight gain.

Do you know any answer to question if one eat Y of fats,  he/she (in equal conditions) will gain X gram if they were saturated fat and Z gram if they were polyunsaturated fats?

Gaining in the sense ?

Weight i mean - are these two types of fat similar considering weight gain

weight gain is a complex issue. it is not that straightforward. I added an answer to that question but it is in the sense of amount absorbed in the body.


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Do bacteria grow on pure dry glucose?
I've accidentally touched pure glucose with my bare hands (fingers to be specific), which was intended for cell-culture.
I'm worried that bacteria from my skin may start to grow on the glucose and contaminate my animal-cell cultures.
Should I be worried about this really and get another glucose packet for it or just proceed to feed cells with that one?

Bacteria or other microorganisms cannot really grow on anhydrous (totally dry) glucose because they need water.
However, they can remain there and cause contamination. Even if you haven't actually touched the glucose sample, there are many bacteria suspended in the air and they may settle down in your glucose packet. When you take the glucose out for weighing, then also bacteria that are in the air, on your gloves, on the paper that you use for weighing, can settle on the glucose sample. In fact any substance, for that matter (salts in PBS, water etc).
That's why before using solutions in cell culture, you have to sterilize them by autoclaving or filtering. Glucose solutions should not be autoclaved because the heat chars glucose. You should filter them using a 0.2 micron filter. All the materials that are to be used for cell culture purposes should be opened only inside the laminar hood.

I wasn't aware of it ! Thank you very much !!!


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What is the role of TATA box in transcriptional regulation?
I know what is the TATA box, but I wish to know whether it has specific roles in transcriptional regulation.

what have you searched? there's a lot out there - even on non-scientific sites like wikipedia...

@VanceLAlbaugh, I have searched, but I've not found the specific role of TATA box in transcriptional regulation.

TATA box serves as a binding site for the TATA-binding protein (TBP; and its associated factors, together comprising the TFIID).
TATA-box is one of the basic promoters present in many genes and therefore TBP is a general transcription factor i.e. TATA-box and TBP do not have specific roles. TATA-box is like a minimal promoter.

TATA box simply is a type of promoter sequence, which specifies to Transcription Factors where transcription begins - which is usually 30bp downstream of TATA Box. Transcription factors can bind to the TATA box and recruit the RNA polymerase enzyme to synthesize RNA.

Specific transcription factors don't bind to TATA box. TBP does, and it is a general transcription factor.

@WYSIWYG Thanks but I am sorry I didn't get you. Where is my answer stating about Specific TFs?

TATA box is bound by the TBP. You said "Transcription factors bind to TATA box", which may imply any transcription factor.

@WYSIWYG Thanks! I got you now. What do you mean when you say "TBP is a general TF"?

See http://biology.stackexchange.com/a/44732/3340. Basically, it means that is required by a lot of genes to carry out transcription and it is constitutively expressed.

@WYSIWYG Thanks man! Opened a new thing for me.

From Nature:

A TATA box is a DNA sequence that indicates where a genetic sequence
  can be read and decoded. It is a type of promoter sequence, which
  specifies to other molecules where transcription begins. [...]. The
  TATA box is named for its conserved DNA sequence, which is most
  commonly TATAAA. Many eukaryotic genes have a conserved TATA box
  located 25-35 base pairs before the transcription start site of a
  gene. The TATA box is able to define the direction of transcription
  and also indicates the DNA strand to be read. Proteins called
  transcription factors can bind to the TATA box and recruit an enzyme
  called RNA polymerase, which synthesizes RNA from DNA.


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How many rounds of TCA Cycle would a complete oxidation of a triacyl(15-Carbon fatty acid)-glycerol, give?
This was a trickier question on a previous test, and I'm still not sure why, but the answer was "at least four". I answered "more than 22" and got it marked wrong. I assume that each fatty acid chain would break down into 1 propionyl CoA and 6 Acetyl CoA, but I'm not completely sure how many rounds this would give us. Can anyone help me out here? Thanks!

I am not too sure but this is my logic:
There would be in total of 18 molecules of Acetyl-CoA which means 18 TCA cycles. Propionyl-CoA gets converted to Succinyl-CoA which is a TCA intermediate (at about half of the cycle). If you do consider this, the 3 molecules of propionyl-CoA would only give you 3 partial rounds (or lets assume 1.5 rounds) of TCA cycle. Still 19.5; less than 22. Even if you consider the metabolism of glycerol, then 1 molecule of glycerol will give you 1 molecule of pyruvate i.e. 1 TCA cycle. So, the total is still 20.5 rounds i.e. less than 22.
I don't know what the other options are but "more than 22" is certainly not correct.


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Cell cycle-regulated genes and mRNA
I am a mathematician and my knowledge about biology is close to zero. I am reading a bioinformatics paper and I would like to understand a bit more about the biology task they are talking about. I cite here the first paragraph of the paper:

The identification of cell cycle-regulated genes through
  the cyclicity of messenger RNAs in genome-wide studies is a difficult
  task due to the presence of internal and external noise in microarray
  data. Moreover, the analysis is also complicated by the loss of synchrony
  occurring in cell cycle experiments, which often results in additional
  background noise.
  [De Santis, Marianna, et al. "Combining optimization and machine learning techniques for genome-wide prediction of human cell cycle-regulated genes." Bioinformatics (2013): btt671.]

I've searched online for some explanation of this topic and I understand that cell-cycle is a set of events that cells go through for duplicating themselves. I also understand that there are some molecules that are responsible for the regulation of the cell cycle. I know that mRNA is a class of nucleic acid that is responsible for transferring the informations from the DNA inside the nucleus to the ribosomes in order begin the amino acids synthesis. Microarrays are matrices obtained by DNA sequences inside some chip.
What is the cyclicity of mRNA? How is it related to the cell cycle?
I just need a very simple explanation, without any detail, as it is not my field but I am concerned to understand the background.

It is assumed that in order for a cell to divide it must progress through a series of gradual stages. At each of these phases certain proteins have to be manufactured through mRNA and/or modified post-transcriptionally in order to serve an specific proliferative or anti-proliferative role, which overall eventually orchestrates the transit to the subsequent stage.
Conventionally the cell cycle is comprised of 3 "interphase" stages prior to execution of Mitosis itself: G1 (growth, metabolically active), S (synthesis of DNA to duplicate genetic material in preparation for its splitting into two daughter cells), and G2 (gap phase where a numerous of quality control checks are undertaken in the form of surveillance of the newly produced DNA for example to ensure viability of the progenies).
Under these premises, the protein content of a cell at an specific phase is expected to cycle or oscillate in accordance with its requirements, and this is linked to mRNA cyclicity as the most direct responsible process for modulation of protein abundance. It is then related to the cell cycle in the sense that in order to transit from the G1 phase for instance, proteins involved in DNA synthesis will need to be produced, and thus protein factors released for the transcription of those certain mRNAs to take place.
Experimentally such dissection of cell cycle-regulated genes is tricky. Extracting mRNA from pure sub-populations of cells at specific stages of cell division is challenging as the isolation of such cell sub-populations is normally through chemical enrichments and sub-optimal synchronisation procedures. The signal to noise ratio is not ideal under these circumstances.
In brief, the cell cycles through stages in order to divide and such cycling is in itself due to the cycling of certain proteins, the most renown ones are called precisely "cyclins", which are protein markers of cells division. Cyclin D, E, A, B prevail differently at different stages of the cell cycle as a result of the balanced equation of mRNA transcription and post-transcriptional protein modifications (phosphorylation events mark them for degradation for example).
Overall an intertwined and well-coordinated process.
*** EDIT
For a suitable selection of some basic bibliography on the subject, robust sources covering the subject with rigour (less specific and dense than the journal articles I comment bellow) please refer to the following links:

Molecular Biology of the Cell
Molecular Cell Biology
Cell Cycle Regulation
The Cell Cycle Principles of Control

& even a review of the latter here.
HTH

Welcome to Biology.SE - can you add some references to your answer? it would definitely make it stronger!

@VanceLAlbaugh I think most of this is given in textbooks. Ana, you can add a textbook reference or provide wikipedia links wherever you think they are necessary (cyclins for an instance). The OP can refer to these links. You can also give a reference for one of the genes that undergo such changes (p53-Mdm loop perhaps). I think overall the answer is fine.

@WYSIWYG agreed

Thank you so much Ana. Can you indeed give me some reference? Even just the book you studied from is fine

A quick search in <www.pubmed.com> with the desired key words would bring you myriads of examples. For a recent computational article see here: http://bioinformatics.oxfordjournals.org/content/early/2016/05/20/bioinformatics.btw309.abstract

The work on Cyclins and CDKs (cyclin dependent kinases) received a Nobel prize in 2001. http://www.nobelprize.org/nobel_prizes/medicine/laureates/2001/press.html

Another fairly recent article on the subject, this time from a more experimental angle: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4595013/

Now, although textbooks give a glimpse into the subject, the area is still subject of active investigation as some tuning is still required to gain better insight of cell cycle regulation. The basic solid knowledge was mostly achieved in simpler organisms such as yeast. Mammalian cells, and pluricellular organisms altogether, being more complex have proven a challenging target in the field of systems biology.


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How is the growth of benign tumors suppressed?
A benign tumor  has an outer layer of cancerous cells beyond which are regular cells (I Think).  The Tumor must have some kind of boundary layer like a wall where somehow the cancerous cells can't affect any more normal cells outside the wall. A Benign Tumor I think can be inactive for many months; it might never grow anymore. Might it be that the cancer cells at this Benign Tumor Wall are inhibited from affecting any more cells? Could there be an Apoptosis shut-off inhibitor or a cell-death pathway shutting-off inhibitor in this case?

Immune system fights cancer ...

Are inhibitors part of the immune system?

There are some cells...I think NK cells..search NK cells on wikipedia

The primary difference between a benign tumor and a malignant tumor is that the former cannot metastasize; therefore they remain within the tissue boundaries.They grow slowly and are are not very de-differentiated thereby retaining some of the tissue organization.
Another point to be considered is that benign tumors do not cause vascularization (formation of blood vessels in the tumor tissue; triggered by secretion of VEGF), which also limits its growth.

I think the first part of your answer is more a definition than a mechanism. In addition, I thought benign tumors were bound within a certain structure that prevented them from growing out of control and from metastasis (I am definitely not an expert!) Perhaps a reference would be in place in your answer?

@ChrisStronks Yes it is a definition only. I cannot find a reference for the wall preventing its overgrowth. Metastasis happens because of a cellular differentiation event (such as EMT). It is not a wall that restricts the escape of the rogue cell. I need to add references, I am looking for a proper one.

Does a benign tumor have some chemical or gene expression that blocks the secretion of VEGF?

Is a benign tumour unable to metastasize because it can not cause vascularization (and then maybe there is no oncogenesis)?. Also does the apoptosis mechanisms in a benign tumour still 'work'?

This is not entirely correct. A benign tumor is not cancer, for example, a skin tag. A malignant tumor is cancer, for example, astrocytoma. The distinction is not the ability to metastasize, though this does tend to be a characteristic of malignant (cancerous) tumors and not of benign (non cancerous) tumors. There are exceptions that can help clarify this. For example, most malignant CNS tumors do not metastasize. See Chapter 7 of Robbins and Cotran for these definitions. Malignant means cancer. Period.

@DeNovo Yes you are right about CNS tumours. I don't have a great expertise in classification of cancers. It would be great if you can add an answer.


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How to study the effect on tau protein isoforms on microtubule based transport?
From what I read, A-beta plaques inhibit microtubule based transport of mitochondria when tau protein is present in the cell. How would I be able to do a test to see if one isoform of tau is more effective at conferring this A-beta sensitivity than another isofrom?

You can do a microscopy based assay to quantify the transport rate (both retrograde and anterograde). Mitochondria can be labeled with fluorescent proteins such as mito-dsRed, and its movement along the axon can be tracked by live cell imaging. You can check this paper; they have done this experiment. (Others have also done it but I remember this paper because someone told me about it recently).
How do you plan to see the effect of different isoforms? It may not be that easy. You will have to replace the common isoform with the others. It is not very easy to control splicing. So you may have to make lines that express only one variant (exon deletion). Though this study reports that alternative splicing can be controlled by using antisense oligonucleotides, the technology is not standardized yet; you can try it nonetheless, because making knockouts is difficult (you would have to make KO mice and then culture neurons from it).

Reference The transport is anterograde. I just need to think of an assay that will test which naturally occurring isoforms of tau will confer the greatest sensitivity to A-beta inhibition of MT based anterograde transport. Are you saying I would have to generate different lines, each expressing only one isoforms, and compare their vesicles transport rates along the MTs?

does this answer your question ? The test that you intend to do is not that straightforward

Could I just take a tau KO line and introduce different tau isoforms to different neurons and then measure vesicles transport rate and compare them?

You can do that too. But I am skeptical if tau KO mice will survive. Another trick is to intoduce loxP sites near exons/the gene and delete it by induction. You may also try working with neuroblastoma cell lines (e.g. Neuro2a) or PC12 cell line instead, for the ease of growing and manipulation. They can be differentiated to neuronal phenotype by retinoic acid/NGF treatment.

Ah I hadn't even thought of introducing loxP sites. That's a good idea. Thank you for all the help.