speculative - Why Didn't Evolution Cause the Human Body to become Streamlined?

If streamlining makes movement/locomotion quicker and easier, why didn't the apes evolve into life-forms that had streamlined bodies (much like fish)?

As with everything in Evolutionary Biology, you must ask yourself: Gain vs. Cost?

In your specific case, the Gain is very little. Air isn't nearly as dense as water, so a streamlined form won't show a major benefit unless the organism is traveling very, very quickly. This is why you see it in birds; raptors can travel over 100mph while diving, and at those speeds small changes in drag can mean the difference between dinner and starving. Smaller birds often make very quick turnabouts and changes in direction mid-flight where, again, small changes in efficiency can mean the difference between life and death. The cost was is worth it.

For apes and monkeys, moving very quickly isn't a case of living or dying. That's what we evolved opposable thumbs and prehensile feet(/tails) for. You don't need to run fast when you can climb a tree and simply get away from any predators on the ground. After we came down from the trees permanently, our larger brains allowed us to use tools to fend off predators - which, again, is much simpler than evolving an aerodynamic form that won't make a difference until you're running at the speed of a car.

So, in lieu of becoming a land-shark, we have hands that can use keyboards and minds that can invent the keyboard. Unfortunately, while the gains are many, the costs do include both a very long period of time where humans are helpless without parents, and an absolutely terrible form of locomotion with our upright stance on forward-pointing knees. Though you won't catch Cheetahs digging sewers anytime soon.

genomics - Sequencing the genomes of polyploid organisms

I've done some transcriptomics work in the past with a polyploid organism, and this presented some unique challenges in the data processing and analysis. Since then, I have been brainstorming about the technical challenges one may face when sequencing and assembling the genomes of a polyploid organism. As far as I am aware, there are no polyploids whose genomes have been sequenced.

If one wanted to sequence, for example, a tetraploid organism, one approach would be to prepare and sequence all of the DNA together and then rely on post-sequencing analysis to tease apart the two co-resident genomes. However, it would be difficult, if not impossible, with this approach to distinguish inter-genome variation from intra-genome variation.

An alternative approach would be to isolate DNA from both co-resident genomes separately, and then sequence and assemble the genomes separately, so that inter-genome variation and homology need not be considered. However, I'm thinking at a very high level and have little intuition as to the technical feasibility of this approach. When there are two or more co-resident genomes, is it be possible to isolate DNA from only one of those genomes? What would this rely on (for example, would thorough cytogenetic/cytogenomic characterization help)? If this task is not possible, what types of limitations must be overcome to enable it?

Is the "Great Pacific Garbage Patch" beneficial for marine wildlife?

There are very few things in the world that aren't beneficial to some lifeform. Even if you were to, say, spill a mixture of persistent broad-spectrum poisons on an area that killed off 99.9% of all species there, the remaining 0.1% that did survive would benefit from the lack of competition.

The "great garbage patch" is hardly so extreme a phenomenon, but similar effects can be seen there: some species suffer, others benefit. In that sense, it's no different from any other changing habitat.

From a conservation viewpoint, there are two issues here that one might find worrying:

1. First, novel, extreme or rapidly changing habitats tend to have lower than average biodiversity, at least initially: the few species that thrive in the new environment tend to proliferate at the expense of others, forming a relatively simple (and often not very stable) food web. Of course, over evolutionary timescales we'd expect the surviving species to adapt and diversify and the ecosystem to settle into a more stable state, but that tends to take a long time compared to the human timescale on which such novel habitats are created.




2. Also, the effects of the "garbage patch", or ecological changes in general, are not limited to the directly changed area. Creating a new habitat in one part of the ocean is one thing; disrupting the ecosystem of the entire ocean is something else, as doing so leaves no unaffected refuge for the species that are harmed.

   
   
   

   For example, fish, birds and marine mammals passing even just occasionally through the patch might end up swallowing plastic and accumulating it in their gut; meanwhile, even for less motile organisms, the patch might act as a population sink, depleting their population density in nearby areas. And if some organisms, such as the sea skaters mentioned in the article you cite, thrive in the patch, the increased population will likely spill into other areas, potentially harming their competitors or prey species.

As for why the news are focusing on the beneficial effects of the garbage to the sea skaters, well, that's what the study that prompted this current batch of news stories was about. It's also seen as newsworthy precisely because it seems so unexpected: we've all heard stories of plastic flotsam harming wildlife, so finding out that some species are actually benefiting from it has some "man bites dog" style news value.

Also, it's a lot easier and more convincing to observe something that is there than something that isn't: we can directly see these insects laying their eggs on the bits of plastic, giving direct and incontrovertible proof of a causal connection. Meanwhile, simply observing that some species used to be more common in the area of the patch than it is now is a lot less direct and informative: we might never be sure just how the patch is harming that species, and it always leaves skeptics an opening to claim that the decline might be caused by other factors. With the sea skates, on the other hand, we're not just observing the effect, but the direct mechanism as well.

homework - What is the main general difference between Mitosis and Meiosis?

I found such a clause:

The general principle is that mitosis creates somatic cells and
meiosis creates germ cells.

However, I cannot agree. Each gametogonium needs to go through mitosis before it can enter meiosis I. So in that case mitosis is happening with germ cells so the clause is false.

I would rephrase the sentence to be

The general principle is that meiosis creates only germ cells with the possibility of a decrease in chromosome number, while mitosis can create both somatic and germ cells while the ploidy stays constant.

Ok, not perfect.

How would you say the main general difference between mitosis and meiosis?

immunology - How does herpes (HSV) infection suppress HIV?

Alright, having read the citation linked, and doing a little poking of my own, here's my approach at an answer:

Some human herpes virus infections may compete with HIV infection. Essentially, some strains (not the ones you normally think of) infect CD4 cells - the same cells targeted by HIV. These strains down regulate transcription in CD4 cells, which in turn interferes with the HIV infection process. This pertains, it appears most notably, to HHV-7.

However the actual impact on HIV disease isn't clear. Strain competition triggers some fascinating evolutionary pressures, but HIV is notoriously prone to mutation, and competition for CD4 cells might not impact HIV infection on a clinical - rather than microbiological - scale.

Additionally, the two most commonly thought of forms of herpesvirus infection, HSV-1 and HSV-2 are associated with increased acquisition of HIV infection. The clearest reasons for this are genital lesions and inflammation at the site of HIV infection. There's also some interesting dynamics in play for active coinfection, such as the impact of acyclovir treatment for HSV impacting HIV, or HAART treatment for HIV impacting HSV.

genetics - Pedigree Probability of Autosomal Recessive Trait

Starting with the left hand side of the diagram:

• III:2 is definitely a carrier (Tt) as one parent (II:2) is affected (tt).


• III:1 is also definitely a carrier (Tt) as when mating with III:2 they produce an affected (tt) offspring (IV:1)


• This means that we can work out the possibilities for IV:4 as we know the parent genotypes. It follows the standard arrangement for two carrier parents giving the options of:
  
  • TT (1/4)
  
  
  • Tt (2/4 = 1/2)
  
  
  • tt (Normally 1/4 but in this case 0 as individual not marked as affected).
  
  


• Therefore for this scenario, the probabilities for IV:4 are :
  
  • TT (1/3)
  
  
  • Tt (2/3)
  
  

Now if we look at the right hand side of the diagram.

• IV:5 is definitely a carrier (Tt) as one of their parents (III:5) is affected.

This gives two possible Punnett squares to be examined:

|-------------------------------------------------------------------------------|
|                                        ♂ (IV:5)                               |
|                          T                                   t                |
|            -------------------------------------------------------------------|
|           |                                |                                  |
|         T |              TT                |                Tt                |
|           |                                |                                  |
| (IV:4)    |-------------------------------------------------------------------|
|    ♀      |                                |                                  |
|         T |              TT                |                Tt                |
|           |                                |                                  |
|-----------|-------------------------------------------------------------------|

This gives nil affected offspring so we can disregard this option for your question (as we are ONLY looking for scenarios which produce affected individuals).

Therefore the alternative is:

|-------------------------------------------------------------------------------|
|                                        ♂ (IV:5)                               |
|                          T                                   t                |
|            -------------------------------------------------------------------|
|           |                                |                                  |
|         T |              TT                |                Tt                |
|           |                                |                                  |
| (IV:4)    |-------------------------------------------------------------------|
|    ♀      |                                |                                  |
|         t |              TT                |                tt                |
|           |                                |                                  |
|-----------|-------------------------------------------------------------------|

Giving 1/4 affected offspring.

As mentioned above, in order to have affected offspring then IV:4 must be Tt. There is a 2/3 chance of this being the case. If this is the case, then there is a 1/4 chance of the child being tt.

Both conditions need to be true for this to happen so we multiply the fractions:

2/3 * 1/4 = 1/6

molecular biology - PDB Mining: Why Do I Find Atoms Less than 1 Angstrom Apart?

I am attempting to find potential Hydrogen bonds between Hydrogen donors and aromatic ring acceptors. I do this by predicting the location of Hydrogens on residues and then calculating how far these Hydrogens are from aromatic rings. If a certain Hydrogen is <7.0 Angstroms from a certain aromatic ring, then I take it under consideration: I form the N-H vector, which is the vector created by the Hydrogen under question and the Nitrogen in the backbone of the residue that the Hydrogen belongs to. I test that this N-H vector is pointing toward the plane of the aromatic ring, and I also test that the point of intersection between the plane of the aromatic and the N-H vector is within 6 Angstroms of the center of the aromatic ring.

If all of these conditions are met, then I consider it a Hydrogen bond between the Hydrogen and the aromatic ring. However, my data must be incorrect, because I am seeing situations where a Hydrogen is < 1.0 Angstrom from the plane of the aromatic. Atoms should not be getting that close to each other.

I thoroughly tested my method by hand using an example situation where my code identified one of the sidechain Hydrogens on an ASN is 0.3 Angstroms from the plane of the aromatic of a TRP. Unfortunately, I could not find any bugs. You can find a PDF of this verification here.

Any suggestions on how my method might be flawed would be greatly appreciated.

terminology - Calculating Protein Concentration from Kilo Units (KU)

The figure of 350 - 600 Units per mg refers to the specific activity of the enzyme.

The Unit is International Unit or IU and is usually defined as that amount of enzyme that will catalyze the transformation of 1 micromole of substrate (or product) per min, under defined assay conditions (such as pH, temperature, substrate concentration, presence of Mg⁺⁺, etc). It is thus a measure of activity.

When the enzyme is pure (no other extraeneous proteins present), the specific activity provides important information about the catalytic capacity of the enzyme.

It is usually calculated by measuring

• the activity of the enzyme preparation under defined assay conditions


• the protein concentration of the same enzyme preparation (using, say, the Lowry or Biuret method for protein estimation).

  Alternatively, if the E(1%, 280) is known (see below) and the enzyme is pure, measurement of the absorbance at 280 nm gives a very good estimate of protein content (and the enzyme may be recovered 'unharmed' at the end of the measurement).

Thus, taking a figure of 450 Units/mg for the specific activity of pyruvate kinase,
25 KU (25 Kilo-Units, I presume) contains 500/9 mg (~55 mg) protein.

I notice that the Sigma product sheet provides a figure for E(0.1%, 280) = 0.54.

This means that a 1 mg/ml solution of the protein will have an absorbance at 280 nm of 0.54

E(0.1%, 280) can be used as a very convenient measure of the protein content provided that the enzyme preparation supplied by Sigma is pure.

A 'rule of thumb', useful when the E(0.1%, 280) is unknown, is that a 1mg/ml protein solution has an A₂₈₀ of 1.

Thus if, say, the A₂₈₀ (absorbance at 280 nm) of the resuspended lyophilized powder is 1.08 and you have 5 ml of this, the protein concentration is 2mg/ml and you have 10 mg of protein in total. You may wish to assay the enzyme yourself to determine an accurate specific activity.

The EC (Enzyme Commission) Number may also be of interest. For pyruvate kinase (EC 2.7.1.40) see here.

For a great ref on PK (pdf may be downloaded) see here (Ainsworth et al.)

---

For your second question, I do not have access to that paper from home.

However, if calmodulin has a specific activity of 40 000 Units/mg,

• 25 000 Units is equivalent to 0.625 mg; this is in a volume of
  0.5 ml. Therefore, the calmodulin concentration is 1.25mg/ml.



• Taking the molecular weight of calmodulin to be 16 000,
  then 16 000 mg /ml (theoretical) would be a 1 Molar solution.
  Thus a 1.25 mg/ml solution is about 78 micromolar.

immunology - Harmless virus? - Biology

It is possible for viruses to live in mutualistic relationships with their hosts, these associations are often overlooked due to the devastating effect that many viruses can have.

To give an example in humans, when HIV-1-infected patients are also infected with hepatitis G virus, progression to AIDS is slowed significantly (Heringlake et al., 1998; Tillmann et al., 2001). Also hepatitis A infection can surpress hepatitis C infection (Deterding et al., 2006).

There are many other notable examples within plants, fungi, insects, and other animals, reviewed by Shen (2009), and Roossinck (2011), in two excellent papers.

The table below, summarises some beneficial viruses across all organisms, and is taken from Roossinck (2011).

References

• Deterding, K. et al., 2006. Hepatitis A virus infection suppresses hepatitis C virus replication and may lead to clearance of HCV. Journal of Hepatology, 45(6), pp.770-778.


• Heringlake, S. et al., 1998. GB Virus C/Hepatitis G Virus Infection: A Favorable Prognostic Factor in Human Immunodeficiency Virus-Infected Patients? Journal of Infectious Diseases, 177(6), pp.1723 -1726.


• Roossinck, M.J., 2011. The good viruses: viral mutualistic symbioses. Nature Reviews Microbiology, 9(2), pp.99–108.


• Shen, H.-H., 2009. The challenge of discovering beneficial viruses. Journal of Medical Microbiology, 58(4), pp.531 -532.


• Tillmann, H.L. et al., 2001. Infection with GB Virus C and Reduced Mortality among HIV-Infected Patients. New England Journal of Medicine, 345(10), pp.715-724.