Do dogs have something different about their physiology that allows them to pant without hyperventilating? I was wondering this as I considered how effective panting would be for humans as a means of cooling.

This article quotes a professor of respiratory physiology that says "dogs are built to pant just right. The mechanics of their lungs and chest set a precise rate for panting that minimizes the amount of work while maximizing cooling power." They also don't breathe fully when panting, so they can still cool themselves without increasing gas exchange. This is different than humans, who will hyperventilate to get rid of carbon dioxide (or you can intentionally hyperventilate and cause respiratory alkalosis).


Why is bacterial meningitis worse than viral meningitis? My field is not biology related, but it is commonly said that bacterial meningitis is far more dangerous to the individual than the viral kind. It seems to be true even with antibiotic treatment. What is the biological reason for this?

If this question has already been addressed or this is the wrong stack exchange, feel free to redirect this question to the more appropriate place.

One needs to be careful making broad generalizations about meningitis. The term simply refers to inflammation of the meninges (the outer layer surrounding the brain and spinal cord). Meningitis can occur due to a number of causes, most notably viral and bacterial infections, but can also also be due to fungi, parasites, toxins, cancer, etc. There is a vast range in severity of meningitis depending on the aetiology.

For example, rabies infection can progress to a fatal meningitis. Rabies is a virus. You therefore cannot say that bacterial meningitis is worse than viral meningitis.

That being said, what you have likely heard is that viral meningitis tends to be less severe than bacterial meningitis. This is true not necessarily because viruses are worse at causing meningitis than bacteria, but because the common causes of viral meningitis are often more easily cleared by the immune system.

Non-polio enteroviruses and herpesviruses are the most common causes of viral meningitis. These are the same groups of viruses that commonly cause mild cold or flu-like signs. Usually, when we have these signs, we don't go to the doctor to be treated with antivirals, because in healthy individuals our bodies are usually good at clearing the virus. The same is true when the virus is affecting the meninges. However, this does not mean that these viral infections cannot be severe in some cases.

The most common bacterial causes of meningitis in people are Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae type b. The pathogenesis of disease is broadly speaking similar to that caused by viruses, but the inflammatory response of the immune system tends to be more severe with these bacterial organisms compared to the common viral causes of meningitis. Bacterial meningitis is also typically accompanied by sepsis affecting other organ systems. While antibiotics exist that are effective at treating these bacteria, many antibiotics do not cross the blood-brain barrier, which makes treatment of bacterial meningitis challenging.

Finally, it is worth mentioning that widespread vaccination may have had an effect on our perception of meningitis severity. For example, at one time polio was a major cause of viral meningitis, but vaccination has vastly reduced rates of this disease in many parts of the world. Similarly, mumps and measles used to be more common causes of viral meningitis, however due to widespread use of the MMR vaccine these are now less common causes of viral meningitis. On the bacterial causes, there are now several common vaccines such as meningitis B/C/Hib/pneumococcal vaccines which are effective at reducing rates of infection with these bacterial organisms.


Why aren't native predators in Australia able to handle the mice problem? Australia is currently dealing with a mouse infestation problem, but Australia is awash with different types of predators that presumably eat lots of mice like animals.  Snakes in particular are well suited to kill mice, especially in close quarters. Snakes can fit in places most other predators can't due to their size. Additionally large invertebrates (like huntsman spiders) should also be able to take on some of the mouse load.
And it would be one thing if this was the first time the population ever boomed like this, but mice population booms have apparently have happened since Australia has existed. So why aren't we seeing large spikes in those predators when mice populations boom like this?

The mice aren't invading Australia, they are invading the wheat producing zones, where the tractors are leveling the land and putting on pesticides. The local frog, amphibian and snake populations downstream of the farmer's fields is strongly affected by the farmland, and so are the birds of prey, if they weather the pesticide use, they have to hide in dense trees, hollow logs, caves, and old barns, which are very lacking in Australian farmland.
If the government enforced laws for field edge habitats for local ecology, then there would be less mice.
Have a look at the map of wheat producing areas.
Rodent Outbreaks: Ecology and Impacts pages 225-238
PDF Google book
The map of mice infestations:

From pestsmart.org.au, though no longer available.

and a map of Australian climate:

wikimedia


How do plants 'tell time' for circadian rhythms based on a ~24 cycle? I've read that many plants have some sort of circadian rhythm where they perform a certain action on a cycle of about 24 hours, like the mimosa plant opening and closing its leaves. Obviously, this is done in order to synchronize with the sun, but many such plants continue to perform these actions even when left in constant darkness or light. It follows that this is the result of some sort of biochemical pathway, but whatever internal 'clock' is used is also independent of temperature.
How can these plants perform certain actions every 24 hours at different temperatures when the chemical reactions most biochemical pathways use are temperature dependent?
It would seem like the length of the cycle should vary widely according to the temperature as it affected the reactions involved, but instead it stays at a very constant length very close to 24 hours. How can this be?
(This is in my textbook, but unfortunately the book doesn't cite any studies. I would greatly appreciate it if anyone could help me find one to link to so I can improve the  question. :)

The short answer is that it is because the reaction chains dispensing time and enzymes doing those reactions have evolved to negate the impact of environmental factors.

The true answer is that the plant clocks do gradually lose sync with 24h cycle when put in stable lighting conditions and move to some more-less random characteristic frequency of their  molecular clock which is quite likely dependent on environment (still it is obviously close to 24h) -- the sad truth is that every clock needs syncing to work properly.


Recommendation of Ecology books What are some of the standard books to study :

Biological Interactions: Symbiosis, Mutualism...etc
Concept of Limiting factors
Niche concept
Resource partitioning
Concepts of community change
Theories of climax
Models of Succession

P.S. I am looking for a book for beginners for studying ecology at UG level.

A classic standard textbook that I've used a lot myself (earlier editions) is Begon, Harper & Townsend. This book is very broad and comprehensive, but I know that some students dislike it's back-and-forth discussion style (fewer definite answers). I see this as a strength though.

Another good choice, that is much shorter, is Gotelli's A Primer of Ecology. This one has a slight theoretical leaning (many standard mathematical models), but can work well in a  introductory course. I don't have the book in front of me, but, looking at your list of topics, I suspect that A Primer... might be weak in some of them (e.g. climax, succession).


Why is green fur not a thing? In most biomes on earth, and certainly in the most densely-populated, the best camouflage color or pattern for an animal would be a variant of green, so as to blend in with the leaves and grasses of the surrounding environment.  Whether predator or prey, the art of not being seen is hugely important in the natural world, and yet to the best of my knowledge there isn't a single mammal on the planet with fur that is even partially green.

Is there a reason for that?  It seems like animals have evolved some pretty crazy color patterns to break up their silhouette or blend into the background, but why haven't any mammals taken the obvious route of "look like leaves"?

Is it really THAT not-easy being green?

The technical answer is: Because the coloration of skin and hair is done by the two forms of melanin: Eumelanin, which is dark brown to black and Pheomelanin which is yellow to red. This enables colors from white (not pigmentation) to black (dense eumelanin pigmentation) and also colors in between by different ratios of the two pigments.

The evolutionary answer is that it obviously made no evolutionary advantage to have other colors. If you look closer at this, you will see that most habitats are not green or only for a part of the year. If you think about african plains, these are mostly brown, something like artic landscapes are only green for a very short timeframe in the summer, for the rest of the year these are white to brown. And even tropical rainforests are mostly dark to brown on the ground. They would clearly stick out of the environment with green colored hair.

For all these different habitats the animals living there have adapted their hair color. It is not uncommon for artic animals to change their hair color with the course of the year, dark to brown in the summer and white in the winter (artic foxes and snow hare) for example. Animals which live in deserts will have a paler color than those which live in dark colored mountain areas.

See this article for more information: "The Adaptive Significance of Coloration in Mammals"

Also interesting in this context is this article which looks at the reason for zebra stripes: "The function of zebra stripes"


What nutritious insects exist to farm that require the least attention? What nutritious insects exist to farm that require the least attention? I'm looking to automate simply, in a self regulating way.

Edit: To add detail, I imagine the insects would live densely in a large tank and be isolated from the outside. They would be able to breed and would co-exist with a plant that is also able to propagate, that could if needs be even be an air plant, that is eaten by the insects, dead insects either return to nourish the plant, or leave through a funnel, water also evaporates and falls as rain inside the tank.

The idea is to produce food without human effort. This could be in the form of a very cheap to use coin operated vending machine. The insects could be compressed and dry fried into a block to be dispensed, maybe like a bar, the machine could be solar powered.

The silkworm Bombyx mori is farmed for silk, but the pupae are also eaten across the Far East. Since these insects (larvae) have been domesticated for centuries there are well-established procedures for growing them.


ChIP-seq vs ChIP-exo I'm currently investigating ChIP-seq vs. ChIP-exo for finding binding sites.

As far as I can tell, ChIP-exo seems to be better in every way than ChIP-seq... but then again, I'm not strong in this area.

Are there any weaknesses in the ChIP-exo approach?

ChIP-exo does seem to be the "ChIP-seq killer." I've seen Dr. Pugh present it a few times, and the audience is pretty much always impressed.

One thing I'd do if I were of the "experimental bent" would be to add random degenerate barcodes in the library prep to control for potential PCR artifacts. I imagine that since the "peaks" in ChIP-exo seem to be quite a bit narrower than ChIP-seq, I reckon it'd harder to use some coverage-in-local-neighborhood to remove such biases (assuming you wanted to do so).

To give you an idea of what I'm thinking of -- it would be somehow similar to what is depicted here.


What is this insect? 6 legs and red body I'm in Brazil, southeast region, urban area. I've found these 6 legged insects with red bodies and black heads. They have long antennae (about as long as their limbs) and they walk around like ants, but slower. Their bodies are about 1.5mm in length.
I have also found a cluster of what I imagine are eggs they laid or got out from (there were 5 or so next to them last night).
Can someone identify them?

These appear to be the nymphs of the red-shouldered bug (Jadera hematoloma), which eat the seeds of the Sapindaceae family (Soapberry family) throughout South America, Central America and the southern parts of North America.
There is a close-up picture of one of these at bugguide.net, and further images here on the same website.


Can one see flickering of a light bulb at 50 Hz? Yesterday I had a BBQ with some friends. The sun had already set and the only light source left (besides some ambient light from the world around) was a low energy light bulb.

After a while I started to see lighting changes in the faces of my friends and the number plates of their cars. It felt like someone toggled the light very fast. When looking at the wall or the light directly I didn't notice any flickering.

In my country the power grid is running at 50 Hz. Is it possible that I actually saw the flickering caused by the alterations in the power grid or am I just going insane?

Short answer
Yes, the flickering of a light bulb may be noticeable, and yes, that's directly related to the mains frequency. However, since the flickering of a bulb is about two times higher than the temporal limits of our visual system, it is unlikely to be perceivable.

Background
The temporal resolution of the visual system can be quantified in a number of ways. As you are referring to a relatively simple flickering stimulus, the critical flicker fusion frequency is probably the most relevant. At a certain critical frequency, a flickering stimulus will appear as a continuous stimulus. This critical flicker fusion frequency limit is around 50 Hz, but variable between 5 - 50 Hz, dependent on the lighting conditions (Kalloniatis & Luu), see Fig. 1 below.

For example, the turn signal of a car is obviously flickering (flickering in the 1 Hz region). But an object displayed on a standard flat-screen computer seems steady. A monitor's refresh rate is typically 60 Hz, which is indeed above the critical flicker fusion frequency (Holcomb, 2009).

However, the good old CRT screens can sometimes seem to be flickering. The mains, as you indicate, is indeed 50 Hz (Europe, Australia) or 60 Hz (US), and indeed the flickering is at this frequency. Similarly, well functioning fluorescent tubes seem to flicker on occasion (when they are reaching their end they start to flicker too, but that's because of a failure of the device rather than the mains frequency peaking through). Due to a similar effect, light bulbs may seem to flicker too. However, because of the sine wave characteristic of the mains alternative current, featuring two peaks per wavelength (a negative and positive peak, the flickering of a light bulb is actually two times the mains frequency, or 100 - 120 Hz. This is quite far above the critical flicker fusion limit and hence will likely not be noticeable.

It's interesting to see that you mention that it was around sunset. Scotopic vision (night vision) is mediated mainly by the rod photoreceptors. The rod visual system mediates gray scale vision at low-lighting. While spatial resolution is poor, it's very well adapted to process fast-moving stimuli. Hence, the flicker fusion frequency under scotopic viewing conditions may indeed be higher; i.e., flickering of light bulbs may not be perceived during the day (Federov & Mkrticheva, 1938). Nice add-on there.

To add to this as alluded to in the comments, whether the flicker of mains-grid powered appliances are actually visible depends on a lot of factors other than flicker frequency. CRT screens, for instance, may have improved phosphors that have delayed response times, 'smearing' out the flickering into invisibility. In other words, it's not a simple matter of 'ON' and 'OFF'. Likewise, light bulbs heat up and hence the temperature difference might not be noticeable to us, as the temporal flickering depends on heating and cooling of the wire.

Fig. 1. Flicker fusion as a function of stimulus intensity. Note that the shape of this graph means that photopic vision is less sensitive to temporal changes; the intensity scale relates to the stimulus intensity, as alluded to in the other answer. Scotopic vision to promote the temporal resolution of vision in the sense mentioned in this answer alludes to the ambient lighting conditions conditions. source: Kalloniatis & Luu (2007)

References
- Federov & Mkrticheva, Nature; 142: 750–1
- Holcomb, Trends Cog Sci 2009; 13(5): 216-21
- Kalloniatis & Luu, WebVision, chapter "Temporal Resolution" 2007


Question on the concept of mitochondrial Eve My question is about the very definition of this common ancestor.

Why shouldn't be the mother of mitocondrial Eve the real Eva m (and so on to grand grand ...mother)? All I know on the subject comes from Wikipedia. My question comes from the idea that mitochondrial DNA is passed from mother to daughter. I do not see where to stop back in time.

Please consider that here I am not asking for details or controversies. Just the significance of mitochondrial Eve.

As the Wikipedia article says:

  In human genetics, the Mitochondrial Eve (also mt-Eve, mt-MRCA) is the matrilineal most recent common ancestor (MRCA) of all currently living humans

Note the use of the words "most recent".  The mother and grandmother of the actual Mitochondrial Eve were living before Mitochondrial Eve, and thus are less recent than she is.


Why did viruses evolve in the first place? This question might seem kind of strange, but it's something I've been chewing on for ages, and I can't really think of a good answer.

Viruses just seem to be floating around passively until they encounter a host cell. Then they enter the host cell, wreak havoc and use the host cell machinery to make more copies of themselves. Then these copies float around passively, until they find host cells.

So what's the point of all this? Infecting the host and causing so much trouble for the host, I mean. The only thing I could think of was something like the "selfish gene" hypothesis, i.e. the genetic material of the virus wants to make as many copies of itself as possible, and in order to secure the machinery for replication, it must infect a host cell. But it's not a very satisfying answer, somehow. All other living organisms at least have their own replication machinery. Then what kind of organisms are viruses? (Are they even organisms?) How and why did they evolve and stay around on the earth for so much time (till the present), if they depend on hosts for their replication?

The are different theories about virus evolution, some speculate that they were evolved before the cells, some speculate they are evolved to spread genetic information, a sort of specialized conjugative pilus others say that they are cellular parasites. Still, none has the final answer yet, but thanks to the boost of DNA sequencing, many new pieces of the puzzle come out lately so keep updating your knowledge!

Whether they are alive or not is also matter of discussion and it pretty much depends on the definition of life itself.
If you define life as the property of reproducing, transmitting genetic information and evolve, then viruses are life forms. But if you want to include in the definition that a life form must have all the biomolecular machinery encoded in the DNA (I really disagree on this point), then they are not. To me, they look quite a living thing.

About your sentence:

  So what's the point of all this? Infecting the host and causing so
  much trouble for the host...

I think you are looking only at the "negative" side. Viruses can transfer useful genetic information, plus they are involved with the evolution itself. We humans have lot's of viral DNA in our genome, so no viruses, no humans as we know them. Think about it ;)

There are plenty of resources around to get a better insight please have look at the following links to get started.

https://en.wikipedia.org/wiki/Viral_evolution

https://en.wikipedia.org/wiki/Evolution_of_influenza

http://www.sciencedirect.com/science/article/pii/S0042682215000859

https://link.springer.com/article/10.1007/s00239-013-9601-0

https://www.nature.com/search?order=relevance&q=evolution%20of%20viruses


most different human tissues with respect to gene expression profiling Is there a PCA showing the relative distance in terms of gene expression / functional genomics among the different human tissue types?

So far I have found:

(1) A paper based on gene expression with some tissues/tissue groups, not many:
https://genomebiology.biomedcentral.com/articles/10.1186/gb-2010-11-12-r124

(2) A paper based on gene expression signatures and aging:
https://www.nature.com/articles/npjamd201614/figures/1

(3) A paper on Gene and Protein Expression in Normal and Cancer Tissues:
https://www.nature.com/articles/srep24799/figures/3

You can navigate the GTEX project. PCA section.

https://www.gtexportal.org/home/histologyPage?tab=PCA

You have different samples for many tissues. Currently you can navigate it tissue by tissue but perhaps there's a way of visualizing the whole dataset (or you can ask for it).


What is the name of this series? My biology teacher used to show us videos (actually animations) on the human immune system. What I remember is that one video was on a virus (represented as a purple colored sphere with spikes) that a woman (who is a part of a music band) inhales in an elevator when a man sneezes.

The documentary shows how the virus travels to her throat and enters one cell, multiplies, and spreads. Then the video shows how white blood cells and T-cells defend the body. In the end, when she drinks coffee, she leaves the virus on a coffee mug and her friend takes on that virus when he drinks from the same mug.

Other videos of the same series include a documentary on fractures, another one on obesity, another one on a disease transmitted when one eats chicken, etc. Can someone tell me what is the name of that series?

I think (not sure) it is a national geographic series?

The Body Story.

--Have to add some characters for the system to be happy--


Identification of a moth It is from Bangladesh. Is it hawk moth? I am not sure. Please help.

It looks like a Hesperiidae (Skipper), not a hawk moth (Sphingidae). There are more than 3500 species of skippers worldwide though, and I don't know what species this is. However, I'm sure that somebody who knows butterflies in Bangladesh could identify this to the genus level.

One suggestion/guess/starting point might be Baoris pagana, but this is merely based on a quick glance at skippers found in India.

(picture from http://www.ifoundbutterflies.org/)


Are these images of carpenter ants? When I searched carpenter ant in Google, this looks kind of like some of the images. Some other images show reddish or winged ants and I have not seen any of those.

I've seen 3 or 4 of these big black ants in the last month we've been in our new house, wondering if I should be concerned.

Correct color? Yes
Proper antenna shape? Yes
Thorax shape? difficult to assess
Pinched waist? Yes
Heart-shaped head? Yes

Generally speaking, carpenter ants are black/brown in color, have bent antennas, a pinched waist, a round thorax, and a heart-shaped head.

And to address your confusion from seeing winged ants when searching on Google.. winged carpenter ants appear a few years after a nest/colony has been formed, so if you're not seeing any wings, it may be a relatively new colony.

One last thing.. carpenter ants (should) have hair on their abdomen. From your pictures I'm not seeing any hairs.

Conclusion: I'm 90ish% confident that's a carpenter ant.


Are Lambic beers the product of quorum sensing? Lambic beers are a Belgian specialty which is still made by open-air "inoculation" by airborne microbiota first, followed by additional yeasts, LAB bacteria and more joining in at the time of transferring to used wine barrels. (No yeast is "pitched" or added intentionally.)  As many as 200 organisms may play a role, and they seem to take turns, partly regulated by rising acidity and alcohol probably, but with some such as Brettanomyces seeming to simply wait their turn compared to what they will do in a single strain fermentation.

Lambic (or American Coolship Ale hereabouts) fementations can take up to 3 years.  Often a thick fluffy "pellicle" or "film" forms on the top of the barrel, like "flor" on sherry, evidently in response to and protection from oxygen. (Sure seems like a bio film.)

(There have been a few studies tracking the staggered blooms of various organisms, including one done 2 years ago at Allagash and one this year at Cantillon, but no discussion about how the sequence is orchestrated. So this is a speculative question about the evolution of these beers.)

Could interspecies quorum sensing be at work?    How could that be confirmed?

Almost certainly not. Species occupy different niches due to their differing growth rates and tolerances. Interspecies quorum sensing and the symbiotic relationship that implies do exist(see: lichen), but open-air inoculation is unlikely to produce them.

Why would the Brettanomyces simply kill time waiting for 'their turn'? It's likely they don't grow as fast as S. cervisiae or other early fermenters, and as a result they're outcompeted until alcohol content rises enough to slow or stop other species. Brettanomyces isn't 'waiting', they're eating and growing as fast as they possibly can.

Many microorganisms form spores or simply hibernate until conditions are favorable for growth. For highly acid and alcohol-tolerant species, perhaps they sporulate until the mix is acidic enough to guarantee them habitat. This is a form of quorum sensing, but the transmission medium is pH and alcohol concentration.


What is meant by "a codon codes for an amino acid"? What is meant by "a codon codes for an amino acid"? Does it mean in order to build that amino acid you must combine those three nucleotides?

Does it mean anything more than provides the instructions for manufacturing that amino acid.

It does not means "provides instructions for manufacturing an amino acid".  How could three little letters encode so much?

A codon is a three nucleotide sequence that matches the anti-codon of a t-RNA molecule capable of carrying one kind of amino acid.  The GGG codon, for instance, binds the t-RNA that binds to glyceine.  So the codon GGG in an mRNA ends up amounting to "put a glyceine here in the amino acid chain"


Very high 260/230 absorbance ratio of an RNA sample After my most recent RNA extraction, the RNA samples had very high 260/230 absorbance ratios, (ranging from 5 to 25).

I've never gotten numbers like this and I know the ratio is supposed to be ~2 in general.

What could be the reason for such a high 260/230 absorbance?

Gergana is right about the effects of the Guanidine isothiocyanate, but not the details there of.  Guanidine isothiocyanate absorbs strongly at 260 and NOT 230 (guanidine hcl is the one that absorbs strongly at 230).  As such if your RNA is highly contaminated with guanidine isothiocyanate, which is used in at least one buffer in just about every RNA prep kit, your 260/230 is going to be much larger then 2 (also the "concentration" will be artificially high.  So if you are getting a 260/230 of 25 and have a "concentration" of "1000 ng/µL" you may actually have less then 200 ng/µL of RNA and a ton of Guanidine isothiocyanate throwing everything off.)


Mechanics of Chromosomal Crossover When chromosomal crossover occurs, two matched chromosomes swap matched sections of their chromosomes. My question is: how does the cell select where to to make the break on both chromosomes? Is it based on some attempt to match sequences on the two chromosomes, or purely on distance from the centromere? The mechanics of the former could be achieved by breaking the two strands of each chromosome at different places. The mechanics of the second is a simple walk from the centromere with a random(?) selection of where to cut.

The purpose of this question: if the process is based on distance from the centromere then it would provide an explanation the presence of junk DNA. Successful crossover requires that the number of functioning genes on the two chromosomes not be radically altered in quantity. A failed crossover would result in at least one of the gametes being non-viable, reducing fertility. If crossover is based on centromere distance then the location of genes becomes a factor in the success of a crossover, erecting a fitness barrier between populations with radically different gene placement, even if gene content is identical.

If this is a question without an answer, currently, one way to address it would be to try to cross breed knockout mice that don't have junk DNA with ordinary mice that do. If the fertility of the cross breeding is significantly lower than than knockout with knockout and normal with normal, or if the cross breeds are less fecund, then that would provide evidence for position based crossovers, and a function for junk DNA in the crossover process.

How does the cell select where to to make the break on both chromosomes?

There are proteins that direct the selection of a site where a double strand break will be made on one chromatid.

  Crossovers are not randomly distributed: The histone methyltransferase PRDM9 recruits the recombination machinery to genetically determined hotspots in the genome and each incipient crossover somehow inhibits formation of crossovers nearby, a phenomenon called crossover interference. Each chromosome bivalent, including the X-Y body in males, has at least one crossover and this is required for meiosis to proceed correctly.
  Credit; Reactome

.

  Is it based on some attempt to match sequences on the two chromosomes, or purely on distance from the centromere?

The sequences are matched but not as you have assumed. Following the introduction of a double-strand break in one chromosome the regions around the break are processed (by proteins) and these processed ends invade the opposite chromatid. The formation of a Holliday junction follows, these are the "X" structures between strands in the image below, and they requires base-pairing;

Image credit; EMW2012


Bohr effect in respiration Would I be correct in saying that the Bohr effect is ONLY related to the concentration of [H+] in the tissues.

Obviously the concentration of carbon-dioxide can contribute to this concentration by producing protons (through carbonic anhydrase) but it isn't directly involved in the effect?

Would I be correct in saying that the Bohr effect is ONLY related to the concentration of [H+] in the tissues.

I would say no. Because oxygen binding affinity is inversely related to both [1]:

high $[H^+]$ concentration and
$CO_2$ increase (which is can be a consequence of the first)

$CO_2$ is involved in the Bohr effect:

  The biological significance of the negative influence of the carbon dioxide pressure on the oxygen binding of blood is obviously very big. [...] During the bloods movement through the body the oxygen-pressure will decrease to a relatively low value, whereas at the same time the carbon dioxide-pressure rises. This will greatly support the oxygen release from the blood, resulting in an improved efficiency in oxygen usage [2].

References:

Wikipedia contributors, "Bohr effect," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Bohr_effect&oldid=618215597 (accessed August 4, 2014).
Chr. Bohr, K. Hasselbalch, and August Krogh. Concerning a Biologically Important Relationship - The Influence of the Carbon Dioxide Content of Blood on its Oxygen Binding. Available from http://www.udel.edu/chem/white/C342/Bohr%281904%29.html (accessed 04.08.2014)


Can germs spread by tissues out of box? Firstly, I don't know if this is the best site to ask this question. Please guide if its not.

Now my question:

If we take out a tissue out of its box, a new tissue comes out partially so we can easily take it next time. Now that tissue can easily collect germs from sneezes and coughing of other people around us.

Can that cause problems/infections? Why doesn't tissue box have a better design?

This definitely possible. Due to the microscopic scale of bacteria and viruses, even very light forces(like those from pulling a tissue out of the box) will lead to those bacteria and/or viruses being tossed to the rest of the box.

However, a large portion of the infectious viruses in humans will struggle to survive on the dry, low nutrient substrate of the tissues and box for extended periods of time(especially given high absorbance), albeit the above comment show many that can(depending on the surface).

To answer why there is no better design, I think the simplest explanation is monetary incentive. There is little incentive to create something better both due to R&D cost and inevitable increase in product price, as well as a steep consumer education cost to let customers know, why this is better. However, if you have a good solution in mind that does not raise product cost beyond a few cents per unit, you should a decent shot(if you patent) to license it to the big players.


Why are animals afraid of the vet? I can understand why people are afraid of the doctor, because they have mental concepts of health and medicine.

But why should an animal be any more afraid of the vet than the post office or any other public space?

It doesn't seem like they would understand why they are there or what possible consequences it could have, the same way a human would being in a hospital.

Most animals are not afraid of the vet. When I was in practice, many dogs and cats waltzed in perfectly happily.

Of those that were afraid, I presume that many picked up expectations from their owner.  The owners who tell themselves "My dog is going to be afraid of the vet!" will be tense and nervous themselves, and of course their pet will detect this and react the same way. Many owners were far more distressed than their pets were, expecting some huge negative reaction to the vaccination or something (the pet often didn't even notice the injection, until the owner squealed or shrieked with anxiety).

Finally, animals that experienced something negative on a previous visit -- perhaps a bad interaction with another animal in the waiting room, or their owner being afraid of needles, or actually having some unpleasant procedure -- will of course remember this.


Introductory book on cell biology I am studying the human circulatory and respiratory systems to develop tools for automated diagnosis of disease.

During the past year, I have read basic books about respiratory physiology, electrocardiography, etc.

At the moment, I feel that my lack of understanding of basic cell biology is prohibiting any further progress. I would like to find a very introductory book on cell biology, which would teach me

what kind of cells there are in humans, what are they made of, and what are their main components
basics of cell cycles, how cells are studied, how they look under the (various kinds of) microscopes
etc

The ideal text would probably be on the undergraduate level and not be much longer than 300 pages. Any suggestions? So I just want to find something to start with.

Lot of classic books available, most famous (at least in India) are

Molecular Biology of the Cell by Alberts et al [ Free Online | Amazon ] -- Simple language, good figures and my personal favorite
Molecular Cell Biology by Lodish et al [ Free Online | Amazon ] -- Very detailed with good examples
Gene IX by B Lewin [ Amazon ] -- Nice examples and figures. Lessons are in different order than most cell biology books.

If you want to just learn quick concepts, use online resources like Scitable by Nature. Pretty nice information with references and recommended reading.


What's superposition and thread in RosettaCM? I'm a beginner in structural biology.
I had a question while reading a paper on RosettaCM.
What does RosettaCM's superposition and thread mean?
I googled it.
As a result, the following results were obtained.

The term structural superposition refers to rotations and translations performed on one molecular structure to make it match another structure or structures. Inherent in the definition of structural superposition is an assumed measure of structural similarity. The optimal superposition is the one in which this similarity measure is maximized. Alternatively, one can define superposition in terms of a difference measure, such as root-mean square deviation ( RMSD ). In this case, the optimal superpositon is one in which the RMSD is minimized. The program ASH uses the former approach with similarity defined by the NER score.
Also, implied in any superpositon is an alignment, or mapping, between points in one structure (usually atoms) and those in another. Sometimes alignment and superpositon are used interchangeably.

Is this correct?
I also think of threads as part of a protein segment, is this correct?
In other words, in Rosetta CM's 1-step Global Superpotion, after aligning, the templates are stochastically determined, and the unselected templates are superposed so that RSMD is smallest.
Furthermore, the superposed template is a thread.
Is the above correct?

Threading:
Start with a homologous protein. This protein can be thought of as two parts: (1) a backbone conformation and (2) a sequence of amino acids attached to the backbone. Threading occurs when you switch out the amino acids to those of your protein with unknown structure, but do not change the backbone conformation.
I believe the origin of the term is like beads on a string. The "string" does not change (the backbone geometry stays the same) but new "beads" (amino acids) are threaded onto certain positions.
The definition of superposition you found online is the correct definition for RosettaCM.


Autoimmunity and central tolerance Where in the body are self antigens important? In terms of central tolerance and autoimmunity, but also in terms of T cell activation?

There can be many responses. They are important for alloimmunity (so by transfusion, transplantation, etc...), for recognizing pathogens, cancer, virus, etc... By T cell activation, the regulator T cells recognize these antigens as self, and prevent the autoimmune reaction.

I guess they were thinking on MHC1 and MHC2. MHC1 shows the inside of the cells, so e.g. by viral infection or cancer non-self oligopeptides (from degraded proteins) bind to MHC1. These non-self antigens are recognized by CD8+ T cells, which destroy the affected cells. MHC2 is used by APCs to present possible pathogens to CD4+ T cells in a similar way.


Why does absorption (at 260nm) of ssDNA increase with temperature? In the graph below, I understand why A260 of double stranded DNA would increase with temperature increase, as more of the DNA becomes single stranded (and A260 of ssDNA is higher than that of dsDNA because the aromatic bases are more exposed, which absorb the light).

However, I do not understand why the absorbance of ssDNA also increases... I know that individual nucleotides also absorb more than ssDNA (as shown in "inequality" below), but I doubt that the covalent bonds holding the nucleotides are breaking at 80 degrees centigrade. Would this maybe be the effect of an increase in temperature increasing absorption? (I have read that increase in temperature increases collision of photons hence increases absorbance, but I am not quite sure). Thank you.

"inequality" showing which has higher A260:

  single nucleotides > ssDNA/ssRNA > dsDNA

It seems canadianer's intuition is correct --

Base stacking still occurs in ssDNA, so I suspect that is why you see a temperature dependence

-- based on this paper:
Conformational Changes in Single-Strand DNA as a Function of Temperature by SANS
Motivation --
UV absorption-based measurement of DNA melting temperature is reliant on the assumption that the DNA duplex dissociates into the same single-stranded DNA (ssDNA) random coil conformations at all temperatures.  However, calorimetry studies (citations 2 and 3 quoted below) have suggested that temperature-dependent conformational changes occur in ssDNA, too.

Early results from calorimetric studies on the dissociation of a 13-mer DNA duplex have shown, however, that the conformation of the single complementary ssDNA does depend on temperature (2). This was evident in the absolute difference between the heat of dissociation of a 13-mer DNA duplex of 490 kJ mol−1 determined at 74°C determined from differential scanning calorimeter (DSC) measurements and the heat of association of the duplex of −236 kJ mol−1 directly determined at 25°C from batch calorimetry measurements (2). This difference was attributed to the additional thermodynamic contributions from conformational changes in the complementary single strands implied from UV absorption changes upon heating solutions of each of the complementary strands from 25°C to 74°C.
...
More recent results also show a large disparity between the free energies of the dissociation of 10-mer duplexes extrapolated from DSC measurements at high temperature to 25°C and the free energies determined directly from isothermal titration calorimetry measurements on the binding of the single strands of the duplex at this temperature (3). This was again attributed to free energy contributions of the change in the single-strand random coil conformations as the temperature increased from 25°C to the melting temperature of the duplex (3).

Methods --
The authors used a 2 μM solution of 10-mer ssDNA (5′-ATGCTGATGC-3′) in 10 mM sodium phosphate buffer, pH 7.0, containing 0.1 M sodium chloride and 0.1 mM ethylenediaminetetraacetate.  Temperature-dependent changes to this solution were measured by three methods:

Small-angle neutron scattering (SANS) at 10°C increments from 25°C to 80°C.  Normalized scattering data were used to compute the geometry of the ssDNA using the LORES algorithm (PDF).
Optical density measurements (260 nm) between 20°C and 90°C, with a heating rate of 1 K per minute and measurements taken every 30 seconds.
Differential scanning calorimetry with continuous measurements from 5°C to 105°C at 1°C per minute.

Findings and Conclusion --
Taken together, the SANS and calorimetry data suggest that the change in shape of the ssDNA with increasing temperature is due to unstacking of bases, corresponding to an endothermic transition.

... [the ssDNA] undergoes an expansion in the diameter direction that causes a slightly shortened length as the temperature increases from 25°C to 43°C. Then, as the temperature increases further from 43°C to 53°C, it expands in the length direction as the diameter decreases. Finally, the ssDNA increases dramatically both in length and diameter as the temperature is further increased from 53°C to 80°C.
...
These conformational changes correspond to the unstacking of the A and G purines as well as the T and C pyrimidines in 5′-ATGCTGATGC-3′ as the temperature is increased. The unstacking is manifested in molecular motion of the nucleotides in and out of the cylindrical axis (an increase in diameter) and in the stretching of the helix or cylinder (increase in pitch). The increase in the optical density upon melting of the single-strand substantiates the SANS results since the optical density changes indicate exposure of the purine and pyrimidine bases to a more polar (water) environment.

And, as with liliae's figure, the results of the ultraviolet absorbance scan show density increasing with increasing temperature.

Figure 6. Normalized UVM scan of a 2-μM ssDNA solution. The solid line is the least-squares fit of a two-state, A↔B transition model to the data points. The broken horizontal lines are the extrapolated pre- and post-transitional base lines and the broken vertical line indicates the temperature at the midpoint of the transition.


Lifespan of connective tissue cells This post is regarding a follow up on my initial post on "Properties and life cycle of chondrocytes and tenocytes".

I am elaborating on my question on the lifespan of tenocytes and chondrocytes.

From what I have read, tenocytes and chondrocytes form from mature stem cells, more specifically Mesenchymal stem cells. These cells can replicate through mitosis, and are present in the body in different tissues like bone marrow. These cells are the key in the regeneration of diverse tissues.

When the cells that inhabit tendons or cartilage die, do new MS cells travel to the tendon or cartilage area and diffentiate into a new tenocyte or chondrocyte? Are tenocytes and chondrocytes continuously replaced?

Not that I'm aware of. There isn't any blood flow to either tendons or cartilage as an adult, so the pathway for migration doesn't exist.

Tendons and cartilage are tissues composed of dead cells after their formation (the cartilage growth plates cease to exist in your teen and completely ossify, tendons I'm not sure on). Damage to tendons and cartilage is permanent, and can cause arthritis (when the cartilage is completely worn away and bone-on-bone contact occurs at joints).

Unlike living tissue, because tendon cells are dead, they are much, much easier to transplant - they do not produce any signaling molecules or have any surface proteins which would trigger an immune reaction for the vast majority of people. Shoulder surgeries often utilize this to the benefit of the patient, especially acromio-clavicular injuries.

If living cells are brought to the dead tissue, some repair is initiated, as I do recall a technique where surgeons tapped into the marrow of a patient's femur to stimulate cartilage reconstruction, but I also remember reading that the new cartilage formed wasn't the same hyaline cartilage produced by chondrocytes of the growth plate, so the repairs were temporary.

Artificially produced tendons do exist, and many are braided in order to foster interaction with host tissues (when you suffer from tendonitis, the tendon itself isn't repaired - the tissue around the tendon is repaired and strengthened). I'm not aware of any successful attempts to regrow tendons.

Attempts to grow cartilage in vitro have been successful, but re-introducing it into the body to produce a surface to articulate against has presented significant difficulties. Because we cannot (currently) reproduce biological articular surfaces, joint replacement often uses composites or surgical grade metals (both of which present problems of their own, but arthritis is not one as there's no living tissue to feel pain).


Can someone who cannot talk still whistle? Can someone who has a damaged larynx, which does not allow them to talk, still create a tune when they whistle?

I know that the larynx is what allows a person to manipulate their pitch and volume, but whistling sounds are just air making a noise as they are through the lips.

Would a person with a damaged larynx be able to whistle physically, but it would just be a toneless noise?

If this is so, is there any situation where a human would not be able to talk, but could still whistle with a tune and understand the speech of others perfectly? (i.e. having not suffered brain damage or are deaf)

Sounds such as certain phonemes are made merely with the use of air flow and movement of the lips or tongue, without the need for action of the vocal chords. Think of 'f', 's', 't', k in the English language. These are called unvoiced phonemes in phoniatrics (see the phonemic chart). Also, clicking sounds and whistling can be made without use of the vocal chords.


How does the brain avoid feedback loops? The article Ants Swarm Like Brains Think really helped me to understand the way that neurons which are pretty dumb on their own (like ants) can work together to create a pretty genius system (a brain or an ant-hive). The idea is that both the neurons and the ants function majorly via positive and negative feedback, which is really neat to understand.

However as shown in that article, sometimes groups of ants get caught in something called a feedback loop. They can repeat the same action over and over because the positive feedback is just being relayed from ant to ant to ant in a circle, and the ants can do something unhealthy such as walk in a circle for days. I don't know any examples of negative feedback loops but they would presumably also be unhealthy.

As noted in the comments, this is an analogy, but not without a good reason: The brain does work via positive and negative feedback. And that does create the potential for feedback loops.

So I'm curious about what biological features in neurons help to avoid these feedback loops in our brains. How does the brain avoid feedback loops?

Normally, after an excitatory neuron fires, it becomes more resistant to firing again for a period of time (refractory period). This is due to electrical changes within the excitatory neuron.

After depolarazing and reaching an action potential(firing), the neuron enters the refractory period, in which its charge will go back to normal (resting potential). This refractory period can be divided in two phases: Absolute and relative. During the Absolute refractory period, the neuron cannot be discharged again, since the sodium channels are inactive.

It's the relative refractory phase, however, that is more relevant to your question. During this period, the neuron enters a hyperpolarization states, meaning that it's resistant to firing again, unless it receives a greater stimulus.

So, basically, after firing and for a while, a neuron requires greater stimulus to be fired again. This works as a Feedback control, since even if you overstimulate a neuron it can fire only so often.

Inhibitory and excitatory neurons (and inhibitory and excitatory neurotransmitters) also play a role in the feedback control. Inhibitory neurons reduce the likelihood of a postsynaptic neuron to fire while excitatory neurons do the opposite.

However, sometimes these mechanism fail.

For instance, in Epilepsy, the resistance of excitatory neurons to fire during the refractory period is decreased. A group of neurons begin firing in an abnormal, excessive, and synchronized manner, resulting in a wave of depolarization known as a paroxysmal depolarizing shift, causing seizures.

In Parkinson disease, decreased dopamine causes increased inhibitory output (excess negative feedback) of the motor circuit, which leads to hypokinesia.

In contrast, excess dopamine and dopaminergic neuron activity seem to be related with Schizophrenia.


What are these little bugs? I recently found at least 50 of these little bugs roaming around my window  sills indoors in my bedroom right behind the head of my bed. I can’t seem to find what they are. I’d love tips on what they are or how to get rid of them. They’re extremely small probably no larger than 1 mm. I tried vacuuming them away but I still see plenty of them.

These are very likely mites (notice their small size and 8 legs). Based on their size, appearance, and abundance, I'd guess they're bird mites (family Macronyssidae). Since they're near your window, I assume you either have a bird nest outside your window or frequent bird visitors to your window.

 Credit: user Aewills on bugguide.com

you can find existing posts about bird mites on Bio.Stackexchange below:

Help identify this mite?
Bug Identification: Tiny Bugs
Tiny white very hard cell bug! Please help to identify!


What's the fastest legal way for the nutrients in a dead body to re-enter the ecosystem? Apologies for weirdness.

Of the various legal methods of disposing of a human corpse, which one ensures the nutrients which compose the body get back into the wider ecosystem the fastest?

Unless I've overlooked something (which is likely) the answer would seem to boil down to:

Burial, in which case soil microbes have relatively free access to the body but will initially restrict their nutrients to the sub-soil ecosystem.
Cremation, in which case most of the nutrients are converted into heat and light energy by the furnace, although this energy, and the remaining nutrients, are then made available to the wider environment much more rapidly.

The Parsis and other Zoroastrians dispose of their dead in a so-called Tower of Silence, where the body is left on a raised platform to be eaten by scavengers, particularly birds such as vultures.

This is possibly (probably?) the quickest way for nutrients to re-enter the wider ecosystem, as scavengers usually work a whole lot quicker than microbes.

Tibetan tradition also contains a ritual known as the Sky Burial, which achieves the same sort of thing. The Tibetan version may be even quicker, as once the scavengers have stripped the body, the bones are ground into a paste along with flour and yak's milk/butter to be fed to a second round of scavenging birds.


What does curated gene mean? I see in databases "curated" or "not curated" for genes. What does that mean?

"Curated" is mostly synonymous with "manually curated", which means that these genes have been experimentally validated. Most non-curated genes are just predicted by a software.


How exactly does mitotic recombination help repair damaged DNA? I understand the utility in crossovers during meiosis, but how exactly is mitotic recombination useful for dealing with DNA damage? If one sister chromatid is damaged, the other can supply a functional replacement for the defect part, sure, but then the donor chromatid will lack that section. Isn't that a zero-sum game? What am I missing?

Note: the technical term is homologous recombination (as DNA repair is actually its primary function), and this answer focusses on lesions affecting both strands at approximately the same level (as a lesion affecting only one strand at a particular location can easily be repaired by using the clean strand as a template), such as symmetrical double-strand breaks (where both strands of the double helix are severed at the same level; commonly caused by [and responsible for the main lethal effects of] overexposure to ionising radiation; used as the example type of damage for the purposes of this answer).

Short answer

The homologous DNA serves as a template for synthesis of new DNA to repair the damaged area.

Long answer (paraphrased from here)

If both strands of a chromosome are severed at or near the same location, special enzymes unwind the broken ends, and other enzymes then clip off a length of one of the strands from each end (the strand that gets clipped off is always the one with the exposed 5-prime end, in case you were wondering), leaving an exposed single-stranded flap on each side of the break.

At this point, other special proteins grab onto these flaps, and take them looking for an intact homologous piece of DNA (that's why it's called homologous recombination), which can be either a sister chromatid (which is guaranteed to be either identical or very nearly so, and is, thus, the preferred solution when possible) or a homologous chromosome (which is always available, except for haploid cells [such as human gametes], but is virtually guaranteed to be not-quite-identical, and, thus, is a less-optimal solution).

With the help of the aforementioned special proteins, one of the flaps then butts into the homologous double helix, base-pairs with the strand it's complementary to (forming a structure known as a Holliday junction [well, technically, seven-eighths of a Holliday junction, as one of the junction's four arms has only a single strand, rather than two]), and kicks the other strand out of formation.  The displaced strand forms a single-stranded loop hanging off to the side (known, unsurprisingly, as a displacement loop, or D-loop), while a DNA polymerase latches onto the bare 3-prime end of the invading strand and lengthens it, using the homologous DNA as a template.1

At this point, things can go in either one of two ways:

In the simpler pathway (the synthesis-dependent strand annealing, or SDSA, pathway), the polymerase simply continues to lengthen the invading strand until enough DNA has been added to the end to bridge the gap between the two broken ends and base-pair securely to the flap on the other end; at this point, the invading strand backs out, allowing the invaded DNA to reassume its double-helical dignity, and the newly-lengthened flap grabs onto the complementary flap on the other broken end.  More DNA polymerases fill the remaining gaps, and a ligase seals the helix back up.  The SDSA pathway is the major homologous-recombination pathway for cells not planning on undergoing meiosis.
In the more complicated double-strand-break repair (DSBR) pathway, the exposed flap on the other broken end also gets in on the action, base-pairing to the exposed D-loop and likewise being lengthened by a DNA polymerase.  When enough new DNA has been synthesised to completely fill the single-stranded gaps, the exposed ends are joined together by ligases, forming a structure with no exposed ends and two complete Holliday junctions.  To turn this back into a pair of separate bog-standard double helices, two of the four strands in each Holliday junction are cut by endonucleases, causing the two DNAs to separate.  (There are rules as to which two strands are cut; either both of the two strands that cross over in a given Holliday junction, or else both of the two strands that don't cross over in said junction, but never one crossing and one non-crossing strand [as this would merely create a new double-strand break at the location of the junction].)  Depending on how the Holliday junctions are severed, the portions of the two chrom[atid/osome]s distal to the original break may or may not be exchanged between the chrom[atid/osome]s; if both junctions are severed on their crossing strands, or both on their non-crossing strands, this distal DNA will not be exchanged, while, if one junction is cut on its crossing strands and the other on its non-crossing strands, said DNA will be exchanged.  Due to its possibilities for swapping bits of genetic material, this is the preferred pathway for cells that are planning on undergoing meiosis (although it also occurs to some degree even in somatic cells).

Here's an image to illustrate the process:

(Image by Emw at Wikimedia Commons.  Blame them for the typo in "Strand invasion", not me.)

1: This is why the 5-prime strand got pruned back, and not the 3-prime strand; all DNA polymerases known to science lengthen DNA strands in exclusively the 5-prime→3-prime direction, and can only add nucleotides to exposed 3-prime ends (exposed 5-prime ends need not apply).


How does a ribosome gather tRNAs at a fast enough rate for Translation? There are many animations of the ribosome in action, and all I have seen show the correct tRNA neatly entering the ribosome and its amino acid being added to the growing protein chain. My question is this: is it really possible that mere brownian motion and diffusion are responsible for getting the right tRNA out of 20 possible types to that point? Presumably that would require tRNAs of every type arriving and most being rejected until the right one meets its codon and is used. Not only that, you would expect orders of magnitude more tRNAs to be arriving at almost the right place but being the wrong way round or hitting the wrong place on the ribosome.
Has anyone in the field ever done any calculations using dynamics equations, along with the known volume of cytoplasm and tRNAs to see if this is even feasible?

The answer is simply due to the random walk of the amino acids. Over small volumes, this process is incredibly quick and is also responsible for nucleotide delivery to polymerases as well proteins searching for their substrates, in fact, only a few enzymes/proteins are limited by the rates of random walk motion. I'm sure there are lots of papers which discuss the rates of trna movement in the cell, but this is the first one that I found: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2727733/
(You are completely right about competing tRNAs and the orientation of the tRNA entering the ribosome, all of these factors are taken into account in calculations. Ribosome animations are also a massive oversimplification, they illustrate certain points well but they are by no means accurate, they are useful for reaching purposes!)


Where does craniocaudal closure of anterior neuropore start? Closure of the cranial neuropore is bidirectional, and final closure occurs in the area of the future forebrain. Closure of the caudal neuropore is strictly craniocaudal and finishes at the level of the second sacral segment.

This is what Larsen's Embryology says. I understand that neurulation starts somewhere in the area of the first five somites and then proceeds in both directions - cranial and caudal. The caudal neuropore is closed on day 26 by neurulation in this direction.

But, the cranial neuropore is closed not only by this cranial wave of neurulation but also by another one incoming craniocaudally and the point where they both meet is of final closure. (hence bidirectional)

My doubts - pls correct if any of my interpretations are wrong. Where is this second craniocaudal wave originating? Where is the final point of meeting (I suspect linea terminalis or anterior commissure) ? Could anyone post a picture or a reference to understand this visually (both waves of neurulation)?

PS. I am not talking of primary and secondary neurulation. Which is different and concerns the caudal eminence.

Where is this second craniocaudal wave originating?

It begins in the prosencephalic region adjacent to the chiasmatic plate.

  Where is the final point of meeting (I suspect linea terminalis or anterior commissure) ?

Cranial linea terminalis represents the zone of closure of cranial neuropore.

  Could anyone post a picture or a reference to understand this visually (both waves of neurulation)?

Sources:

1: https://www.ncbi.nlm.nih.gov/pubmed/11948562

2: https://goo.gl/RLmQcj


Influence of temperature on transcription, protein binding and decay rates I am the kind of biologist who doesn't know much about molecular genetics and about the dynamic of biochemical reactions.

Question

My question concerns the influence of temperature on the dynamic of molecular genetic processes. Typically, I'd like to know how (quantitatively speaking, looking for the $Q_{10}$ for example) the following parameters get modified with temperature.

rate of transcription

UPDATE See How is the rate of transcription influenced by temperature?

protein binding to a DNA-binding-motif

UPDATE see influence of temperature on protein binding and decay rates

rate of protein decay

UPDATE see influence of temperature on protein binding and decay rates

rate of mRNA decay

UPDATE answered by @Chris below

Why do I ask this question?

In order to know what kind of default parameters values I should enter for modeling purposes in evolutionary biology. While our scope is large we decided we would consider parameters values that are observed in yeast.

This sounds straightforward when thinking about it but finding hard evidence is not really easy. As this is too long for a comment, I have to put it in as an answer. Just a few thoughts: All enzymatic reactions are of course temperature dependent and usually have a temperature optimum at the specific living temperatures. For yeast this is around 27°C, for thermophiles this is much higher. For transcription an number of other factors including accessibility of the chromatin and the availability of cofactors play an important role besides the higher activity of one enzyme. This paper might be interesting for you: "Direct measurement of transcription rates reveals multiple mechanisms for configuration of the Arabidopsis ambient temperature response".

DNA binding should be a statistical process between association and dissociation at a given binding site. At higher temperatures the turn-over at the binding site should be higher (because there is more energy available to promote dissociation). T

The thermodynamics of DNA structural motifs
Thermodynamics of specific and nonspecific DNA binding by two
DNA-binding domains conjugated to fluorescent probes.


Do mutations in one bacterial strain have the same effect in other strains within the same species? I would assume so, since they are the same species after all. I am asking this because I am doing a bioinformatics project for school and I cannot find any protein mutations for the specific bacterial strains that my department has managed to isolate. The proteins I have identified as stress proteins are within their genomes, but there is no known mutations I have found while perusing the literature. Mutations for these proteins are present in other strains though. Any help would be greatly appreciated.

Different strains of the same species have differents genotypes (ie different alleles and therefore express different proteins).So if your protein A in strain 1 has some effect, it could have the same effect in strain 2, but not necessarily.
Indeed lets imagine that protein A interact with protein B in strain 1 to produce an effect. If protein B is absent in strain 2, or different, protein A will have no effect. My point is if you have a mutation in one strain, the same mutation would not necessarily have the same effect (although it is very likely) in an another strain beacause both strain don't express the same proteome.


Questions about "parasite recursion" So imagine a parasite of a parasite. Imagine a parasite of that parasite. Then imagine a parasite of that parasite, then a parasite of that parasite, and so on and so forth.

Is there a formal term for this?

How frequent does this occur in nature? If it varies, what does it vary by? How many levels down do parasites typically go?

What is the deepest level that has ever been observed, and with what organism?

Thanks

Hyperparasitism is one possible term. According to the linked article it is commonplace in certain types of insects, but also in fungi. Apparently the cases of at least three levels are known: a fungus on a fungus on a fungus on a tree.


Why are the walls of the bronchioles folded? The bronchiole shown in the section above has folded epithelium, why is this so?

Those foldings are called as mucosal folds, formed by the contraction of smooth muscles , are also present in trachea, and in many other organs such as gallbladder etc.

Physiologically: This folding causes an increase in area for better action of mucus which protects the body from entry of dirt, pathogens and loosing the moisture.

Anaomically: as @Bryan pointed out that the folding permits the  contraction and relaxation of smooth muscles around the bronchioles.

Source 1

Source 2


Do I need to serially dilute E. coli cultures for optical density measures? I am expected to track cell growth by measuring the incubating culture's cell concentration every 30 minutes or so. So my questions are: Why do I need to do serial dilution (assuming that I do)? Why can't I just fill up a cuvette with the cuvette's volume's worth of incubating culture and measure that against the blank every 30 minutes? And if I do need to dilute, how far should I dilute (1:100, 1:1000, etc)? This is for a culture filled with E. coli.

One is not normally required to serially dilute E. coli cultures for spectrophotometric measurements, at least in the experiments where the OD value is important.

For most protein expression work, the consensus is to start the induction at OD 0.6, and for most chemically competent cells, the optimal OD ranges from 0.3 to 0.8 depending on the competency protocol. At no point in time do you need to perform dilutions, as they are all within the linear range of cell count:OD ratio.

The only time you need to dilute the culture is when you want to find the OD of a very concentrated culture (for example after 24 hours of vigorously shaken incubation).


Why are Oxyuranus snake species named Taipan? It is interesting, why are Oxyuranus species called Taipan. The snakes are Australian but taipan looks like of Chinese origin word (it means big shot - important person).

An answer is found at the Wikipedia page for Taipan:

  The common name, taipan, was coined by anthropologist Donald Thomson after the word used by the Wik-Mungkan Aboriginal people of central Cape York Peninsula, Queensland, Australia.

This passage is citing Sutton. 1995. Wik Ngathan Dictionary as support. I cannot evaluate the truth in this statement though.

For another reference see McKnight. 1981. The Wik-mungkan concept Nganwi: a study of mystical power and sickness in an Australian tribe. Bijdragen tot de Taal-, Land- en Volkenkunde 137, which refers to Taipan as the Rainbow serpent (an Aboriginal mythical creature) of the Wik-Mungkan tribe.

Even more folklore is found in McNamee. 2000. The Serpent's Tale: Snakes in Folklore and Literature in "Taipan the snake and the blue-tongued lizard".


Is it possible to identify this chrysalis? At least I believe it's a chrysalis. I found it hanging from my gate the other day.

I'm in Western Arkansas:

More photos here

Based on the image and location, I'd say you've got the chrysalis of a bagworm moth (family Psychidae) or some related species of case-building moth.

There are over 1350 species of Psychidae, and I am not certain of the exact species.

Caterpillars of this family are known to create protective cases out of local debris. Because this debris can vary, so too will the appearance of the case. Different species likewise prefer to use different materials. Sticks, leaves, tree scales, etc. have all been known to be used in their chrysalii. As a result, Googling for images should produce a wide variety of chrysalis structures. Here is one example using Eastern Redcedar scales in NC:

The University of Arkasnsas has a locally-relevant page about Thyridopteryx ephemeraeformis, one species that is often considered a "pest".


Why does higher venous volume increase atrial pressure? If the cardiac output stays the same (hypothetically, although obviously it doesn't stay the same), then why does higher venous volume increase right atrial pressure? Shouldn't the flow rate be conserved (with a constant cardiac output) so that the venous return to the right atrium is no different than before, and therefore the pressure is no different?

Imagine the circulatory system is an amusement park ride.  The ride is the left ventricle and the arterial system.  After riding, people go around and get back in line to go again.  The line and the building housing it are the venous system.  Maybe the lungs are some sort of staging area where you get ready to get on the ride.

The right atrium is the end of the venous system.  Venous pressures are right atrial pressure.

When all is well the line is moderate and people wait a short time before riding again.  But now 100 more people arrive.  If the park workers can speed up the ride or loading rate to accommodate the extra riders then great.  But if the ride cannot go any faster then the line backs up.  If you imagine that it is raining out, all the people in line bunch into the building housing it.  Venous pressure increases.  It will stay increased unless the number of riders (blood volume) decreases or the heart improves its output to accommodate the load.

Congestive heart failure is a useful example.  The ride speed (cardiac output) cannot increase because the heart is weak.   If riders increase (blood volume) it backs up into the waiting line or venous system.  This increase in volume occurs if someone with CHF eats a salty meal – water follows salt and blood volume increases, which backs up in the venous system because the heart cannot increase its output to accommodate the increased volume.  These sick folks are said to be volume overloaded.  You can see increased venous pressure as the signs of CHF – for example dilated external jugular veins.

Among many adaptations to deal with increased venous pressure is atrial natriuretic peptide.  When increased venous pressure stretches the right atrium this peptide hormone is secreted which is a cue to the kidney to dump sodium, and with it fluid volume.


BLAST(Basic Local Alignment Search Tool) is heuristic? How can we say that BLAST is based on a heuristic algorithm, as after finding one common word in the query sequence and a database sequence it performs pairwise alignment by dynamic programming - which is an exhaustive algorithm? Also, BLAST provides quantitative analysis by giving bit scores and E-values. As it gives quantitative results, why do we say it is based on a "heuristic algorithm", such as 'word algorithm'?

You might be confused about what "heuristic" means. "Heuristic" doesn't mean random or arbitrary, instead, an algorithm is termed "heuristic" if it employs a shortcut which means that it does not necessarily yield the theoretically best result.

For BLAST, this shortcut is the assumption of first matching the fixed-length words prior to extending the match. Hypothetically, there could be a query sequence and a database where the best scoring match for the query sequence doesn't contain any k-length sequences in common with the database sequence. In this case, BLAST would be unable to find that match. - So the heuristic portion of the algorithm isn't in the dynamic programming portion, it's in that first step of finding pairs which are to be aligned.

The failure of BLAST to find a match is likely to be rare, though, especially with short word lengths. If you find a decent match, it's highly likely that there is a 3-mer (5-mer, etc.) of identical sequence in the pair. But because it's not a guarantee, the use of k-mer word in the process means that BLAST is a heuristic algorithm.

The ability for BLAST to provide quality and statistical metrics is not limited by its heuristic nature. To build an e-value, you don't need to know that BLAST is able to find the absolute best match. Instead, you just need to be able to build a model of the sort of matches BLAST would find by spurious random chance, when applied to a similar database with no "true" matches. Similarly for bit-score. You don't need to know what the absolute best match would be, you just need to know how BLAST would behave on a hypothetical true-match-free database of similar properties.


What were the main discoveries in Biology? What were the greatest achievements in Biology? Can you please provide a short list of discoveries that you would consider as being the most important discoveries of the history of Biology.

Here are a few things coming to my mind

Discovery of cells by Robert Hook
Discovery of bacteria by Antonie Philips van Leeuwenhoek
Discovery of antibiotics by Alexander Flemming
The basis of heredity by Gregor Mendel
Evolution (On the origin of species by C. Darwin)
Watson and Crick discovery of DNA structure
Vaccination
The concept of ecosystem


What is this tree growing in my town? Can anyone tell me what kind of tree this is? I took this picture today. It's in Iowa City, Iowa.

It looks like a white crab apple or an obscure cultivar of apples, of which there are many.

The best identifier will be the fruit. Because there are not millions of flowers, It looks like there may be less fruit and bigger than a crab apple, although it varies by year.

The fruit of crab apples are small apples which can be used to make jelly. Crab apple trees can grow to 10m, a lot bigger than table apples.

White flowering crab apple:

https://en.wikipedia.org/wiki/Malus

comparison images.


The information carried by nerve signals Action potentials carry nerve signals in individual neurons and somehow encode information. My question is if it is possible to read that information carried by the nerve signal and feed it into a computer to understand what information it contains?

Neural info is contained in spike trains, mainly in terms of spike frequency and related parameters. These spike trains in individual neurons can be measured by techniques like patch clamp and Ca2+ imaging. These techniques are all pretty sophisticated and computer assisted for sure.

However, by recording of action potentials in e.g. the optic nerve, we cannot  possibly know what the person is seeing. Nonetheless, by cleverly mapping responses of conglomerates of neurons we can make estimates of what the information carried in the nerve fibers mean. For example:

Mapping the responses of an ensemble of place neurons in the hippocampus has been successfully used to predict where a mouse is exactly located in a maze (Guger et al., 2011);
Gross potentials measures with EEG can be used to move artificial limbs, as shown in physically handicapped people. In essence, by mapping out the responses of motor areas in the brain, it can be predicted where a person is thinking their limb is moving.

Reference
- Guger et al., Front Neurosci (2011); 5 85


What does the presence of 6 molecules of water in this equation indicates to? so I was studying biology today and I went over this weird question that says:

The presence of 6 molecules of water in this equation:
C6 H12 O6 + 6O2 --> 6CO2 + 6H20, Indicates that the:
a) Complete Glycolysis of a glucose molecule (Obviously not correct)
b) Occurrence of Krebs cycle Twice
c) Complete occurrence of oxidative phosphorylation process
d) Storage of energy in NADH and FADH2 molecules

Alright so this is the oxidation of one mole of glucose equation (Without the ATPs) but till now I don't exactly know the correct answer for this question, but to not create any confusion this question is related to the Aerobic respiration (Glycolysis, Krebs Cycle and Electron transport chain).

Here's how I approached this question:

(a) is obviously not correct because the products of glycloysis are 2 pyruvate molecules and 2 ATP molecules so I checked off this choice.

(b) However seems correct because the products of 2 Krebs cycle is 4 CO2 and there is already 2CO2 when the pyruvate acid formed the 2 acetyl CoA molecules so in total that's 6CO2, but still what about the 6 Water molecules?

(c) is a very debating choice because when there is a "Complete occurrence of oxidative phosphorylation process" so that means 2 Krebs cycles had already occurred and formed the 6CO2, and during the oxidative phosphorylation process Water molecules are formed. and ATPs too? I don't exactly know about the ATPs, but aren't they supposed to be in the equation's products in order for this choice to be correct?

(d) This choice indicates to Krebs cycle but the water molecules only are formed during oxidative phosphorylation only.

So basically all the choices seems very debating and confusing and if I were to choose then I'll go with (C) because it's the only choice that makes sense for the water molecules (and the question asks for water), but I want someone to please answer this question with a brief explanation to why he chose this answer,

Thanks :)

This reaction only means complete oxidation of glucose to 6 molecules of carbon dioxide and 6 molecules of water.

Reaction presented in question is very generalized, but the presence of six water molecules only means complete cellular respiration. Check out the actual biochemical pathways which take place to oxidize one glucose molecule.

And other options do not represent the complete cellular respiration, so there will not be formation of six water molecules, only option C means complete oxidation of glucose.

Via: https://en.wikipedia.org/wiki/Cellular_respiration

Water molecules shown by solid blue arrows.

During glycolysis, One glucose molecule releases two water molecules. This is the 9th step  of glycolytic pathway controlled by Enolase. Two water molecules are produced because two reactions are taking place.

(Image source:  https://johncarlosbaez.wordpress.com/2016/01/08/glycolysis/)

During Citric acid cycle, 2 water molecules are used in two enzymatic reactions performed by  Fumarase and Citrate Synthase. And Aconitase performs the  isomerisation of citrate to isocitrate so it has no net effect on water molecules. So, 4 water molecules are used here.

(Image Source: http://www.biosciencenotes.com/citric-acid-cycle/)

During Electron transport chain, 12 water molecules are produced due to oxidation of NADH (FADH2).

As electrons in this chain are passed, they move from higher to lower energy state, and release energy. Some of the energy is used to transport hydrogen ions across the membrane. This creates electrochemical gradient. And electrons are transferred to molecular oxygen to form water.

This makes net total of 10 water molecules. But 4 water molecules during cellular respiration are used in substrate level phosphorylation. Check out its explanation here   (Via : https://onlinelibrary.wiley.com/doi/pdf/10.1016/0307-4412%2895%2900140-9)

(Image Source: https://www.khanacademy.org/science/biology/cellular-respiration-and-fermentation/oxidative-phosphorylation/a/oxidative-phosphorylation-etc)


What determines the direction in which motor proteins go? I know that kinesin motor proteins move towards the positive (beta) end of the microtubule, while dyenin motor proteins move towards the negative (alpha) end of the microtubule. However, because the microtubule is composed of repeating alpha and beta units in ABABABABAB fashion (as shown in the picture below), what causes motor proteins to move to the positive rather than the negative pole?

For example, if one "leg" of the kinesin is bound to a beta tubulin while the other leg is up and ready to bind again, what determines which alpha tubulin it binds to (since there is alpha in front and in back of the beta tubilin it is bound to)?

While you're entirely correct that the ABABAB sequence is symmetric to a motor protein cruising along, the individual $\alpha$ and $\beta$ monomers themselves are not symmetric along the axis of movement (or any axis at all, as far as I can tell). This produces a polarity that can be seen in the figure below, from the original 1998 paper describing it.

The figure you use above to display the microtubule is slightly misleading in this way; it shows the subunits as blobby spheres. However, the motor proteins are able to distinguish the top of these molecules from the bottom, seeking a unique set of loops and helices to attach to. As it walks, then, the motor protein can only bind to one side (pole) of the subunit and is unable to walk backwards.


Which tree's root can grow the longest? In a recent TV documentary it was said that a particular tree root could grow miles long. However, I forgot the name of the tree and I don't remember the name of the TV program as well.

I searched on the internet but I could not get it. Does any one know about this tree and how tall its roots can grow?

Was it Pando? Pando is a single, massive 80,000 year old Populus tremuloides (quaking aspen) individual, that is assumed to have a single, massive root system covering 106 acres.


What did Darwin mean by "degraded flowers"? One of the chapters of The Origin of Species says that "Certain plants, belonging to the Malpighiaceæ, bear perfect and degraded flowers;" Full passage for context

Do you know which plant characteristic was he referring to? Is this morphological difference still recognized? Is there a new name for it?

Perfect flowers have both male and female parts.
"Degraded" isn't used anymore - just "imperfect".

"A bisexual (or “perfect”) flower has both stamens and carpels, and a unisexual (or “imperfect”) flower either lacks stamens (and is called carpellate) or lacks carpels (and is called staminate). Species with both staminate flowers and carpellate flowers on the same plant (e.g., corn) are monoecious..."

ref https://www.britannica.com/science/perfect-flower

Found by searching for "perfect flower"


Are gametes diploid or haploid? Some sources say that gametes are haploid, some say that they are diploid.

I'm confused.

Actually there is some confusion here, and that's quite excusable, because it's extremely common reading that monoploid and haploid are synonyms and have the same meaning. However, they are different terms. According to Hartl and Ruvolo (2012):

  The potential confusion arises because of diploid organisms, in which the monoploid chromosome set and the haploid chromosome set are the same.

As we, human beings, are diploid organisms, it's easy to see why haploid and monoploid ended up being considered as synonyms.

However, a more precise terminology would be:

Monoploid: the total number of chromosomes in a single complete set of chromosomes (this does not change whether we are talking about a somatic cell or a gamete).
Haploid: half of the total number of chromosomes in a somatic cell. The haploid chromosome set is the set of chromosomes present in a gamete, irrespective of the chromosome number of the species.

That being said, diploid and haploid are not antonyms nor mutually exclusive terms. A cell can be diploid and haploid at the same time. Let's exemplify this with organisms that perform gametic meiosis:

Human beings have diploid somatic cells, with 46 chromosomes. When a somatic human cell perform meiosis, it produces haploid cells which are monoploid. Human gametes are haploid and monoploid.

In wheat (Triticum aestivum), somatic cells are hexaploid, having 42 chromosomes (that is, 6 full sets of 7 chromosomes). When a wheat cell perform meiosis (producing micro and mega spores, and later on gametes), it produces haploid cells which are triploid. Wheat gametes are haploid and triploid.

The same whay, a tetraploid organism would produce, by meiosis, a cell which is haploid and diploid. Thus, depending on the number of chromosome sets in the somatic cell of a given species, you can say that a gamete is diploid (as stated in this other answer).

In a nutshell, a gamete that was produced by meiosis (there are life cycles where the gamete is not produced meiotically) is always haploid, regardless the number of chromosome sets it has (which will determine if it is monoploid, diploid, triploid, hexaploid etc...).

Sources:

Hartl, D. and Ruvolo, M. (2012). Genetics. 1st ed. Burlingham, Mass.: Jones and Bartlett Learning.
Genetics-notes.wikispaces.com. (2017). genetics-notes - Ploidy. [online] Available at: https://genetics-notes.wikispaces.com/Ploidy [Accessed 1 May 2017].


How many Watt-hours can an electric eel produce in a day? Electric eels are cited as being about to produce about 860 watts of energy. But I haven't been able to find information on how long they can sustain their charge.
https://www.youtube.com/watch?v=y9wktSQdyaE
In another question, it was shown that they can continually power a Christmas tree, albeit the lights flicker, just when it's hanging about and doesn't appear to be defensive. This suggests that it has some ability to sustain a low level of current... so I'd be surprised if there is no study that has measured the potential Wh. Sadly, I cannot find it.
Does anyone know any estimates for the energy an electric eel can produce over the course of a day?

This research states that an eel whose size is 90 cm can provide 6.05 mW, which is 145 mWh every day. They say you'd need 165 eels to be able to read for 24 hours using a 1W lightbulb like the one on a phone.
An electric eel should be able to flash a 0.6W L.E.D. light for 10 milliseconds at full power every second, which would be very visible in daylight, and would light up the room.


Are there chromosomes that we inherit that are not recombinated? We do have chromosomes that recombinated ,but aren't there pure chromosomes that are not recombinated that people would have?

As you say people, I will assume you are talking about humans only.

Except for the small pseudo-autosomal regions (PAR1, PAR2), the Y-chromosome and the X-chromosome do not recombine together. This means that if you are a girl, then you have inherited a X chromosome from your father who did not recombine in your father (but might have recombined in your father's mother if that's where this chromosome come from). If you are a boy, then you have inherited a Y chromosome from your father who never recombines.

There is also mitochondrial DNA (mtDNA) that does not recombine but mtDNA is not organized into chromosome.


How Much DNA do Siblings whose Parents are First Cousins Share? On average, two siblings generally share 50% of their genome. How much does this increase if the siblings' parents are first cousins?

Before I actually answer your question, let us clear up some problems in your assumptions. The fact that you expect 50% similarity in siblings is a full of several assumptions.

Imagine a case of a simple diploid organism with 2 traits. To restate your assumption, if both the parents are heterozygous in either of the two traits, and the alleles present in either parent for each trait are different (four different alleles possible for each trait), then the probability of getting two children who share 50% of the same alleles is more than any other percentage sharing.

Let us break this down. We'll gradually add complications.

For the 2-trait organisms, let us assume the genotype of the parents to be $\text{AB,EF}$ and $\text{CD, GH}$ where $\text{A,B,C,D}$ are the alleles controlling trait 1. Hence, for their first child, the possible genotypes are $\text{ACEG, BCEG, ADEG, BDEG, }$ and so on.... Since there was no allele match in the parents, each of these genotypes is equally likely.

For the second child, the same possibilities with equal probabilities exist. Now, I computed a matrix which has each possible genotype for child 1 as rows, that of child 2 as columns and the values are the proportion of alleles shared (i.e. common between the two). .

So, all proportions of the sharing is possible between the two kids. But, to find out the most probable configuration, we plot another kind of plot.

Technical note: Although the barplot has frequencies of appearing in the above similarity-matrix, it is equivalent to the probabilities since each genotype was equally likely.

Hence, the case with the two siblings sharing 50% of the genome is most likely for this case. Now, if we expand to 3 alleles, here's the corresponding plot.

It shows, that even if we increase the number of traits (as we gradually approach the human case), the maximum likelihood still includes the sibling-organisms sharing 50% of the genome.

Now, what if the parents already shared some genome? Let us say, the 2 trait organisms already shared 50% of the genome. It is equivalent to say that in the genotypes elucidated above, $\text{A=C, E=G}$. With this assumption, I ran the same kind of simulation to get the following graph.

Another technical note: Although the plot still shows frequencies of appearing in the matrix,the repeats of the same genotype along rows/columns in proportion to their probability of forming will make these frequencies equivalent to probabilities.

So now, the siblings with 75% similarities are the most likely outcome.

Let us now ask, for the 2 trait organisms we are working with, that if the grandparents had zero genomic similarities, and their two kids in-breed, what will their two kids share? For this, we take the probabilities of the first generation (children of the grandparents, sorry for the semantic mashup) for each %overlap, and multiply it with the probabilities of their kids having the various overlaps and plot a final graph.

This shows that they will most likely share 50% or 75% of their genome.

Limitations of this analysis:
 It does not account for linkage of genes. It assumes totally independent assortment of the alleles. It models all similarities to be in alleles of different traits initially and then allows for same diploid pairs, i.e. it does not allow for the observed probabilities of forming a same diploid pair, i.e. case where the similarity (genomic sharing) between two individuals is because of two same alleles for the same trait. It is also blind to any parental imprinting. Homozygosity is not yet incorporated in the simulation, will do in a while.

Below is the two-generation probability simulation for an organism with 4 and 5 traits.

The maximum likelihood of %similarities in genome, as you can appreciate, for a large number of traits would be somewhere around 63-64%.

I shall post the R code in a while, after I format it properly. For computations for greater than 5 traits, I shall write a better engine in a day. Sorry for the improper formatting of the question. Shall rectify in a while.


Mathematical modelling of omics data I'm interested in modelling host-pathogen interactions using mathematics. I know there are good resources in Pubmed but seems I'm looking for a book or introductory reviews.

My background in maths is limited, knowing the basics about calculus and algebra, and more recently some machine learning.

The paper inspiring this question is this one:

Front Microbiol. 2015; 6: 235.
A review on computational systems biology of pathogen–host interactionsA review on computational systems biology of pathogen–host interactions

I'm a bit confused because your title and your question description don't seem to align perfectly (-omics data versus host-pathogen interactions). If you are interested in host-pathogen dynamics, in my opinion, the best general introductory text in this area is Keeling and Rohani Modeling infectious diseases and humans and animals.


Generate mesh surface from protein structure What tools are most widely used for generating a mesh surface of a protein from an x-ray crystallographic structure (from the PDB)? Pros and cons would be appreciated.

I'd prefer the output to be a watertight triangle mesh of the protein surface.
Also, I'd like the tool to be scriptable (i.e. no need to open a GUI).

So far, I've been playing with MSMS and EDTSurf. But I was wondering what was standard in research, as well as if there was anything in the standard bioinformatics libraries.

PyMOL and Chimera can do that, and both can be script-driven. The PyMOL wiki is full of examples, and probably already has some how-to that would get you started. Chimera also has a complete documentation.


Blood and hair follicles from 25 people put on the Moon; enough to regenerate a human population? Discussion on the question Why were blood and hair follicles from 25 people put on the Moon? calls into question whether this is a stunt or might have any basis in science.

There's two parts to my question:

If somehow preserved well, do hair follicles and blood samples from a group of humans provide sufficient coverage alone to reconstruct a human population as far as the DNA content is concerned? Ignoring that you don't have an egg to put it in, is enough DNA present, or would there be key bits of DNA missing that you'd need a germ line sample in order to get? I suppose this can be asked as "can we clone people from blood and hair follicles alone?"
Would 25 individuals be enough to obtain a viable population of clones?

Background from the linked question:

The Wired.com article A Crashed Israeli Lunar Lander Spilled Tardigrades on the Moon says:

  Spivack had planned to send DNA samples to the moon in future versions of the lunar library, not on this mission. But a few weeks before Spivack had to deliver the lunar library to the Israelis, however, he decided to include some DNA in the payload anyway. Ha and an engineer on Spivack’s team added a thin layer of epoxy resin between each layer of nickel, a synthetic equivalent of the fossilized tree resin that preserves ancient insects. Into the resin they tucked hair follicles and blood samples from Spivack and 24 others that he says represent a diverse genetic cross-section of human ancestry, in addition to some dehydrated tardigrades and samples from major holy sites, like the Bodhi tree in India. A few thousand extra dehydrated tardigrades were sprinkled onto tape that was attached to the lunar library.

If we assume for a moment that the samples could be successfully cloned, 25 individuals is probably not enough to maintain a stable human population for more than a few hundred year without experiencing severe inbreeding depression and eventual extinction.

In population biology, there's a general rule of 50/500 for minimum viable population sizes. Essentially, a minimum population of 50 is needed to prevent inbreeding depression, and 500 to stabilize genetic drift. Of course that's a generalization used in management situations, and lots of factors go into making a calculation like this with any amount of precision.

One estimate gives a minimum viable human population (for generational space travel and permanent colonization) of ~40,000 humans in order to maintain genetic diversity. But that only applies to a population carefully screened and selected to maximize the effective population size. Another suggests 160 people could be enough for a stable population, as long as they return home to mix it up with the rest of humanity every 200 years or so.