text:
Are similar smells usually based on similar chemicals?
Building off of this question: Why does freshly cut grass smell like a watermelon?, is it usually the case that things that we perceive as having similar smells are, in fact, the same or a similar chemical hitting our noses (as in the case of cis-3-hexanal in watermelon/cut grass), or is it often a cognitive thing (we're bad at parsing smells, so when confronted with a new smell, we fish around in our experience to find something that seems familiar, even if there's not much chemical similarity)?

With regards to the similar chemicals having similar smells, it does seem that there are trends with smell association and functional group.  This wiki article has a good list of compounds and their smells, and some classes definitely give similar types of smells, amines are rotting/fecal smells (hence the names putrescine and cadaverine), while esters are often fruity.  As you can see its not perfect, but there are definitely patterns.
There are some weird dose-dependent effects like in the case of indole which is labeled as flowery/fecal, which are two pretty distinct smells.  Apparently its fecal at high doses, and smells like jasmine at low doses.  My guess is that this has to do with different binding affinities of the different olfactory receptors (ORs) that are expressed in the olfactory receptor neurons (ORNs).  Many odorants will bind to multiple ORs, which means they will stimulate a characteristic sub-population of ORNs.  The binding to the different ORs will of course have different affinities.  This probably means that at low concentrations of indoles, you stimulate a certain population of ORNs that your brain recognizes as nice flowers, but as you increase the concentration you get the activation of ORNs with ORs that have a weaker binding to indole, changing the population of activated ORNs to one that your brain recognizes as feces.  Its definitely a strange pairing though..
I'm not familiar enough with the literature to know if the similar smelling things have similar ORN activation patterns, but my guess would be that they do.  If you have a population of different ORs that your odorant is binding to, a slightly different odorant will probably bind to a similar subset of ORs, just off by a few if its missing or has gained a functional group that is in the binding pocket of some of the ORs.  This probably means that if you are presented with a chemical that you have never smelled before, it will probably activate a similar ORN population as other similar chemicals, and your brain will probably say it smells like one of those similar chemicals.


text:
Why are women more susceptible to radiation?
The answer to this question on the Space.SE indicates women are more susceptible to radiation in space than men.

Why is this the case? Is it merely that women have less muscle mass (which being more dense than fat) and therefore may receive a greater dose when exposed?

It's actually because of the greater risk "from breast, ovarian, and uterine cancers" (article).  There's a more scientific write-up here, and while I don't have access the abstract implies that a more rigorous update of the exposure criteria upheld sex differences.  From a more terrestrial perspective, The Nuclear Information and Resource Service (nirs.org) has this rather incensed piece on the issue.  They cite a 2006 NAS report which

finds that harm to women (cancer) is 50% higher than the comparable harm to men from radiation doses that fall within the legal limit to the public over a lifetime.

Basically, it looks like females are more likely to get cancer from radiation, and once they do, those cancers are more likely to cause more harm.  According to the executive summary of NASA's 2014 in-depth report:

[A] 45-year-old man has a 344-day limit versus a 187-day limit for a 45-year-old woman, due to radiation exposures on the space station that would be typical at the time of solar maximum.

The effect of body size, however, could be the opposite.  Taller women get more cancer, with that study showing a 16% increase in incidence for every 10cm (4in) height increase.  That increase, however, is among certain types, such as melanomas, and not the above-mentioned "breast, ovarian, and uterine cancers."  Males, being taller, could therefore get more cancer overall; it turns out males usually die more from most cancers, just not (obviously) "breast, ovarian, and uterine cancers."

source: Stack Exchange

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sort: votes


text:
What is the difference between these worms: Caenorhabditis elegans and Eisenia fetida?
I love worm composting (I use red wiggler worms), but wondering how similar or different the Caenorhabditis elegans and Eisenia fetida are?

It's possible that the gardening stack exchange might provide better answers if you're interested in their differences in regards to composting.

@Mys-721tx's answer (excellent, by the way!) is the type of response you'll get here.

Caenorhabditis elegans is a nematode. Eisenia fetida is an annelid. They both are lophotrochozoans (more specifically, trochozoans).
Time of Divergence
According to Michael Lynch, there are about 41 amino-acid substitutions per site between Annelida and Nematoda. According to Lynch's data, I estimated that this difference is roughly equal 100 million years.
Therefore, assuming the rate of molecular evolution was constant, their common ancestors lived about 100 million years ago.
Difference on Anatomy
Nematodes have pseudocoelom while annelids have eucoelom. Therefore nematodes do not have a vascular blood system. However, annelids do have one. Nematodes also lack a layer of circular muscle, which annelids have. This layer of muscle allows annelids to move by shorten and elongate their bodies.
C. elegans in particular does not have a female gender. There are only male worms and hermaphrodite worms. Only the male can fertilize other worms.
E. fetida is hermaphroditic and two of them can fertilize each other.

The time of divergence within the nematodes is already estimated to be >500 million years http://www.timetree.org/pdf/Blaxter2009Chap28.pdf -- so the divergence of annelids and annelids must be even earlier

What does "there are about 41 amino-acid substitutions per site" mean?

@MichaelKuhn It's probably true. Also notice that the Lynch paper was published in 1997, the sequence data he used might simply be not good enough.

@JackAidley Lynch compared 10 proteins encoded by mitochondrial genes between organisms in 12 phyla. The "substations per site" are the differences in protein sequences coded by homologous genes in two compared organisms.

@Mys_721tx: I don't see how you can have 41 amino-acid substitutions at a single site between two homologous genes. Surely you can have at most one substitution per site on each gene?

@JackAidley I think by site Lynch meant the entire gene.

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text:
Why do Type II Restriction Endonucleases cleave at palindromic sequences?
Type II Restriction enzymes usually cut only at palindromic sequences. Is there any specific reason for that? Is there any advantage for bacteria if they cleave phage DNA at this type of sequence?

First, not all restriction enzymes cut at palindromic sequences.
A lot of them do though, simply because it is more effective. Recognising a palindromic sequence enables them to cut both strands of DNA at the "same" site, because the strand will have the same sequence only in different directions at that site.
See Wikipedia for example.

Of course..you are right but what advantage did a bacteria have by evolving such enzymes (which cut at palindromic sites)?

That it's going to cut both strands. So it is more efficient.

Yes you are right.Many of the bacteriophages are double stranded. Thanks :)

Short Answer

The palindromic symmetry of the restriction site allows a dimeric
  enzyme to bind the DNA in a manner that bends the double helix in a
  way that facilitates the endonuclease reaction.

More Detailed Answer
The ‘palindromic’ nature of the recognition/cleavage site of restriction endonucleases, such as EcoRV (illustrated here) results in a form of symmetry (A) that allows a dimeric enzyme — that forms a tunnel — to bind symmetrically at that site in the DNA (B).

This binding causes the DNA to bend (C) bringing a catalytic magnesium ion into a position in which it can interact with phosphate of the phosphodiester bond that is being cleaved (D). (The dimeric nature of enzyme allows force to be exerted at two points, to produce the bend. Compare bending a thin pipe over one’s knee, applying equal force with both hands.)

Methylation of the adenine nucleotide in the recognition sequence prevents hydrogen bonding of the enzyme to the DNA. DNA lacking the recognition site is not cleaved by the restriction enzyme because it does not bind specifically to the protein so that the magnesium ion remains too far away.
Reference
This answer is based on chapter sections 9.3.2 and 9.3.3 of Berg et al., which is available online at NCBI Bookshelf and is well worth reading in full. There is also a PDB Molecule of the Month item on this, although unfortunately the bending of the DNA is not apparent in the images there.
Comment on Last Two Sentences of Question
There is no particular “advantage for bacteria”  other than “it works”.  So I think the last sentence is looking at things from the wrong perspective.

This late answer was provoked by a recent duplicate question. I felt that none of the answers to the original or duplicate covered the reason why the recognition by an enzyme dimer was important to the cleavage.

These REs, that recognize palindromes, are mostly homodimers and hence the same sequences (for each monomer)for recognition, only they are reversed. This explains the palindromes.

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text:
Factor causing Methicilin-resistance in MRSA?
I think the main reason is the natural selection that is causing methicillin-resistance.
However, I am not completely sure what this means practically.
Here, the original question:
MRSA was isolated in the throat secretion of patient hospitalized with bronchitis. Which of the following
statements best characterizes this microorganism?

a. its MIC is increased to methicillin, but not to penicillin
b. methicillin-resistance is associated with production of β-lactamases
c. Methicillin-resistance is caused by changes in configuration (mutation) of PBP

What is the right answer?

Thanks for editing and adding the full question.  I will update my answer.  Just to clarify what you meant, in your answer you say that you think the answer is B but then describe C?  I would edit it, but I want to make sure which you meant.  This doesn't change my thinking on the matter.

I think you can normally think about similar pressures leading to extended-spectrum beta-lactamase (ESBLs) and  methicillin/oxacillin-resistant Staphylococcus aureus (MRSA).
Going to the core of your question:
"Currently, the reported mechanism of methicillin resistance in S. aureus is the production of a distinctive penicillin binding protein 2a (PBP2a), which exhibits low affinity toward β-lactams"
But to really read on it you need to back to Liu et al.
Again Todar's is a great source for a good broad reading on staph including MRSA.
Response to Edit [inclusion of full question]:
TSDR: The answer is C.
Let's break down the three options given in the question and learn about MRSA along the way.

a. its MIC is increased to methicillin, but not to penicillin

First, for people who may not know, MIC is short for minimum inhibitory concentration.  Simply, the MIC is a basic measurement of how much of any given agent is need to stop the growth of a bacterial colony.  Often we think of current medical antibiotics when thinking of MIC, but even simpler things like table salt and sugar have a MIC for a given species.  Thus this sentence is making the assertion that the bacteria found in the patent have an increased resistance to methicillin but not to penicillin.  This leads us to ask the obvious question:
Can Staphylococcus aureus (staph going forward) be methicillin resistant but not penicillin resistant?
This is a bit of a trick question, but let's break it down to the needed components: What is Methicillin, what is/are penicillin(s), and how are staph resistant to them.
First that it should be noted that penicillins can actually refer to a whole class of antibiotics which all use β-Lactam and the specific set of antibiotics:

benzylpenicillin (penicillin G), procaine benzylpenicillin (procaine
  penicillin), benzathine benzylpenicillin (benzathine penicillin), and
  phenoxymethylpenicillin (penicillin V). (from wiki)

It should be noted that more correct way to address the whole class of antibiotics would be β-Lactam antibiotics, not penicillins, and that if you wanted to talk about more specifically penicillin derived compounds you would be discussing penams.  For even further clarification, penicillin as drug most likely refers to benzylpenicillin, and for the rest of this answer I will use penicillin to refer to benzylpenicillin.
Thus we should think of penicillin as an early antibodic that work by preventing the dividing/genesis of cell walls and certain organelles via binding to penicillin binding proteins (PBPs).
Methicillin is also a β-Lactam antibiotic, and it's MOA is similar to penicillin.  It was developed/discovered after penicillin and was seen a answer to Gram-positive bacteria that were breaking down penicillin via β-lactamase.  Methicillian still works by binding to PBPs, but it escapes the bacteria's counter to penicillin.
This leads us to address how penicillin resistance and methicillin resistance commonly occur in staph.  First, many staph strains and other bacteria use β-lactamases to breakdown antibiotics so they no longer can bind to PBP's (1).  But methicillin is particularly suited by its side chains to not be degraded by β-lactamases.  In their ground breaking work on the subject, Hartman and Tomasz identified that methicillin resistance was not in the acquisition of a β-lactamase, but in a mutation in PBP's that prevented methicillin binding (2).  There they tested 4 strains of staph, two were methicillin resistant (MR), and two were methicillian susceptible (MS).  You will note that all but 1 didn't have β-lactamase activity, and where more susceptible to penicillin than methicillin (ibid).
BUT this does not mean that MR strains are not also penicillin resistant, instead it shows that the resistance can be independent of each other.  Therefore "A" is wrong because it tries to draw a correlation that is not there.  In reality many MR strains are also β-lactamase positive.
This also address the problem with "B."  While it is possible that a β-lactamase could bind to methicilin and lead to degradation of the antibiotic, the main mechanism of methicillin resistance is the mutation of PBPs (ibid, 3), in particular BPB2a (4, 5).
We are then left with the task of figuring out why "C" is the correct choice.  Indeed "C" is the given reason for the failure of "A" and "B," but we can still go deeper into how and perhaps why BPB2a mutated.
For that I think it is best that we turn back to Chambers' review of the subject.  Forgive my over quoting, but it's done so well there and the text is now open.

Methicillin resistance is associated with production of a novel PBP
  that is not present in susceptible staphylococci. Resistant strains of
  S. aureus produce an additional 78- kilodalton PBP (Fig. 1), termed
  PBP2a or PBP2' (assumed to be identical for the purposes of this
  review), that has a low binding affinity for beta-lactam antibiotics.

...

PBP2a is highly conserved. Limited proteolysis of PBP2a from unrelated
  strains of S. aureus (123) and coagulasenegative staphylococci (31),
  whether homogeneous or heterogeneous, generates remarkably similar
  peptide fragments.

...

Presumably PBP2a can substitute for essential PBPs when these have
  been saturated by drug and can perform the functions necessary for
  cell wall assembly (22, 122).

...

In some strains, PBP2a is inducible by beta-lactam antibiotics and its
  production differs according to growth conditions (34, 122, 125, 159).

Unfortunately, they didn't quite have the staphylococcal cassette chromosome mec (SCCmec) figured out at that point.  The genetics is quite complex.
How does MRSA genetically accomplish resistance?
As we already established, the resistance comes from the production of an alternate PBP, PBP2a.  SCCmec is interesting for several reasons.  First of all, it's much larger than a plasmid, and contains information for several genes.  That's why it's called cassette chromosome.  Further it normally incorporates into the same part of the genome in staph, in an area know as OrfX (6).  This means that even during horizontal transfer, that the cassette has to direct it's integration into the genome, which is exceedingly uncommon, or at least there are not many other know examples (7, 8).  This cassette can be spread horizontally between staph, and even with other species (ibid, 9).  Even if the integration site (integration site sequence, ISS) is slightly different, this specificity is carried out by cassette chromosome recombinases (ccr), wich are also on SCCmec (8).  This is carried out by ccr-medated recombination of the target chromosome, and further details on the process are considered outside the scope of this question.
The actual gene that encodes PBP2a is called mecA.  But as we mentioned above, PBO2a production can be induced and regulated.  It is likely less favorable to produce it in the absence of antibodies, and after serial passage of bacteria in antibiotic free broth, you find that PBP2a expression can drop drastically.  Therefore regulatory and other useful proteins encoded by SCCmec.  When placed in a β-Lactamase environment, MecR1 causes a single transduction cascade to start transcription of mecA (10).  Conversely, MecI provides a negative feedback loop to MecR1, and in the absence of β-Lactamase, will lead to the down regulation of mecA (ibid, 11).  The actual action of MecR1 is to cleave MecI, thereby remove the suppression of mecA by MecI.  I actually learned something new when reading the wiki on MRSA, but didn't do further research on the subject:

mecA is further controlled by two co-repressors, BlaI and BlaR1. blaI
  and blaR1 are homologous to mecI and mecR1, respectively, and normally
  function as regulators of blaZ, which is responsible for penicillin
  resistance. The DNA sequences bound by MecI and BlaI are
  identical; therefore, BlaI can also bind the mecA operator to
  repress transcription of mecA.

This represents the general pattern of resistance of MRSA, but there is a rich diversity in the particulars of how each strain manages expression.  Two of the main identifiers are how the mecA gene complex and ccr gene complex are configured (carriage).  The other two identifiers are the ISS and whether or not the ISS is repeated in the target chromosome (and how many times it's repeated) (8).  If we just consider the mecA and ccr carriage, then we get a great summary from IWG-SCC (ref 8):

The mec gene complex is composed of mecA, its regulatory genes, and
  associated insertion sequences. The class A mec gene complex (class A
  mec) is the prototype complex, which contains mecA, the complete mecR1
  and mecI regulatory genes upstream of mecA, and the hypervariable
  region (HVR) and insertion sequence IS431 downstream of mecA. The
  class B mec gene complex is composed of mecA, a truncated mecR1
  resulting from the insertion of IS1272 upstream of mecA, and HVR and
  IS431 downstream of mecA. The class C mec gene complex contains mecA
  and truncated mecR1 by the insertion of IS431 upstream of mecA and HVR
  and IS431 downstream of mecA. There are two distinct class C mec gene
  complexes; in the class C1 mec gene complex, the IS431 upstream of
  mecA has the same orientation as the IS431 downstream of mecA (next to
  HVR), while in the class C2 mec gene complex, the orientation of IS431
  upstream of mecA is reversed. C1 and C2 are regarded as different mec
  gene complexes since they have likely evolved independently. The class
  D mec gene complex is composed of mecA and ΔmecR1 but does not carry
  an insertion sequence downstream of ΔmecR1 (as determined by PCR
  analysis).

And

ccr gene complex.The ccr gene complex is composed of the ccr gene(s)
  and surrounding open reading frames (ORFs), several of which have
  unknown functions. Currently, three phylogenetically distinct ccr
  genes, ccrA, ccrB, and ccrC, have been identified in S. aureus with
  DNA sequence similarities below 50% (Fig. 2 and 3). The ccrA and ccrB
  genes that have been identified to date have been classified into four
  allotypes. In general, ccr genes with nucleotide identities more than
  85% are assigned to the same allotype, whereas ccr genes that belong
  to different allotypes show nucleotide identities between 60% and 82%.
  All ccrC variants identified to date have shown ≥87% similarity; thus,
  there is only one ccrC allotype. We suggest describing their
  differences as alleles by using previously used numbers, e.g., ccrC1
  allele 2 or ccrC1 allele 8.

All of this is nicely summarized in their table:
\begin{array} {|r|r|r|}
\hline
SCCmec ~type  &ccr ~gene ~complex  &mec ~gene  ~complex \\
\hline
I &1 ~(A1B1) &B \\
\hline
II &2 ~(A2B2)&A \\
\hline
III &2 ~(A3B3)&A \\
\hline
IV &2 ~(A2B2)&B \\
\hline
V &5 ~(C)&C2 \\
\hline
VI &4 ~(A4B4)&B \\
\hline
VII &5 ~(C)&C1 \\
\hline
VIII &4 ~(A4B4)&A \\
\hline
\end{array}
To sum up, methicillin-resistance is caused by the encoding of a novel PBP, PBP2a, along with other factors, which is both genetically stable and transferable via the use of SCCmec.
References:
(1) Pathak A et al. High prevalence of extended-spectrum β-lactamase-producing pathogens: results of a surveillance study in two hospitals in Ujjain, India. Infect Drug Resist. 2012;5:65-73. doi: 10.2147/IDR.S30043. Epub 2012 Apr 5. [Note that many of the great sentinel studies on drug resistant bacteria occur in the massive hospitals in India].
(2) B Hartman and A Tomasz. Altered penicillin-binding proteins in methicillin-resistant strains of Staphylococcus aureus. Antimicrob Agents Chemother. 1981 May; 19(5): 726–735.
(3) Liu, H. et al. Detection of borderline oxacillin-resistant Staphylococcus aureus and differentiation from methicillin-resistant strains. Eur J Clin Microbiol Infect Dis. 1990 Oct;9(10):717-24.
(4) Tawil N. et al. The differential detection of methicillin-resistant, methicillin-susceptible and borderline oxacillin-resistant Staphylococcus aureus by surface plasmon resonance.  Biosens Bioelectron. 2013 Nov 15;49:334-40. doi: 10.1016/j.bios.2013.05.031. Epub 2013 Jun 4.
(5) Chambers HF. Methicillin-resistant staphylococci. Clin Microbiol Rev. 1988 Apr;1(2):173-86.
(6) Huletsky A et al.  New real-time PCR assay for rapid detection of methicillin-resistant Staphylococcus aureus directly from specimens containing a mixture of staphylococci. J Clin Microbiol. 2004;42(5):1875-84. DOI: 10.1128/JCM.42.5.1875-1884.2004
(7) Schoenfelder SM et al. Success through diversity - how Staphylococcus epidermidis establishes as a nosocomial pathogen. Int J Med Microbiol. 2010 Aug;300(6):380-6. doi: 10.1016/j.ijmm.2010.04.011. Epub 2010 May 6.
(8) IWG-SCC. Classification of staphylococcal cassette chromosome mec (SCCmec): guidelines for reporting novel SCCmec elements.  Antimicrob Agents Chemother. 2009 Dec;53(12):4961-7. doi: 10.1128/AAC.00579-09. Epub 2009 Aug 31.
(9) Stürenburg E. Rapid detection of methicillin-resistant Staphylococcus aureus directly from clinical samples: methods, effectiveness and cost considerations.  Ger Med Sci. 2009 Jul 6;7:Doc06. doi: 10.3205/000065.
(10) Jensen SO and Lyon BR. "Genetics of antimicrobial resistance in Staphylococcus aureus". Future Microbiol 4 (5): 565–82. doi:10.2217/fmb.09.30. PMID 19492967
(11) Oliveira DC, de Lencastre H.  Methicillin-resistance in Staphylococcus aureus is not affected by the overexpression in trans of the mecA gene repressor: a surprising observation. PLoS One. 2011;6(8):e23287. doi: 10.1371/journal.pone.0023287. Epub 2011 Aug 2.

Clear answer and well summarised! Please, cover in more detail the SSCmec thing. You left out mecA gene which is located in SSCmec. Bacterial resistance to methicillin and related penicillins is mediated by acquisition of mecA that codes for a novel penicillin-binding protein, PBP2a, that has a low affinity for methicillin and related penicillins and cephalosporins. This is all what is covered in Murray Microbiology book.

@Masi Sure thing.  I didn't want to go into a tangent, you could probably write a whole dissertation on this.  I will update before the end of the bounty.

@Masi  Sorry about the delay, but I think that probably covers what you were looking for.  If you know how to better format that table, I couldn't get it to look right.

Acquisition of a new PBP (eg methicillin resistance in staphylococcus aureus), source Murray.
So I think the answer is C: change in configuration (mutation) of PBP, which can interpreted as acquisition of a new PBP.

I noticed that you still haven't edited your own awnser.  I think you mean to say the awnser is C.  I would like to point out that the alternate for of PBP, PBP2a is not really new, mearly has upregulated expression vs classic PBP.  Are you looking for information in how the binding site structure changed?  I want to make sure I'm adding the kind of clarity you are looking for.


text:
Which strains of C. diphteria are causing Diphteria toxin?
I got this question:
Diphteria toxin is produced only by those strains of C. diphtheria that have which of the following characteristics?

Encapsulated
glucose fermenters
lysogenic for b-prophage
only mitis-strains
sucrose fermenters

I think the right answer is lysogenic for b-prophage, since Freeman found out that toxic gene is encoded by lysogenic phage infecting all toxigenic strains in 1951.
However, I am not sure what "b-" means in "b-prophage".
Which part is "b-" in Prophage?

Real simple: Beta!  Often called "phage beta" b-prophage is a more modern way to write it.  I knew that one off the top of my head, but I like to refer the general public interested in bacteriology to Tadar's online text.
It's nicely done, and I wish that it had been around when I was studying bacteriology.
Specific to your question:

Hence, Corynebacterium diphtheriae can only produce the toxin
  responsible for the disease if it carries a temperate virus called
  phage beta. Only lysogenized streptococci  produce the erythrogenic
  toxin (pyrogenic exotoxin) which causes the skin rash of scarlet
  fever; and some  botulinum toxins are synthesized only by lysogenized
  strains of C. botulinum.


text:
Can acid-fast M. tubercolosis obstruct alveoli?
I am not sure which word is the best here for colonisation of alveoli by acid fast-mycobacteria. I found this question, and I am getting confused by the term obstruction of alveoli because I tend to relate it to COPD which is not a case here:
Which of the following is the predominant pathogenic mechanism of tuberculosis?

a) cell-mediated hypersensitivity
b) obstruction of alveoli by large number of acid-fast mycobacteria

I think the right answer is "obstruction of alveoli by large number of acid-fast mycobacteria", but I am not sure if you can say that acid-fast mycobacteria obstruct alveoli.
Are acid-fast mycobacteria "obstructing" alveoli or just colonizing?

Mycobacteria are on the order of 2µm in length and 0.2µm in diameter.  Alveoli are on the order of 200µm in diameter.  Obstruction is possible, but M. tuberculosis grows rather slowly.  Too slowly, in fact, to avoid being engulfed by alveolar macrophages.
Furthermore, obstruction does not sufficiently explain the predominant symptoms of tuberculosis:  bloody sputum and the tubercles themselves.

I certainly agree it's not the myco colony obstructing the alveoli, but rather the elicited immune response does a pretty good job of that.  Muc5, Il13, etc are all slamming in to cause mucin production and inflammation.

Thank you for your clear answer! So obstruction is possible and it is mostly theoretical model by large number of acid-fast mycobacteria. However, can we still say that obstruction of alveoli by large number of acid-fast mycobacteria is the predominant pathogenic mechanism of tuberculosis?

@AtlLED Is this "cell-mediated hypersensitivity" more right answer? Or what would you say is the predominant pathogenic mechanism?

To answer this homework question, consider "What causes tubercle formation?"
http://en.wikipedia.org/wiki/Tuberculosis

"In most forms of the disease, the bacillus spreads slowly and widely in the lungs, causing the formation of hard nodules (tubercles) in the respiratory tissues and form cavities in the lungs." So the answer must be B, because it implies that bacillus is causing it as a factor. Great! Thank you!

I don't know what all of your possible answers were to this question, but I think you should reread the part about tuberculosis being a granulomatous infection.


text:
Model for fluctuating selection
Is there any mathematical model to predict the behaviour and long-term consequence of counter-acting selection at different time scale?
For example, let's consider the bi-allelic gene A, with alleles A1 and A2. During a long period of n1 generations A1 is slightly beneficial (differential of selection: s1). After this period, follows a short period of n2 generations when A2 is highly beneficial (differential of selection: s2).
What mathematical model describes the frequency fluctuations of alleles and which allele will get fixed at the long term given the initial frequency ( f0 ), assuming infinite population size and random mating.

Unsmooth changes like you describe are normally hard to use in an analytical model. You could build a model of smoothly changing selection using a sine wave or simulations (which would be easy to build).

That remainds me the famous case of Biston betularia

Biston betularia is a moth that lives in England and has a light color in order to mimetize with the bark of trees. However, about 1% of the population presents melanism, and its camouflage fails. During the industrial revolution, the trees became dark as a result of the pollution. When that happened, the proportion of melanistic moths inverted, to almost 99%. During the 20st century, when the industry independized of the coal, the trees got light again, and the proportions restored once again.

This might be a gross oversimplification but could you not use sequential univariate breeders equations, model the response during the s1 phase, this will erode variation in favour of the A1 allele, then you could then apply the univariate equation to the s2 phase. If all variation was lost in the s1 phase then the response in the s2 phase will be 0, and increase dependent on the strength of selection and size of remaining variation.

GriffinEvo's response sounds right. But does the fluctuation continue indefinitely? In that case you might use the idea of step functions from EE to model the process.

Sounds interesting. I welcome you to develop a bit the idea and make an answer out of your comments. I have never heard of the step functions from EE (what does EE stands for?).

I'm going to look at some of your questions over the evenings this week and hope I will be able to answer them - no idea what is meant by EE @daniel

@GriffinEvo: electrical engineering.

The frequency fluctuations will be determined by a standard model of selection as found in any basic population genetics text. In this scenario they take a very basic form: during each long period $i$ the frequency of $A_1$ increases from $f_i$ to $f_i\cdot (1+s_1)^{n_1}$ and during each short period $j$ the frequency of $A_1$ decreases from $f_j$ to $f_j\cdot (1/(1+s_2))^{n_2}.$ Thus over each pair of periods the frequency of $A_1$ changes by $(1+s_1)^{n_1}/(1+s_2)^{n_2}$. If this quantity exceeds 1, $A_1$ goes to fixation; if it is less than one $A_2$ goes to fixation.
More generally, for an infinite population in a fluctuating environment, the allele with the higher geometric mean fitness will go to fixation. Early discussions of these results are due to Dempster (1955; Cold Spring Harbor Symp. Quant. Biol.), Haldane and Jayakar (1963; J. Genetics), and Lewontin and Cohen (1969; PNAS).

Nice answer to a very old question! Thank you. I edited your answer just to clarify that $f_i$ and $f_j$ multiply the thing in parenthesis and are not function of the thing in parenthesis. just in case someone could have a doubt...

If I am not mistaken, this model is a good approximation when the two phases are short enough. If the phases were to be too long then fixation may occur during the first phase and allele frequencies would never be affected by the second phase. This is even more important when $N$ and/or $s$ are high. It might be interesting to have such model for finite population.

Glad this was helpful. In the specific way that you formulated the question, we don't need to worry about fixation because the population is infinite and thus fixation can never occur. But as you note in the real world, or in a finite population model, fixation becomes a major issue. Off the top of my head I don't see how to derive a simple expression for the fixation probabilities of each allele in this case.


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Why can't we propose a solid theory regarding origin of life?
What  information is greatly lacking which does not allow us to propose a  solid theory for origin of life ?

The problem is not that scientists are baffled as to how life could have arisen. Rather, the problem is that scientists have many explanations as to how life could have arise, to the point that the appearance of life seems almost trivially obvious; it's just unclear which of the many possible routes was actually followed, and it's difficult to find clues that sort that out. It's as if you found a quarter at the bottom of a hill. The question isn't "Could that quarter have possibly rolled down the hill?" It's "Which path did the quarter follow when it rolled down the hill?"

I think this greatly overstates our understanding of the origin of life. I'm certainly not an expert on this, but as far as I know there are large gaps in all current hypothesis.

The first animal must have produced only 1 simple protein/product in large numbers... like mucus for example... in a long chain with no end, and then the second animal must have been when the long chain of mucus incorporated a copy of the first animal in it. they would have had no cells, no nucleus, just a complex molecule that made a huge amount of mucus, or another simple product which served as protection and food simultaneously. that's a fairly good theory for the first animal. the first animal was perhaps just a 50 atom molecule that made mountains of mucus out of heat and co2 and water.

Because the planet was sterile, the first animal didn't have to defend itself against anything, it just required the right PH of pure water, and an energy source, like sulphur, or volcanic vent compounds, it didn't need an outer shell that much, because everywhere was pure minerals and water.

What do you mean by "solid theory" because supported theories do exist.

First of all, we do have some solid theories to explain the origin of life. That said, the main thing missing in order to be able to accept one of these theories with a decent amount of certainty is the ability to run a planetary scale experiment for a few billion years.
The theories are fine, the problem is that we cannot really test them. In order to test a theory that describes the origin of life, we will have to recreate the original conditions (think of a test tube the size of the Earth) and then pump energy into the system and watch what happens over the next few billions of years. This is not really feasible, for obvious reasons. I really doubt you will be able to get funding for an experiment that will run that long.

The mice are working on it as we speak...

@Amory I just hope they finish before the Vogons get here.

@Amory I am certain it is 42

The reason for no single, solid origin of life (OOL) theory is that there are
many and none of them explain or resolve the overall or the detailed issues of OOL, encompassing wide differential and even conflicting approaches, e.g., reproduction vs metabolism, and RNA vs DNA. Further, all are using naturalistic processes, requiring validation by the laws of physics and experimentation. While there are numerous theories, they are either geochemically irrelevant or outside the laws of physics. Whether RNA world, panspermia, hydrothermal vents, small warm ponds, all embrace various levels of chemical evolution for the initial, intermediate and ultimate biochemical assembly of increasingly more complicated levels of organic elements considered vital to OOL. No viable processes have been found to naturalistically create life.
Increasingly, wild speculation of geochemical conditions and trivialization of biochemical assembly, metabolism and reproduction are being proposed. The intractable problems that apply to naturalistic theories begins with the fact that chemical evolution of non-living compounds produces no viable pathway to increased complexity, that is, there are no cosmic evolutionary processes capable of the complex structure, design, order and operation of biochemical systems required for even the simplest organism.
The universal challenges that must be fully resolved in all theories include:
1. The homochirality essential in nucleotide amino acids,
2. The homopolymerization of the DNA side chains,
3. The nucleotide coding using information design,
4. The cell membrane formation essential encapsulation.
5. The chicken and egg issue of proteins and complex structures.
These are affected by requirements for colocation. coincidence, contamination mitigation and concentrations that are absolutely precise.
Finally, lab experiments must accurately reflect geochemically relevant conditions and not overly manipulated by experimenters, which would simulate intelligent design but produce questionable results.
The number of sources that could be listed is extensive. A simple search internet of the main descriptive words would provide detailed definition and additional detail. Regarding the 5 universal challenges: 1. homochirality relates to the right/left handedness of the amino acids since they are not symmetric. DNA amino acids must be 100% left handed or DNA will not work. One of the challenges to get comprehensive sourcing is due to the reluctance of present biological entities to fully acknowledge the delineated intractable issues.

Welcome to Bio. Can you add sources to your answer?

The high number of sources that could be listed are very extensive. A simple search internet of the main descriptive words would provide detailed definition and additional detail. Regarding the 5 universal challenges:

If there are so many sources to find it shouldn't be too difficult to put a few in your answer. Your answer is downvoted because it lacks references. Sources allow other users to background-read on your post.

"DNA amino acids" do you mean nucleotides? With errors like this sourcing becomes even more important.


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How to distinguish those flowers in outskirts: hawkweeds (Hieracium), hawksbeard (Crepis) and hawkbits (Leontodon)?
How to distinguish those flowers of the forest outskirts: hawkweeds (Hieracium), hawksbeard (Crepis) and hawkbits (Leontodon)?
I am not asking about concrete species it should be extremely hard since they have hundreds forms, but what are observable differences between genus?
I have read wikis articles but still not sure that I could distinct those flowers in the field right way.

http://en.wikipedia.org/wiki/Leontodon
http://en.wikipedia.org/wiki/Hieracium
http://en.wikipedia.org/wiki/Crepis

It's quite hard to answer this question and the best would be to follow a flora, which I'll not just copy informations from to past here.
So following are general observations subject to numerous exceptions.
Hieracium generally have lanceolate to oval leaves, not or little toothed, most hairy.
Crepis and Leontodon have generally Taraxacum-like leaves, that means, dentate to lobed.
Some Crepis have leafy stems (but some don't), while Leontodon always have their leaves concentrated to the base, forming a rosette.
[edit on 2014, october 2]
Be aware that there is another genus of the Asteraceae family which may be mistaken with the Crepis/Leontodon/Hieracium group, although it's easier to distinguish. It's the Hypochaeris genus.
Hypochaeris have few but not so homogenous species as there are within the other genera.
Hypochaeris radicata (which may be the most common species in France and wester Europe) have all its leaves basal, forming a rosette and sticking to the ground (never erected). These leaves are always lobed (neither entire, nor toothed), with erected hard hairs covering there upper faces.
Hypochaeris maculata may be mistaken with some Hieracium : it have hairy smooth entire leaves wich are (all or mostly?) basal forming a rosette.
[Addition on August, the 5, 2014]
Also Leontodon and Hypochaeris have hollow stem just below the capitulum(1). When you press the stem just below the capitulum, you fell it flattens under your finger, and if you use the nail to make an incision in the stem, you will see it is hollow like a pipe.

NB : Taraxacum also have hollow stems but they are fully hollow (from the base up to the capitulum), while Leontodon just have the upper part of the stem which is hollow.

Leontodon are almost always monocephal, that means, the stems are not branched : they have only one capitulum per stem, while Crepis and Hieracium and Hypochaeris mostly (if not always) have branched stems carrying several capitula.
(1) the capitulum is the type of inflorescence in the Asteraceae family. It's also called "head" (and actually, "capitulum" is the latin word for head).
You may like to have a look at this page [in french] presenting some common yellow and ligulate weeds from the Asteraceae family to get some illustrations of what I explained here.


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Inheritance of Huntington's disease
People with Huntington's disease have HTT genes with more than 37 copies of CAG repeat. The risk of extra copies being generated is higher during sperm formation than during ovum formation. Why is it so?
Interesting fact: People with HD allele inherited from father develop symptoms earlier than if that allele is inherited from mother.

Excellent question. The answer is that, in general, there is a higher rate of mutation in spermatogenesis compared to oogenesis. This is because there are more cell divisions during spermatogenesis, which allows for opportunities for mutation.
In addition, repeat diseases like Huntington’s sometimes have a phenomenon known as anticipation. This is when the disease gets phenotypically (and genetically) more severe with each successive generation. The exact molecular basis of this is not completely understood, but it is just well known that DNA polymerase tends to make more mistakes in large repeat regions, causing an expansion of the repeat. Anticipation is not linked to gender, I just wanted to point out that these repeats are prone to mutations that will expand the repeat and cause disease
You can see anticipation in this graph. This example is for Fragile X. The higher the repeat number in the parent, the greater the chance the child develops the disease. The parent doesnt have the disease, but what happens is the repeat mutates and gets expanded to the point where the disease will develop.

So, put these two facts together and you have your answer. A male's sperm tends to have a higher overall mutation rate, and the region responsible for Huntingtons is already prone to disease causing mutations as it is. The result ends up being the disease gets ‘inherited’ more often from the father
Picture from here

Awesome answer ! Could you tell me what is the difference between total CGG repeat length and pure CGG repeat length ?

In fragile X the repeat is CGG. But sometimes there are also AGG repeats as well. Pure counts only the CGG repeats, while total includes both. This paper was trying to find the importance of AGG repeats on the disease

If they were trying to find the importance of AGG repeats, then why did they count pure CGG repeats ?


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Do mitochondrial DNA have repair enzymes?
Mitochondria are considered endosymbionts originated from a prokaryote. So, do they have a DNA repair mechanism ?

Yes, mtDNA can be repaired by enzymes coded by nuclear genes.
http://www.ncbi.nlm.nih.gov/pubmed/22992591

Could you provide a brief synopsis of this review article for future reference when others come to find this question?


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RNA-seq analysis - q-values in cuffdiff
I'm using cuffdiff 2.1.1 to look for differential gene expression between two conditions. Each condition has 2 biological replicates. The results I get look promising from a log fold change perspective - lots of genes that I would expect to be affected have the highest fold change values. However, from a q-value perspective very few of the results look promising, having q values > 0.05.
My question is, given 2 replicates, how is the q value calculated? Surely if there was high variance between replicates but the difference between experimental conditions was also large then the q-values would be correspondingly high?
In this case, can I, or should I, really trust the q-values?

http://cufflinks.cbcb.umd.edu/manual.html#gene_exp_diff

If after a few days you don't get good answers here, consider reasking the question here:
http://www.biostars.org/
It's basically stackexchange specifically for bioinformatics.  About a third of the questions over there are about next generation sequencing.

q-value is the corrected p-value to account for multiple testing (i.e. you are testing thousands of genes). Those with q-value <0.05 are significant experiment-wise. Cuffdiff uses Benjamini-Hochberg correction to compute FDR (i.e. q-value). The calculation does not depend on the number of replicates it's based on the distribution of p-values those, yes, are influenced by the number of replicates. The more replicates you have the better).


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How can an infection of lower respiratory tract lead to a skin infection?
I am interested in the multifactorial process about infectious diseases of the lower respiratory system and their progression to a skin infection.
Possible agens are zwitterions, viruses, fungi, amoebas, bacteria and/or parasites.
Zwitterions
Small protein segments, much unknown but their importance is much greater than known.
Viruses
Parvovirus B19

Example of a case: 5 children develop a bright red rash on the face and turns violet after a few days and then disappears. Then maculopapular rash appears on the trunk, buttocks and extremities. It soon fades from the trunk but persists on the thights and forearms. Two children have also had a slight fever and a sore throat, but all were not terribly sick. What is the genetic material of the most likely causative agent?
It is a skin infection. Not so severe. Little upper respiratory infection but not necessary caused by the agent. Infects many so spread probably by respiratory droplets. **But how a respiratory infection can lead to a skin infection?*

Bacteria
....
Amoebas
...
Fungi
....
Parasites
...

I don't have the time to answer this now, but you're thinking about it just in the context of the question which is limiting.  Check out Mycoplasma pneumoniae.

So, my question is are we limiting ourselves to the example case, which seems to have nothing to do with respiratory infection (unless it's measles, but the statement "not terribly sick" somewhat precludes this, and the measles rash turn dark brown, not violet).  Or are we just generically asking the question "how can a respiratory infection lead to a skin infection." which is very different.  I also don't see what your attempt to answer the question has been.

cf. Parvo, Erythema infectiosum, Rubella, and viremia.  You're going to have to give me more before I'm enticed to come back.

Have you determined the the most likely causative agent first?  This still feels like a homework question that hasn't been addressed fully.  I've given you 4 different respiratory infections that causes rashes (M. pneumoniae, measles, parvo, and rubella).  Start with figuring out the causative agent, then ask the question, "How does [P] pathogen cause a rash?"  If you show your effort in answering that, and have trouble, I'd be happy to come back and help.

Perhaps we should continue the discussion in chat?

One might argue that since replication takes place in erythroblasts (Brown, Anderson, & Young, 1993), that it's not actually a respiratory infection either.  Fluids are simply more hospitable to the virus and more transmissible.
As for the rash, perhaps it is because the P antigen receptor that erythrovirus uses to infect erythroblasts is also expressed on endothelial cells, like those in skin (and alveolar) capillaries .


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Assays during drug discovery
After researching the definition of Assay, I am left with the idea that an assay refers to scientific screening. It could be of chemicals, microbes, etc.
I understand that during drug-discovery assays scientists screen for chemical compounds that may make up an effective drug.
But could someone explain, or provide me with some links that further discuss the process of assays, or how they work or take place during drug discovery?
Frankly, I'm also still a bit confused about the definition of "Assay" itself.
Thank you.

An assay may be thought of as a trial or test that is designed to quantitatively determine the amount of a substance in a sample.
Thus a biochemist might use a protein assay to quantitatively determine the amount of protein in a sample, or a pharmacologist might assay a sample to quantitatively determine the amount of drug present, or an enzymologist might carry out an enzyme assay to determine the amount of enzyme activity in a sample.
Let's take the case of the enzymologist. I take a liver sample, homogenize it, centrifuge and take the supernatant (soluble) fraction. I want to quantitatively determine the amount of a given enzyme activity.
I do this by performing a test by (say) adding a sample of the supernatant to a cocktail that 'does something' only if the enzyme of interest is present.  The 'do something' could be a color change, where the cocktail  contains  everything needed for the enzyme to work (all substrates, cofactors etc) and where the enzyme transforms one of the substrates to a coloured product.  I now have an enzyme assay which tells me if the enzyme is present (the trial), which may be made quantitative with reference to the amount of color produced in a given time.
As I remember things, Sherlock Homes was pretty good at the assays, using them to make trials of his geological samples, but I cannot find the quote.

I'm a pharmacy student and I can try to explain how they do to find new drugs.
In fact, there are many diferent ways to do so, it depends of what kind of new drug you are searching for.
Sometimes you're working on a disease which the pathological molecular mechanism of action are well-known and where many drugs are already effective. In this case, the 'assay' may just be about improving a well-known molecule by adding or changing a small part of the molecule (replace a ketone by an alcohol for exemple). Always in this case, you know on what molecular receptor you have to act, its 3D structure, its composition, its location in the human body and maybe the most important (but you don't know this every time and in this case, you could begin by this point) how and what part of your drug acts on any part of the receptor.
Then you have molecular libraries where you can search your new drug. They are alimented by different ways: someone who found a new chemical reaction that can add a chemical function where you could not before and generate several new compounds by applying his new method. All this compounds can be given to a national library where access is possible. You can also find intermediate compounds of reaction. This happens in public research because private laboratories keep their discoveries secret.
Sometimes you're working on a disease where the usual drug doesn't match really with the receptor, in this case, you have 3D tools that can modelize molecule and receptor in order to quantify how they match. This is achieved on many many molecule from this library and these methods generate few drugs that match the best.
Then you work on these drugs to improve them and make them compatible whith digestive barriers if you want an oral drug, or with the galenic form you need. This point is about improving the matching with the receptor by changing few parts of the molecule.
In fact when you know on which molecule you want to act, it all start with IT tools that mesure interactions between this molecule you want to act on and other random molecules.
When you don't know molecular mechanisms of your disease, you have to find it before, otherwise you're gonna work double-blind.
This is a few part of the reality, I hope that answered the last part of your question.


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In our solar system which other planet could have been in the "habitable zone" in the past?
With changes in our solar system, such as planets moving away from the sun and the reduction in solar radiation, which other planets in our solar system could have been, in the past, in a suitable zone for life to originate?

I think this might be more on topic in the physics SE, no?

I'm not sure what physicists would know of biology (origin of life).  It seems on-topic to me.

Cf. http://biology.stackexchange.com/questions/8972/why-must-a-planet-be-in-a-stars-habitable-zone-to-have-life?rq=1

@AtlLED it is equally suited here as it is specifically asking about where conditions are suitable for life.

@Oreotrephes do you think what I have below is biological enough?

Looks, great to me. IMO the word "habitable" makes biological enough. OP should accept!

This answer is also speculative, but according to the planetary habitable zone models proposed by "Habitable zone for Earth-like planets in the solar system" (Franck et al. 2000), a key finding was that:

an Earth-like planet at Martian distance
  would have been habitable up to about 500 Ma ago while the position of Venus was always outside the habitable zone.

So, Mars could have been habitable, but as it is much smaller than Earth, it has a smaller gravitational field presumably a major factor in how it lost much of its atmosphere.


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Abnormal Prolactin Level
I want to know what makes the balance of the Prolactin abnormal. Is that related to the presence of a nodule near the pituitary?

It could be, but this website is NOT for medical advice. If this is your personal condition, please seek a qualified medical professional. If this is a hypothetical condition, please clarify exactly how Prolactin levels are abnormal (hyper- or hypo-) and what you mean by 'nodule near the pituitary'.

The main abnormality in prolactin levels is hyperprolactinemia, meaning blood levels of prolactin above the normal range, not during pregnancy or lactation.
The major cause of these abnormal prolactin levels are tumors consisting of pituitary lactotroph cells--called prolactinomas--which secrete prolactin. This is generally corrected with synthetic dopamine analogues, as dopamine negatively regulates secretion of prolactin in lactotroph cells.
Here is a 2010 review with further detail:
http://joe.endocrinology-journals.org/content/206/1/1.full.pdf

I am not sure whether I understand your question right, but prolactin levels can be abnormal under several conditions like cancer, drug abuse, stress, breast surgery etc.
Its secretion is mainly controlled (inhibited) by Dopamine. Other hypothalamic factors like VIP, TRH, PRH etc. are enhancers.
Please specify your question for a detailed answer.

Prolactin is a hormone which is produced by the pituitary gland.  Prolactin is named because it was found to be elevated in women who are lactating, its also produced by men and in elevated levels during sleep. Because of this, like many blood factors and hormones it probably has more than a single purpose.
When there is an abnormal growth from the pituitary gland, since the tissue produces prolactin, abnormal pituitary tissue can also produce extraordinary amounts of prolactin. I don't think this means that its a cancer, but its a sign that there is an unusual pituitary condition. It can even be the result of taking some drugs.
Most of these tests are from experience - we find that this happens a lot, but the causes are usually not understood well. Cancers in particular are quite unpredictable and can have many different properties from one case to another.  Pituitary tumors are the most common central nervous system tumors, so common they are found in autopsies 3-27% of the time, often never having been found previously.


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What would happen if you slowly crushed a live brain?
In a hypothetical scenario, if you cut open a person's skull to show the live brain, and then you slowly start to crush it..
At what point would the person loose consciousness?
What would the person be feeling all this time?
Would it cause pain?

I'm voting to close this question as off-topic because it is tasteless and stupid.

just watch a film studying TNT shrapnel inclusions of the brain, javelin skull perforations, and stories of the numerous suicides attempts involving a few nail gun shots to both sides of the head. In some scenarios people have survived with 8 nail gun perforations into their brains. The wording of your question is not at all scientific by the way. It is worded like a nazi experimentor or a horror movie script.

It depends on what part of the brain you are "crushing."
When we do brain surgery we often do exactly what you describe. That is, we open the skull and often remove part of the brain. However, in our case usually the part we are removing is diseased or malfunctioning to begin with.
There are areas of the brain that are known as eloquent and those that are considered "not eloquent." This is an overly simplistic but educationally instructive way to classify things. Eloquent brain regions are those regions that when disturbed will cause an obvious and devastating neurological injury. Examples are primary motor/sensory cortex, broca's area, wernicke's area etc. Noneloquent areas are those that can be damaged or resected and the sequelae are less obvious. For example, you can remove quite a bit of frontal lobe before you notice a problem. However, an appropriate and sensitive behavioral test/instrument may still pick up the deficit.
Damage to the brainstem and thalamus is more devastating and even small injury to this area can cause major deficits and changes in the level of consciousness. Injury to different levels of the brainstem produces different level of consciousness. Again, it really depends on the precise location and extent of injury and there is no single answer to your question.
As the brain itself has no pain receptors the patient would not really feel much pain even if you caused major deficits. However, again it depends on the location. You could theoretically irritate thalamic sensory regions and cause chronic pain syndromes but your lesion would have to be pretty precise.

It seems there's way too many variables here.  Crushing can occur in a number of ways, leading to different primary damage in different regions first and different people have a different level of system failure thresholds.
Technically, there are no pain sensors on the brain, so you wouldn't feel any pain in the classical sense.  However, it's hard to determine how you would affect the pain interpretation circuits (again, "crushing" can occur a number of different ways); you could inadvertently cause pain signals.
Losing consciousness would also depend on when what region of brian is crushed.  And how it's crushed.  Most of our higher processing regions associated with consciousness are on the very outer surface of our brain.  In one scenario, if it just gets compressed, and damage tend to accumulate in the center of the brain first, it would be a different outcome than if it was some kind of shear crushing force that damaged outer brian first.


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What hair color will result in someone inheriting both blond and ginger genes?
Both the genes for blond hair and ginger hair are recessive, so they need both parents to give the same gene for it to take affect. What happens when a person has 1 copy of a recessive gene and another copy of a different recessive gene.
They don't have enough of the recessive genes to have either blond or ginger hair, but they don't have a dominant gene to "take charge"?

Hair color is not so simple as that.  Most traits, especially those as complex as color, are controlled by many alleles at many loci.  That's why there are different kinds of brown, blond, and red hair in the population.  There is no "hair color gene."  A fascinating paper came out a few years ago, identifying dozens of SNPs playing a role in hair and eye color.  It's a deep, deep rabbit hole that we have only begun to plunge into.
EDIT: To summarize, it's very complex.  This paper performed genome-wide association scans looking at two comparisons each for eyes (Blue and green, blue and brown), hair (red or not, blond or brown), and skin (freckles, sun-sensitivity).  The researchers looked in a group of Icelandic and Dutch individuals, which means they only looked at a small portion of human variability (i.e., very few African or Asian genomes, for example).  Still, just from those simple comparisons, their scans:

revealed 104 associations that reached genome-wide significance, accounted for by 60 distinct SNPs, of which 32 showed genome-wide association with only one pigmentation trait, 12 with two traits and 16 with three traits.

That is to say, they found 60 DNA bases that explained their data.  Roughly half of those only affected one thing (eye, or hair, or skin, but only one), a fifth of those single base changes contributed to two different traits, and a full 25% of those SNPs were related with three traits.
That's still pretty hefty.  Basically, they found 60 things that can affect hair, eye, or skin color, and some of those can affect some or all of those at the same time.  And they only looked at people from two countries.  Here's a figure where they summarize the seven strongest SNPs; you can see how tricky it can be to explain colors.

Wait, so Game of Thrones gets its genetics wrong!?

Yeah, that always bugged me.  Also, there are dragons.

I don't have access to the paper. And I doubt that I have the knowledge to understand it. Could you please explain shortly how hair (and eye) color is determined.

@IlyaMelamed Hopefully that helped!

Thanks. just 1 last question. What is the meaning of the stars on the figure?

@IlyaMelamed Asterisks mean highly significant.  In this case, it means there is a less than a 1 in 100 million chance that those findings occurred due to chance.


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Does a fully-resolved phylogenetic tree have to be dichotomous?
I read that wherever there is polytomy there is an unresolved pattern of divergence. I don't understand why this is so.
When divergence takes place, is it necessary that there will be division into only 2 paths? Can't there be more than 2 paths with all the paths being equally related to each other (that is, no 2 paths being related more to each other than to a third path)?
In other words, does a fully-resolved phylogenetic tree have to be dichotomous?

In theory, yes, every tree has to be dichotomous. You can understand a trichotomy in a tree as the summatory of two dichotomies that had happened so close in time that you cannot know wich was first.
Given a certain population, assume that some individuals colonize a new environment, got reproductively isolated and form a new specie. This is the typical speciation process. In this case, the two species, share a common ancestor. If you go back in time, all the individuals of the new specie will descend of only one individual. The same goes for the original specie. If you go back further, this individuals will share an ancestor, too. This is the conceptual meaning of the dichotomy, but normally it is impossible to determinate wich was exactly the common ancestor.
Now imagine that the original population formed not one, but two new species. And that this process happened about the same time as the one described before. It is conceptually possible that a set of three brothers were the origin of three different species (wich will be a true trichotomy), but not only it's very unlikely, but it's virtually impossible to prove. Since two close dichotomies are far more probable than a trichotomy, it's assumed that every tree has to be dichotomous, and that a trichotomy is in fact due to lack of resolution.


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What should be evaluated in food decomposition experiment?
Briefing
Some days ago I noted that 3 cookies left on my desk since 3 months ago are still "fresh", and by that I mean... not spongy like some cookies that get soft after some time outside.
However this particular brand of cookies do get spongy, I'm not sure why don't these do!
I also noted that there is a cockroaches/flies infestation in a home nearby, so these are getting in my house, but none of those insects dare to eat the cookies.
So, I decided to make an experiment inspired in the well known experiment of Watermelon vs McDonalds Burger where a watermelon decomposes extremely quick, and the burger does not. This article even mentions one that hasn't decomposed after two decades!
I understand that watermelon decomposes so fast mainly because of the sugar/water that it contains, but that is another story, let me tell you what I want to do.
Problem
In this experiment the only notable variables taken into account were: Visual appearance (picture), and time.
For my cookies I want to do a similar experiment, but I want to know which variables should I consider, so far I only have these in mind, but I want to know what else can be considered for food products:

Date of packaging
"Best before" date label
Visual appearance (daily pics)
Time gone by before going spongy
Humidity of room (3 daily measures across the day)
Temperature of room (3 daily measures across the day)

And the samples will be:

Being in a closed room (eg. my room)
Being in an open room (eg. dinning room)
Exposing to insects directly (eg. roaches, ants, flies)
Adding a drop of "morning saliva" (mainly for the bacteria)

Question is
In general, what do I need for food experiments? I think these are OK, but maybe I'm overdoing it on some, and maybe I need to consider some other parameters.
My experiment's objective is to see if it decomposes, why does it take X time to do so, or why doesn't it decompose at all, if it is safe to eat, or if it shenanigans like McBurgers.

You could weigh the cookies in a time course to see how quickly the cookies are degraded. Also, you could take some samples and make cultures in Petri dishes to see if there are differences in the microbiota associated with each one. In this line, maybe you'd want to sterilize the samples by some means, just to ensure they have the same microbial conditions. You could also measure the porosity of the samples by pacing them in water and measure how much water it can absorb, or something like that. I assume you do not have an HPLC engine, but you could also make extracts and see how the spectra varies over time.


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How effective are restriction enzymes in protecting bacteria?
Bacteria use restriction enzymes to cut DNA of bacteriophages. Virus mutates really fast. Won't a point mutation in restriction site render the restriction enzymes of the bacteria useless ?
So how effective are restriction enzymes in protecting bacteria ?

Note that a given bacterium will probably have more than one restriction enzyme, so the viral genome probably won't ever run out of targets. Even if it did, restriction enzymes could suffer mutations that may change the specificity. When you talk about microorganisms, it's more accurate to think in populations rather than individuals, since the colony would be able to grow again if they have at least one cell. Viruses need a certain density to spread, so even if the bacteria cannot defend against, it may be able to survive simply because the virus run out of hosts before some cells can be infected. This is even easier if the bacteria have some kind of resistance form.
Moreover, restriction-modification systems aren't the only defense line against viruses. Many bacteria have a system called CRISPR-CAS that acts like an immune system, inserting RNA fragments into the bacterial chromosome and using them as "antibodies" by hybridization. In this context, you can assume that restriction-modification systems, alongside other nucleases they usually carry, act as an innate immune system, while the CRISPR-CAS would be an analog to acquired immunity.

Diagram of the CRISPR-CAS system. Source.
Furthermore, not every environment has the same viral density. Some habitats may be protected against viruses by some means, like the gut microbiota (the carbon intake goes through the stomach acid and tons of hydrolases, which is very destructive for viruses); while some others may have an incredible amount due to lack of biodiversity and high cell densities (this is the case of most extreme environments). E. coli, as a gut bacteria, would probably have enough with only restriction-modification enzymes (In fact, while it have a CRISPR system, it seems to be repressed), while many others will need more defenses.

@ Miguel Angel Naranjo Oritz Awesome answer !! CRISPR-CAS system-very interesting !


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HIV-RT nucleotide contact residues
I'm investigating HIV-RT 3KLF and 1LWF trying to find a perfect pose of thymine. Which residues on HIV-RT is Thymine supposed to contact on 3KLF and 1LWF? Where exactly is the nucleotide binding domain on 3KLF and 1LWF?
Please provide a journal article as proof.

Thymine must make contact in two places on HIV-RT before being added to nucleotide strand. First contact is made with the fingers region then contact is made at the N-Site.
Allosteric Regulation of HIV-1 Reverse Transcriptase by ATP for Nucleotide Selection


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What are the statistical tools for distinguishing molecular analogy from homology?
Scientists have developed statistical tools that distinguish "distant" homologies from coincidental molecular homoplasy in extremely divergent sequences.
What are these tools?How are they used ?
I have very less knowledge about statistics.

What do you mean exactly with molecular analogy?

Let's say you sequenced genomes of 2 organisms and found a common sequence - AGATTA in both. Now , you want to determine whether that similarity is because of homology or because of analogy.

analogy is based on function and any experiment that can measure the functional output can compare analogous features.

@WYSIWYG I am not able to understand what you are trying to say.Could you elaborate?

You may be interested in this question. In any case, analogy and homology are not mutually exclusive. Are you thinking of homology versus convergent evolution?

There are lots of statistical algorithms that allow you to evaluate the similarity between two given sequences. For instance, blast allows you a rapid comparison between your sequence and other sequences in a database; while Clustal, with a similar functioning, allows you to compare a set of given sequences between them. They are very simple algorithms, but very fast and useful, and basically they score an alignment by counting how many positions between the two entries are the same. Other algorithms function in a similar fashion, but they use hidden Markov models to compare your sequence with a consensual sequence in order to identify motifs and domains. I'm sure there are even more advanced programs, but I don't know them and don't think it's the point.
Homology usually refers to things that share the same origin, while analogy refers to things that do the same function but their origin isn't shared. While the algorithms I've described you only search for similarity or identity, you must notice a few things:
a) Homology of function doesn't necessarily correlate with high similarity. Two proteins can have the same global structure and their sequences be completely different. The three-dimensional structure is the same, and probably there'll be key amino acids that will remain very similar. This is very obvious in many proteases, which share only the three catalytic amino acids (catalytic triad) between them, and vary enormously even between strains of the same species.
b) Protein domains vary in size from a few dozen to a few hundred amino acids. The odds that exactly the same sequence evolves in two separate moments are very low. Especially in highly conserved domains, which usually carry out key functions.
c) Proteins usually have a modular structure with more than one domain. New proteins often evolve by switching and combining domains by translocation. So, even if the same domain has evolved in two separate times, the association between these two "twin" domains with other domains will probably reveal its unusual origin.
That's why usually the term molecular analogy is not used, and if so, it would refer for example to structurally different domains that catalyze the same reaction or that share the same structure. Note that even if the analogy as you describe isn't impossible by itself, the software won't be able to differentiate them unless the sequence appears associated with others. Furthermore, the origin of many of the current protein families is so far in the past that it's quite impossible to reconstruct it, even more so with the high diversity in prokaryotes.

As Miguel puts it, homology means similarity of origin and therefore of some structural properties. Whereas analogy means similarity of function (like insect wings and bird wings provide the same function of flying).
A homoplastic trait may still be homologous because same set of genes may be involved, whose DNA/protein sequence may be homologous.
Just thought of an example that was illustrated in PhD comics some days back- about dogs and hyenas- they both have snouts and look similar but hyenas are more related to cats.
This is an example of convergent evolution but the genes giving rise to snout- the structural proteins the homeotic genes, growth signaling molecules or whatever is responsible for this trait is present in both animals. This trait has a good deal of structural homology. Now, the rigor with which we say that two traits are similar is another factor. It depends on how many variables you use to define a trait. For e.g. a snout shape can be defined using- snout dimensions, angles, bone morphology, texture etc. The more variables you add the more rigorous it becomes. Sometimes the extra variables don't give any extra info and you may choose to remove these variables (this is precisely what is done in a statistical method called Principal Component Analysis).
If phylogentic study is based on these common convergent characters (snout) then we'll end up predicting that dogs and hyenas are related which is erroneous. Therefore multiple gene families are to be considered while doing phylogenetic analysis.
If we go back to butterfly-bird example; both have wings that are used for flying but they are structurally very different- therefore the genes responsible might also be different.
Since the structure itself is different you wont be able to compare the two traits using structural variables. You need variables that define function. For e.g. Thrust generated, fluttering speed, angle of attack etc. (of course they need to be normalized with respect to body size).
Once you have the set of variables (random variables in statistical terms) you can apply statistical tests to compare them.

I think you have misinterpreted my question.My question in really simple words is - If I give you 2 DNA strands of DNA each from a different organism and you find that they have a particular sequence in common. Now you want to determine whether this similarity is due to convergent evolution or due to homology . Now, using statistics and remaining piece of DNA , can you distinguish between this?

those tools just measure homology. convergent evolution may give rise to homologous genes. you cannot know if it is convergent evlution or not unless you look at other genes in the organism.


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Is it true that bees and wasps don't sting if struck by hand while they are in flight?
Is it true that wasps don't sting if struck by hand while flying? I know of one person who claims to have done this at least 20 times and has never been stung. And out of curiosity (not that I'd want to kill them), what about bees?

The other answers are fine and good, but I can confirm, using solid anecdotal evidence, that it is indeed possible to be stung when swatting bees and wasps.  I've done it, and I don't recommend it.

I agree with @Amory here as I know of folks being stung when driving cabrio cars. Not struck by hand but by a 80 km/h headbutt :)

I do this often and never got stung, but I saw someone else get stung by a wasp when waving it away from their face - even though the wasp didn't land on their hand at all. So it's mostly matter of chance and speed at which the hand moves. I successfully killed many wasps by clapping my hands on them in flight. But when some got between the fingers, I got stung.

I think what your friend advised is incorrect, or they are very lucky.  According to "Bee and Wasp Stings" from the University of California Davis, they specifically state:

Unless someone accidentally collides quite hard with or swats at a bee or wasp, it is not likely to sting.

Also, if you swat at some species, they are likely to become agitated, making the situation potentially far worse.

I can confirm that I have often enough slapped a wasp or bee in flight without being stung. The reason is probably pure chance.
It is kind of like asking if a human can bite when slapped. If I come up to you and slap you, fast and hard, you will probably not be able to bite my hand because of surprise and the blinding speed with which I hit you. If, however, you happen to be talking to me and have your mouth open at the time, you might be able to pull off a quick bite.
In a similar vein, if I happen to swap a wasp (no anagram intended) and hit it on the sting, I will probably be stung. If I hit it on the side and move fast enough, I doubt it will have the time to reorient itself and sting me before my hand is gone.

I have many experiences with bees. I avoid swatting bees/wasps, since if you do not agitate them, they fly away and are not interested in humans or exploring human skin. (They are also important pollinators.) If you slap them very hard, you can instantly kill a bee, especially if it collides perpendicularly with a wall afterwards. If you swat it a bit less vigorously, like I did yesterday, my finger got slightly red and itchy; I was partially stung and/or the venom was transferred to my finger, which is normally stored in a cuticular sac in the abdomen of the bee and is quite potent, given its small volume.
Don't hurt bees and they can't hurt you. If you agitate bees, they will defend themselves. Any insect of sufficient size and mass can be hurt with a blow of sufficient energy. Tiny fruit flies are too small for a slap, large moths, bees, dragonflies can be slapped down when in flight.

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


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Can food swallowed when a person is upside down reach the stomach?
If a person positions him/herself upside down and swallows food, will it reach the stomach against gravity? If so how?

http://en.wikipedia.org/wiki/Swallowing#Pharyngeal_phase, phase 11. So... yes

The eminent @JanDvorak has basically provided the full answer, but yes, it is possible.  You can easily try this yourself, just lean off a bed and swallow something (small) and see what happens.  Peristalsis in the esophagus is responsible for moving food down into the stomach.  The big proof of this is that astronauts can eat when in space, when weightless.  Their food is moved into the stomach just fine.
It's easier to do it upright (peristalsis + gravity) as opposed to upside down (peristalsis - gravity) but definitely quite possible.

It is not a good idea to experiment with this just like that. A part of food can enter your larynx and bronchi and eventually lead to aspiration pneumonia.

Yes it is possible. As I myself have experienced it.I was doing a headstand when I tried it.It does take a lot of time but does reach the stomach.


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Elevated transaminases after blood transfusion?
This sparks HCV immediately in my mind.
However, there may be other possibilities too.
What can you deduce from elevated transaminases if you only know that the healthy adult patient received blood transfusion in Africa?


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Are there specific conditions that allow humans to see ultraviolet wavelengths
It is fairly common knowledge that the lens in its normal state absorbs ultraviolet (UV) radiation.  An interesting notion has come up from time to time in my reading that suggests there are a small number of conditions that result in humans being able to 'see' ultraviolet.
What conditions may cause this?  Also, those affected, would they 'see' it has a different shade of violet?

You will be interested in Aphakia, which is the lack of an eye lens usually through surgery but sometimes from birth.  These individuals supposedly see UV as a whitish-blue or whitish-violet:

This appears to be because the three types of colour receptor (red, green and blue) have similar sensitivity to ultraviolet, so it comes out as a mixture of all three - basically white, but slightly blue because the blue sensors are somewhat better at picking up UV.1


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What does the evidence suggest about how Neanderthals became extinct?
According to "Neanderthals: Facts About Our Extinct Human Relatives" (Szalay, 2013), Neanderthals dominated Europe during the last Ice Age, but may have died out before the arrival of Homo Sapiens (according to research detailed in "Radiocarbon dating casts doubt on the late chronology of the Middle to Upper Palaeolithic transition in southern Iberia" (Wood et al. 2012).
There are a number of theories floating around in the literature - everything from inability to adapt to climate change  to dietary deficiencies.
What does the latest research suggest as the cause of the Neanderthal extinction?
(refereed papers would be appreciated)

This is one of those active areas of research where there isn't a lot of consensus among researchers. There isn't even consensus as to whether it was an extinction in the strictest sense, because we now have evidence from genomic research that Neanderthals interbred with modern humans. Research is still being done on a lot of different hypotheses.
This article by K. Harvati is a decent short summary of the current state of the field, and includes references to recent articles.


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Human body power consumption in still state
I'd like to know what kind of power human body needs to maintain life, in still state (average daily power consumption of an average man is also of interest). In terms of watts.
I've only managed to find one figure - 1700 kcal per day without physical activity. That converts to 80 watts, which seems (intuitively) a bit low, so I wonder if it's the right figure or not.

1700kcal=7000kJ=a lot of ice turned into steam. Actually @Amory 7000KJ isn't going to turn that much ice into steam If you ask how much quantity of heat is required to convert 1 kg of ice into vapour then you have to add latent heat of fusion that is 336 kj/kg and latent heat of vaporization 2257 kj/kg (these two process occur at constant temperature so need to add rise in tempeature) So it will be:
Q= 1×336 + 1× 4.18 ×100 + 1× 2257
Q = 3011 kj Or 3.01 Mj So you can turn ~2.33 KG ice at 0° into steam at 100° with that energy.

You're basically correct.  I don't know if you've found the Wikipedia article on Basal Metabolic Rate but it's got everything you need, including a bunch of formulas you can use to figure out an average value for a given body type.  There are also many online calculators, such as this one.  You can easily figure out averages, which I think is what you want, but between two individuals the number can change quite a bit.
Why does 80 watts sound so low?  This is more of a physics.se answer, but Watts are a unit of power which mean they measure energy use over time; W=J/s, or Joules per second.  Every second.  Have you ever touched a 75 watt lightbulb?  They're hot as hell.  If your human does nothing all day, s/he will be like an inefficient incandescent lightbulb on for a full 24 hours.  Maybe that seems low but electricity is relatively cheap these days.  To use another classic physics experiment, 1700kcal=7000kJ=a lot of ice turned into steam.
No wonder my father always made me turn the light off in the bathroom...

A bulb is exactly what I thought about. Temperature is inversely related to surface area. Body has much higher area than a bulb, so will have much lower temperature given the same power dissipated, and it has to maintain 37C. And not all power consumed by body dissipates as heat. But that's just intuition, like I said. I didn't do the math.


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Does animal fat and meat contributes differently to our body?

Is animal fat harmful to our body or is it harmful if the amount eaten exceeds a certain amount?
I have heard fat is more concentrated than protein. If I am correct then we can get more energy from fat. Then why is fat not desirable?
Our ancestors used all the parts from their hunt, even the fat. How did it work for them?
Would eating fat be beneficial for an athlete? (May be for different purposes: power, endurance or building muscle)

Have you read the Wikipedia article on Fat?  It has literally all of the answers you are seeking.  However...
1: Every single thing is bad for you if you get too much of it.  Animal fat, sugar, water, you can over-do it on anything.  Fat can be bad for you but it is definitely required.  In particular, "Vitamins A, D, E, and K are fat-soluble, meaning they can only be digested, absorbed, and transported in conjunction with fats. Fats are also sources of essential fatty acids, an important dietary requirement."  Fat does a host of other things, as mentioned in the article.
2: Fat is indeed a concentrated store of energy, but there's more to life than just energy.  Protein, like other nutrients, are required for life.  Protein happens to be particularly important, providing the structure for all our cells, is required for muscle growth, and provides amino acids, which are needed to make other proteins in your body.  Proteins are used as hormones, cellular messengers, immune receptors, so on and so forth.  You couldn't live without protein.  Energy, while concentrated in fat, could come from elsewhere.
3: It worked just the same for them as for us.  I will add, however, that our ancestors did not necessarily use every part from every animal, and these days, we actually use every part of many animals, just not always for food.
4: Sure?  Energy is good, but protein is probably better.  "Athlete" is a vague term, as strength-training and endurance activities are very different from each other.  Protein is probably better for strength, carbohydrates are probably better for endurance.  But you can ask over at https://fitness.stackexchange.com/.


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Is this necrotizing skin infection caused by Staphylococcus aureus?
A 5-year-old boy returns from summer camp with several minor cuts and abrasions on legs. He has fever
and extensive cellulitis, subcutaneous tissue and muscles are involved. Necrotic tissues were surgically
reomoved and broad spectrum antibiotics were used. Which of the following microorganisms usually
causes necrotizing fasciitis?

a. bacillus cereus
b. clostridium tetani
c. A-group streptococci
d. Micrococcus sp.
e. Staphylococcus aureus

It is so severe that I started think that Staphylococcus aureus is possible.
My previous answer was A-group streptococci, but I disagree with it now.
What is causing the case?

if broad spectrum are being given chances are that it will be staph aureus because nowadays resistance to multiple antibiotics is being found in it.

@biogirl broad spectrum antibiotics are the standard first step in treating just about any infection.

@terdon You are right.I just thought that  because the question specifically states "broad spectrum" it may hint at staph aureus.I may be wrong.

At the moment, I am not sure what is the right answer. I am wondering still between C and E.

It is not mentioned in the question about the time period, how long it took that the surgeon was done from  the incident. If it was done very fast after incident, then I would pick Staphylococcus aureus. However, I do not understand its pathology yet.

I still cannot find any reason for C, since it is not pneumonic. The fever is only related to the symptoms of necrosis. Staph aureus is related with post-operative wounds which may imply that also minor cuts and abrasions can cause it. So most support goes for Staph aureus at the moment.

Murray says that the answer is C for cellutitis and necrotizing fasciitis in a table, but I have found no explanation. I want to understand why.

@Masi Have you read the article on Necrotizing fasciitis on wikipedia ?

Yes, but my books cover the topic much better and deeper. They say that the answer is C by empirical evidence.

Staphylococcal infection is more likely to cause abscesses and Streptococcal infection is more likely to cause cellulitis. It is not clear how a 5 year old did not get medical attantion till he got to this serious state. Why was culture not done? Surgical removal of necrotic tissue due to cut and bruises? doesn't tally with cellulitis. Incision and drainage is a standard proceedure for absecesses, is that what was done? Is this a hypothetical question?

I do not know. I hope it is.

No. It is caused by A-group streptococci. Source Murray and empirical evidence.