bioinformatics - Is there a program that simulates biology on a molecular level?

There is a recent paper that introduced the first molecular-level whole-cell simulation.

Karr, J.R., Sanghvi, J.C., Macklin, D.N., Gutschow, M.V., Jacobs, J.M., Bolival, B., Assad-Garcia, N., Glass, J.I., & Covert, M.W. (2012). A whole-cell computational model predicts phenotype from genotype. Cell 150:389-401 DOI: 10.1016/j.cell.2012.05.044

The authors combined 28 different sub-modules of various biological processes from the literature. Each one operates at the level of macromolecules, although models them in different ways: some by ODEs, some by logic; some by agent-based approaches. If you want to fool around their code is available online and I wrote a basic introduction/summary of the paper.

Here are some related bio.SE questions motivated by that model:

botany - Plant anatomy, what are these stem like filaments growing under the flower

These are "floral spurs" – they usually contain nectar, and are part of the variety of complex flower shapes that orchids and other flowers, like columbines, have co-evolved with their pollinators.

Essentially, in order for the pollinator to reach the nectar down in the base of the spur, it must move into a position where pollen is deposited onto it; then when it moves to another flower, it can transfer that pollen and the plant is able to reproduce.

Of course, long tongues are good at getting nectar from long-spurred flowers, so there is both species filtering for long-tongued species, and presumably also selective pressure within a species for long-tongued individuals. This, in turn, drives selective pressure on the spurs.

Spurs are a classic example of a "key innovation": they have evolved separately in different types of flowers, and when they evolve, they often lead to rapid speciation (because a small change in spur architecture can constitute a barrier to reproduction). (See, for example, publications of Scott Hodges)

human biology - What is the biological mechanism linking temperature and probability to be infected with a virus?

It is common knowledge that when you're cold you could get a cold.

This may be a nice illustration why we need to be wary of “common knowledge”.

What is the mechanism linking temperature and viral infection?

This isn’t clear. There are a few proposed mechanisms but a likely explanation is: “there is no mechanism” – and the assumed correlation between cold temperature and catching a cold might be nothing more than an illusion – a form of confirmation bias.

In fact, we don’t even know for sure that the cold season coincides with cold temperatures.

On the other hand, a 2007 review [1] found that

… most of the available evidence from laboratory and clinical studies suggests that inhaled cold air, cooling of the body surface and cold stress induced by lowering the core body temperature cause pathophysiological responses such as vasoconstriction in the respiratory tract mucosa and suppression of immune responses, which are responsible for increased susceptibility to infections.
[emphasis mine]

So according to their results, potential mechanisms which link temperatures and viral infection are indirect:

• The lowered core body temperature would imply, in my interpretation, that the body has to expend more energy to maintain its temperature, and hence less energy to power its immune system (which is expensive).


• Lack of respiratory tract mucosa removes an important physical barrier between the environment and the body, and allows pathogens to enter the body with much less resistance.

[1] Mourtzoukou & Falagas: Exposure to Cold and respiratory tract infections, in Int J Tuberc Lung Dis. (2007), pp 938–943

zoology - Why is the frog genome so much larger than a fish's?

As we have heard in the summaries of the human ENCODE project, 80 per cent of junk DNA appears to have an essential function. Many fish have a genome with only one tenth the size of a usual vertebrate genome. Why can fish have 1/10th of junk DNA and be still fully functional? What has a frog more than a fish has? I'm especially interested if we can see the difference somewhere, complexity of physiology or anatomy, or such.

Jap. puffer fish genome: 390 Megabases, 47,800-49,000 genes (UniProt)

Medaka genome: 690 Megabases, 24,600 genes

Clawed frog: 1,500 Megabases, 23,500 genes

biochemistry - Melting point of a fatty acid?

(1) Chain Length

Will definitely affect melting point, as this website explains pretty well:

"Melting point principle: as the molecular weight increases, the melting point increases."

(2) Number of Methylene groups.

This is another way of describing unsaturated from saturated fats. The more saturated a fat is, the straighter it is. Methylene groups cause kinks, which disrupts the Van der Waals forces along the rest of the carbon chain.

As such, from the link above again:

"On the other hand, the introduction of one or more double bonds in the hydrocarbon chain in unsaturated fatty acids results in one or more "bends" in the molecule. The geometry of the double bond is almost always a cis configuration in natural fatty acids. These molecules do not "stack" very well. The intermolecular interactions are much weaker than saturated molecules. As a result, the melting points are much lower for unsaturated fatty acids."

(3) Ionized state of the fatty acid.

This will have a very minor affect. The fatty acid generally has an unpaired ester (-ate at the end) which can have a negative charge. However, from the link above again:

"However, in fatty acids, the non-polar hydrocarbon chain gives the molecule a non- polar character."

So even if the ester had a charge, the negative character is miniscule compared to the intermolecular forces exerted by the non-polar tail. Particularly since the charge can distribute amongst the two oxygen molecules which are conjugated, reducing the reactivity further.

(4) Degree of saponification.

I'm not super-familiar with the degree of saponification, but from a quick overview of the process I'd say this wouldn't affect melting point - counter to my comment. The process of making soap involves only the acidic portion of the fatty-acid triglycerides. That portion of the macromolecule is going to be pretty much the same regardless of the fatty acid, so it will have nearly the same reactivity regardless of its chain length and conjugation.

What will not saponify are usually waxes - which are pretty much fully-saturated hydrocarbon chains with very few (if any) acidic sites. Parafin Wax, for instance, does not saponify, and has the formula ${C_{31}H_{64}}$.

(5) Ability to alter entropy of water.

Like the degree of saponification option above, the ability of a fatty acid to alter the entropy of water correlates to the number of reactive sites throughout the molecule. As-such, unsaturated fats (those with methylene groups) are going to be slightly more reactive as pi-bonds are more reactive than sigma bonds.

So, given that this answer relies on a previous option, it's probably better to go with the previous option.

Ultimately, if I were answering the question I'd choose 1, 2 since the rest either depend on those two or are miniscule. However, beware that it's your question to answer and not mine.

human biology - Does making yogurt from non-pasteurized milk work against possible disease bacteria?

In short, 'No.'

Yogurt, in and of itself, is the product of milk with specific strains of bacteria that are not particularly unique. Yogurt is just as hospitable to harmful bacteria as beneficial bacteria.

The two mechanisms which spring to my mind that would prevent infection by harmful bacteria in yogurt would be the following:

*The already dominant beneficial bacteria outcompete for the harmful bacteria, effectively limiting the capacity for harmful bacterial growth.

*The already present beneficial bacteria create extracellular products which damage harmful bacteria.

The second, if it happens at all, doesn't happen on a scale that I'm aware of. The first could happen, but I highly doubt it. It seems, to me, that it would be more likely to happen in cheese when most of the easy resources have been consumed, which in yogurt they haven't.

Yogurt, and all products stemming from milk, are inherently safer not because of any bacteria that take up residence, but because the mammary glands inside the animal producing the milk are effective filters for a variety of infections. Milk is a product that is constructed in the mammary glands, and the cells are selective about the output. Keep in mind, however, that it is by no means sterile. There are dozens of virii and diseases which can be imparted by breastmilk, and nursing women must adhere to guidelines concerning exposure to medications and diet. It's also possible for DDT and other compounds to become concentrated in breastmilk, resulting in harm to the child.

http://www.breastfeedingbasics.org/cgi-bin/deliver.cgi/content/Drugs/pre_pass.html

So, yes, while milk in and of itself is safer than other options, it is not risk free. A virus could easily infect the mammal or herd producing the milk for sale to humans, and only exhibit dangerous symptoms after the milk had been sold. This is why it's illegal to sell unpasteurized milk for human consumption in most U.S. states.

zoology - What is this crow eating, and is it a common part of the corvid diet?

Here's a picture (by Rob Curtis) of a crow carrying and eating the corpse of what looks a bit like a small hawk or falcon:

Other pictures clearly show the crow is eating the dead bird. This image shows the underside of the head and beak; this one shows its legs, which are grayish.

1. What bird is being eaten?


2. Is this bird a usual part of the corvid diet? Or did the crow just opportunistically scavenge a dead bird?