text:
MOL2 to PDBQT conversion via OpenBabel and MGLTools removes hydrogen atoms
I am trying to convert a MOL2 file (includes partial charges and hydrogen atoms) into a PDBQT file for re-scoring in AutoDock Vina. However, both approaches that I tried don't keep the hydrogen atoms from the MOL2 file (the PDBQT file doesn't contain hydrogen atoms).
The command I used for OpenBabel is
babel -i mol2 my.mol2 -o my.pdbqt

When I look at the documentation, they babel has a dedicated "-d" flag for removing hydrogens. So I assume that this shouldn't happen by default?
The same thing happens if I use MGLTools
prepare_ligand4.py -l  my.mol2

Any ideas of what might be going on here?
Thanks for your help!
will append the MOL2 file if someone wants to try it:
@<TRIPOS>MOLECULE
mymol2
   25    25     0     0     0
SMALL
USER_CHARGES
@<TRIPOS>ATOM
      1 C1         -1.0341   29.2934  -14.5590 C.ar      1 <0>       -0.1745
      2 C2         -0.1917   29.9513  -13.6630 C.ar      1 <0>       -0.1483
      3 C3         -2.3919   29.1585  -14.2689 C.ar      1 <0>       -0.1608
      4 C4         -0.7068   30.4744  -12.4770 C.ar      1 <0>       -0.0956
      5 C5         -2.9070   29.6816  -13.0828 C.ar      1 <0>       -0.1543
      6 C6         -2.0573   30.3323  -12.2033 C.ar      1 <0>       -0.0209
      7 C7         -5.0136   30.3602   -8.9792 C.2       1 <0>        0.9092
      8 C8         -1.1556   29.8264   -9.1470 C.2       1 <0>        0.9071
      9 C9         -2.6151   30.8987  -10.9189 C.3       1 <0>       -0.0262
     10 C10        -3.5221   30.2951   -8.6255 C.3       1 <0>       -0.1568
     11 C11        -2.5717   29.8912   -9.7583 C.3       1 <0>       -0.1554
     12 O1         -5.7013   31.2223   -8.3667 O.co2     1 <0>       -0.8817
     13 O2         -0.7003   30.9084   -8.6799 O.co2     1 <0>       -0.8929
     14 O3         -5.3714   29.5329   -9.8669 O.co2     1 <0>       -0.8807
     15 O4         -0.6188   28.6818   -9.1887 O.co2     1 <0>       -0.8571
     16 H1         -0.6331   28.8861  -15.4824 H         1 <0>        0.0899
     17 H2          0.8655   30.0564  -13.8891 H         1 <0>        0.1079
     18 H3         -3.0478   28.6460  -14.9665 H         1 <0>        0.0917
     19 H4         -0.0427   30.9855  -11.7849 H         1 <0>        0.2049
     20 H5         -3.9661   29.5717  -12.8653 H         1 <0>        0.1145
     21 H6         -2.0757   31.8190  -10.6595 H         1 <0>        0.0142
     22 H7         -3.6485   31.2140  -11.1119 H         1 <0>        0.0547
     23 H8         -3.4370   29.5769   -7.7988 H         1 <0>       -0.0109
     24 H9         -3.2268   31.2722   -8.2199 H         1 <0>        0.0482
     25 H10        -2.8394   28.8903  -10.1212 H         1 <0>        0.0739
@<TRIPOS>BOND
    1     1     2 ar
    2     1     3 ar
    3     2     4 ar
    4     3     5 ar
    5     4     6 ar
    6     5     6 ar
    7     6     9 1
    8     7    10 1
    9     7    12 1
   10     7    14 2
   11     8    11 1
   12     8    13 1
   13     8    15 2
   14     9    11 1
   15    10    11 1
   16     1    16 1
   17     2    17 1
   18     3    18 1
   19     4    19 1
   20     5    20 1
   21     9    21 1
   22     9    22 1
   23    10    23 1
   24    10    24 1
   25    11    25 1
@<TRIPOS>SUBSTRUCTURE

EDIT:
The solution to the problem with prepare_ligand4.py would be
prepare_ligand4.py -l  my.mol2  -U \""" -C

to keep the partial charges and hydrogen atoms (oddly, -U "" didn't work for me: prepare_ligand4.py: option -U requires argument)

You saw my last answer of your question? you can do that easily, just use
prepare_ligand4.py -l  my.mol2 -A "hydrogens"

Thanks, I didn't see that you updated it. But one important question: in the help menu it says "-A type(s) of repairs to make:" does it add hydrogens or does it preserve the original ones?

It will add all hydrogens. The algorithm is like that. You can always manually edit the hydrogen in a pdbqt file.

I mean you can always delete extra hydrogen if it isn't present in your original mol2 file.

Thanks, but this is very inconvenient: I like to preserve the input-hydrogen atoms that are present in the mol2 file with their assigned partial charges.

Yes I know.have your tried: -U ""

-U "" alone might stop merging of hydrogen to the nearest carbon.

Did that worked?

I tried it, according to the documentation http://mgltools.scripps.edu/api/AutoDockTools/AutoDockTools.Utilities24.prepare_ligand-pysrc.html it should work, but when I run prepare_ligand4.py -l my.mol2 -C -U "" I get a prepare_ligand4.py: option -U requires argument

Remove the -C, just check finally if it changed your partial charge any way.

Same problem with and without the -C, somehow it is not accepting the empty string for the -U parameter. Thanks for all your help btw, I really appreciate it!

Let us continue this discussion in chat.

Thanks a lot, just got it to work if I use  -U \""" Thanks for all your help, problem solved :)

Wow, all good then. If you have any problem regarding Docking software you can contact me.

What about the other one, you got the vina results?

With other one you mean "OpenBabel"? One of the two would be sufficient for the conversion - got Vina to work after preparing the pdbqt files. However, I noticed that the re-scoring output is less detailed as in AutoDock4.2, for example, it does provide hydrophobic and hydrogen bonding contributions, but not electrostatic energy

In babel:
babel my.mol2 my.pdbqt -xh

-x states options for writing .pdbqt files
-h says keep hydrogens


text:
How much divergence would be needed for classifications as astrobiology?
It is possible that life has invaded mars or the moon by way of probes rovers and other man made tech. How many years or generations of sequential and phenotypical diverge would be  necessary to establish the organism as astrobiology?

Are you asking how long an organism must live in a non-earth environment before it is considered astrobiological?

Yes i am @nbogard

Well, it is just a matter of definition. You can make up your own choice!

I think if life was transferred to either body on a probe, it would not count as alien yet because it could not have had time to develop very far on its own, since all probes are recent evolution wise. These would be offshoots from earth life. Truly alien life would most likely use different biochemistry because it originated in a different planet, it would be a totally different tree of life. However, the presence of life on the moon or mars, even if just contaminating earth bacteria, would be incredibly important for astrobiologists, as it would provide direct evidence that life can survive in these harsh environments. Life on the moon would most likely be dormant bacteria, because there is no air or water or food. However, if bacteria could survive prolonged exposure to space and be revived upon entering a suitable environment, that would provide evidence for panspermia. Read this: https://en.wikipedia.org/wiki/Surveyor_3
If panspermia is true, then those aliens might not be that unrelated after all. But until we find one, we can't make any conclusions.

Awh I learned a new word panspermia thank you

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
How does sucrose protect bacterial cells in lysozyme solutions?
I have a microbiology question.
When we put bacterial cells in sucrose solution with concentration higher than 0.5M we observe plasmolysis - the cytoplasmic membrane detaches from the cell wall due to water loss in order to balance the osmotic gradient.
If after that we put some lysozyme in the solution, the cells become spherical as they turn into spheroplasts, but they are still alive.
If we put lysozyme in a solution that contains bacterial cells, but no sucrose, they die. So my question is how does sucrose protect cells from lysis?

What kind of bacteria did you use, gram positive or gram negative?

Gram positive, Bacillus megaterium.

hemolysis: this term is used with reference to RBCs

I beg your pardon. What I actually meant to say was plasmolysys, I always mistake those 2 words.

This is an interesting question and as often, it has been noted by someone before. In this case it has been a researcher named Claes Weibull, who did his research in the 1950s. He noted (as you did) that sucrose has a protective function on the generation of protoplasts from Bacillus megaterium) with lysozyme. He published the following figure (from the first paper below):

He did not really explain the phenomenon, but speculated about protective function of the sugar in solution when the bacterial cell wall is removed. This also works with PEG in solution (see the third paper below).
He published a number of papers on this (if you look him up in Pubmed, you will find more articles, but these seem most relevant):

The isolation of protoplasts from Bacillus Megaterium by controlled treatment with lysozyme
Characterization of the protoplasmic constituents of bacillus
megaterium.
Osmotic properties of protoplasts of Bacillus megaterium.

It seems also possible to cultivate these protoplasts on agar plates and let them form "normal shaped" bacteria again:

Morphological study of the reversion to bacillary form, of Bacillus
megaterium protoplasts.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Can foxes move their ears independently?
I've read that dogs can do move their ears independently, i.e., point one ear in the direction of a sound without having to point the other one at the same time. Is this a common trait with other canids, such as foxes? Can most eared mammals do this, with humans being an exception (except for a few exceptional humans)?

Yes, they can. Here are a couple pics I found of foxes moving their ears independently:

This is something all canids can do (1)(2) Btw, I can move my ears independantly. It's all in the finding the right muscles.

How can you tell from a still photo that only one ear is moving?

@daniel Easy - because it is swiveled from it's natural position. Red foxes will point both ears at one thing if paying it full attention. The foxes pictured were pointing both ears in different directions, because apparently two things were catching it's attention.

Not easy for me. Your reference (1) does not support your point directly and  reference (2) is to a book with no page number. Can you please find a reference that directly supports the point?


text:
How do ants know where they are going without eyes?
I know that ants have some sense of direction, but what is the physiology behind this sense?

The eyes are easily seen on green ants. In other genera you may have to look more carefully to notice the eyes.

Well, first off, they have eyes, so there's that.
However, a lot of what ants wish to achieve can be done through a combination of a random walk and chemical trails.
When ants are exploring their surroundings, they are essentially wandering about without much in terms of a sense of purpose; laying down a chemical signature as they go.
When they find something interesting, like food, they use their own chemical trail to backtrack, laying down a new chemical trail indicating the nature of what they have discovered, making a kind of smell-road from the hill to the point of interest.
Any ants that subsequently come across this trail follow it, and subsequently join in transporting the food back to the hill.
An interesting implication of this behaviour is the antmill, wherein an ant will lose their trail, and revert to following a nearby ant. If the ant they follow are following them to begin with, this can lead to a spiral of ants that can reach miles in diameter, consisting of confused ants walking until they die from exhaustion.

This is the correct answer. The behaviour just described by Williham is btw so simple (though effective) that it can be modelled in simple agent-based simulations. The underlying set of rules is a very basic one. One example: https://www.youtube.com/watch?v=UZ2HTTeM3aQ

Kindly elaborate more on the "chemical  signature" part? @Williham Totland

@Cupidrex That was just me being unclear; I meant chemical trail as in the other paragraphs; and strictly speaking antmills arise due to ants following one another by sight, not smell.


text:
Why does cracking a joint make noise?
What causes the noise when you crack a joint? Is joint cracking harmful?

The exact mechanism is unclear. Here are some possible causes:

rapid collapsing of cavities inside the joint [1];
rapid ligament stretching [1];
breaking of intra-articular adhesions [1];
escaping gases from synovial fluid [2];
movements of joints, tendons and ligaments [2];
mechanic interaction between rough surfaces [2], mostly in pathological situations like arthritis (and it is called crepitus [3]).

There are no known bad effects of joint cracking [1, 4].

There are no long term sequelae of these noises, and they do not lead to future problems. There is no basis for the admonition to not crack your knuckles because it can lead to arthritis. There are no supplements or exercises to prevent these noises [4].

And no good effects either:

Knuckle "cracking" has not been shown to be harmful or beneficial. More specifically, knuckle cracking does not cause arthritis [5].

References:

Wikipedia contributors, "Cracking joints," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Cracking_joints&oldid=617403659 (accessed July 22, 2014).
The Library of Congress. Everyday Mysteries. What causes the noise when you crack a joint? Available from http://www.loc.gov/rr/scitech/mysteries/joint.html (accessed 22.07.2014)
Wikipedia contributors, "Crepitus," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Crepitus&oldid=615557134 (accessed July 22, 2014).
Johns Hopkins Sports Medicine Patient Guide to Joint Cracking & Popping. Available from http://www.hopkinsortho.org/joint_cracking.html (accessed 22.07.2014)
WebMD, LLC. Will Joint Cracking Cause Osteoarthritis? Available from http://www.webmd.com/osteoarthritis/guide/joint-cracking-osteoarthritis (accessed 22.07.2014)

It might cause your significant other or roommates to go crazy and bop you on the head, though.

I don't really see how anyone can say that there is no benefit.    Only based on my experience, there is a reason for cracking a joint.   Before cracking it, it "feels odd".  Afterwards that feeling is relieved.   Just because we don't know why that is, doesn't mean it's not beneficial.   At the very least, subjectively it was beneficial, immediately.

I believe I read that cracking your fingers causes reduced grip strength for some period of time. I cant recall the duration. I suppose that could be a slight negative but it eventually the grip strength is returned to normal.

I can crack joins all day, so how's this so hard to figure out for scientists? It's not something you need years to wait for, it happens all the time...

I used to crack my fingerjoints a lot, and noticed that my fingers had become a lot weaker. Not sure if actually weaker, but playing piano had become a lot harder. Some anecdotal information if anyone's interested.

Is joint-cracking harmful?  No.  Donald Unger was told by his mother that he'd get arthritis if he cracked his knuckles so he cracked his left knuckles every day for 60 years but never his right knuckles. He had no arthritis or any other problems in either hand and got a publication (D. L. Unger, "Does knuckle cracking lead to arthritis of the fingers?", Arthritis and Rheumatism 41(5):949–950, 1998 – online version for those with appropriate access) and an Ig Nobel Prize (2009) for his troubles.
OK, so one guy's knuckles prove nothing but who can resist the opportunity to cite an Ig Nobel winner?

A paper was just published that explains this phenomenon in PLOS One, found here. It looks like the sound is caused by the formation of a gas cavity in synovial fluid of the joints. They do mention that contrary to what is stated in the most upvoted answer here, the sound does not come from the collapse of the bubble, but rather its formation.
And in response to the comments, as mentioned in the paper, this does not seem to cause any harm to the meniscus or surrounding tissue.


text:
What attracts cells to: pathogens, professional antigen-presenting cells, and cells with an antigen on its MHC-1 protein?
I have a few questions in regards to attraction/stimulation in the immune system.

What attracts leukocytes and antibodies to pathogens in the first place?
What attracts CD4+ cells to professional antigen-presenting cells (APC)?
What attracts CD8+ cells to cells with an antigen on a MHC-1 protein?
What attracts macrophages to pathogens that have been tagged with antibodies?

Is it just a case of everything bumping into each other and if cells (and antibodies??) bump into chemokines and/or cytokines they will be stimulated (and not attracted) to stay around that area moving to an area of a greater concentration of chemokines and/or cytokines?
That said point 1 can occur without chemokines and/or cytokines (in the case of antibodies, they could be taken/administered by the person).  While in case of point 3, (I may be wrong here) but chemokines and/or cytokines may not be present in the case of MHC-1?

What attracts leukocytes and antibodies to pathogens in the first
  place?

They just bump into them. If secreted antibody is already present in the blood then complement system can be activated.

What attracts CD4+ cells to professional antigen-presenting cells
  (APC)?

APC release chemokines. All that is known is that this is a CC-type chemokine and signals via CCR4/CCR8 receptors. See this list of articles (from Google Scholar). This study reports a peptide called Chemrin that promotes chemotaxis via ChemR23 receptor.

What attracts CD8+ cells to cells with an antigen on a MHC-1 protein?

CD8+/NK cells are activated by CD4+ cells before they kill their target. The MHC-1+antigenic peptide is just a mark for the cells that are to be attacked, as far as I understand.

What attracts macrophages to pathogens that have been tagged with
  antibodies?

Complement factors.
NOTE: Many of these concepts are old but still relevant. You should check out recent articles in this area for novel/atypical mechanisms.

Regarding the answer to the first question: yes, if we are talking about circulating pathogens. But if the pathogen has cytotoxic effects on a tissue, the release of damaged cell components may attract immune system cells by chemotaxis.

yeah forgot to add that.. Cells can release type-1 interferons.

Brilliant, thank-you! I've been reading up on the self non-self theory & the danger theory..So was trying to arduously identify some of the danger signals that were already present.  And thank-you @Cornelius


text:
How does Sodium Valproate cause neural plasticity
I have been reading a fascinating paper: Valproate reopens critical-period learning of absolute pitch
18 individuals were given Sodium Valproate (VPA) for a fortnight during which they trained on a pitch-training game. Results suggest that VPA reopens the plasticity window that normally closes by adolescence.
However, the paper seems to suggest that the exact mechanism of action is unknown.

Valproic acid is believed to have multiple pharmacological actions,
  including acute blockade of GABA transaminase to enhance inhibitory
  function in epileptic seizures and enduring effects on gene
  transcription as an histone deacetlyase (HDAC) inhibitor (Monti et
  al., 2009). Of relevance here is the epigenetic actions of this drug,
  as enhancing inhibition does not reactivate brain plasticity in
  adulthood (Fagiolini and Hensch, 2000), but reopening chromatin
  structure does (Putignano et al., 2007). While systemic drug
  application is a rather coarse treatment, the effects may differ
  dramatically by individual cell type (TK Hensch and P Carninci,
  unpublished observations). VPA treatment mimics Nogo receptor deletion
  to reopen plasticity for acoustic preference in mice (Yang et al.,
  2012), suggesting a common pathway through the regulation of
  myelin-related signaling which normally closes critical period
  plasticity (McGee et al., 2005). Future work will address the cellular
  actions of VPA treatment in the process of reactivating critical
  periods. Future MRI studies will also be needed to establish whether
  HDAC inhibition by VPA induces hyperconnectivity of myelinated,
  long-range connections concurrent with renewed AP ability (Loui et
  al., 2011).

So it is saying that the standard use of VPA is to increase GABA levels (which keeps firing rate down -- it is used as an antiepileptic), however it also acts as an HDAC inhibitor, which means it causes unwrapping of chromatin and consequently increased mRNA transcription, maybe even transcription of genes that would normally be entirely deactivated in an adult.
So my guess is that some protein is getting produced that messages neurons to generate new axon/dendrite growth and/or new synaptic connections.
Can anyone clarify how VPA might accomplish plasticity?
EDIT (one month later): I have more detail, but I still can't quite make the connection. Here goes:
Neurites get wrapped by myelin/oligodendrocyte, which produces and exudes some of the chemical messagers {Nogo, OMgp, MAG}. The membrane surface of the neurite contains nogo 66 receptors (NgR-s) that get triggered by these messagers and inform the neuron to inhibit axon-growth. Somehow the 'HDAC inhibition' property of VPA is unwinding DNA enough to alter transcription rates of certain proteins, and one of these must be disabling the NgR.
But how is this happening?

This paper might be of some help http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3907704/

As far as I can see this paper is being a little misleading, by saying "VPA mimics Nogo-66 receptor deletion".
The action of VPA doesn't seem to be related to this receptor.
It seems that blocking this receptor and applying VPA both increase plasticity, but via different mechanisms.
VPA seems to facilitate LTP through increased availability of relevant proteins (as an HDAC inhibitor, it "loosens/unwinds" DNA, allowing for increase in protein transcription). And by increasing protein transcription across the board, it may be increasing the availability of proteins that promote synapse formation.
The principal problem with growing new structure is, as hinted at the end of the question, that the adolescent/adult brain secretes a chemical that gets picked up by Nogo 66 receptor, which signals to collapse the axon growth cone.
It's why adult humans can't recover from spinal injuries. The axons won't reconnect.
It so happens that a small molecule Nogo Antagonist has recently been developed by Professor Strittmatter.  He was kind to reply to my query, and I learned that this molecule is currently in the early stages of FDA approval. It's a very exciting discovery!
I would caution anyone considering taking VPA to balance it with a beta-blocker (e.g. omeprazole). It is an acid, and if not balanced with something to reduce the stomach's ability to produce acid, risks acid reflux, which may force a change of diet, and be longterm/permanent. So, DYOR.
Also of note is that (again discovered by Strittmatter) Ibuprofen has been found to also interrupt the signalling pathway that leads to axon growth collapse. But it requires a high dosage, and ibuprofen also causes a similar imbalance.

Can you provide a link to the paper regarding the receptor antagonist? Also, the anecdotal evidence seems to be very unscientific and I recommend that it be removed.

@MarchHo http://www.ncbi.nlm.nih.gov/pubmed/12037567 -- also, that is a terrible idea to remove valuable information (that, as it happens, has been scrutinised by an Oxford educated medical professional). Anyone considering taking VPA should be forewarned and educated.

@Pi anecdotes as basis for medical advice aren't really appropriate for this site - otherwise very good answer that I'd be happy to upvote.

ok 7 years later, I agree. I have cleaned the answer, and also filled in a couple of blanks from memory.

Please add references while you're on it. -1

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


text:
biologically speaking, what's the difference between sleeping and just resting?
I can lay down in a rested position with my mind at ease, but no matter how relaxed I am or for how long i do it, it seems I'll still need sleep eventually.  What's the difference - what is occurring during sleep that can't occur now matter how relaxed or rested you are?
And if you know of any studies that have been done to try and mimic the benefits of sleep in a waking state - ie during some type of meditation or whatnot - I'd consider that relevant and interesting to know.

I wish i could give a one word answer: brain-activity..

@WYSIWYG As that would be the epitome of "vague", I'm glad you can't. :)

haha sorry but it is the brain activity that is different between sleep and just physical rest.. al you need is details :P

@WYSIWYG you bring up an interesting point actually because I had thought something similar - that your brain must be takin a rest, but then I thought to myself: dreaming has to be pretty brain-intensive, no?  we're often creating scenarios that frequently don't even follow the same rules of existence as our waking world.  It seems to go far beyond normal waking reverie; isn't that taxing on the brain?

@coburne Personally when I dream during my sleep, I think I am not refreshed and I feel weariness.

Difference between rest and sleep
There are many factors which describe the difference between rest and sleep.
Rest
Rest occurs with conscious breathing. This allows the autonomic nervous system (ANS) to rest. The autonomic nervous system belongs to the peripheral nervous system. ANS controls many organs and muscles in the body.
In most situations, people do not know about the workings of the ANS since it functions in an involuntary, reflexive manner. For instance, we hardly notice if blood vessels change size.
This is the same case when our heart beats faster. There are some people who can control some of the functions in the body and can know the heart rate or blood pressure.
Sleep
Sleep it is a natural state of rest for mind and body. It happens in cyclic pattern. This can be one of the reasons to describe the difference between rest and sleep. There are four stages of sleep.
In the first stage of sleep, there is low-frequency, low-amplitude $\theta$ waves. This stage last several minutes before you enters into the next stage of sleep. In stage 2 of sleep, you brain moves into low frequency. In the third stage of sleep, you receive more high-amplitude $\delta$ waves.
During stage 4, the delta waves account for more of your brain activity and then they return back to stage 1.
Resting is more like being couch potatoes.
Rest is important for health and sleep is a necessary factor. You need both for your physical and mental activity to create energy. When the energy level goes down and wastes increase, there is tiredness and body needs rest. When you take rest, energy is restored. All the waste in the body gets extinguished. Rest and sleep are dependent upon each individual’s ability to relax. If an individual is tensed, he cannot be in the state of rest. Rest is taken to counteract fatigue.
Source:
[1] http://www.theatlantic.com/health/archive/2012/09/when-you-cant-sleep-how-good-is-lying-in-bed-with-your-eyes-closed/262484/
[2] http://insomnia.ygoy.com/difference-between-rest-and-sleep/

+1 for Resting is more like being couch potatoes.. Just kidding. This is a pretty good answer.

REST is not a deep sensation. We define various types of waves that are drawn using electroencephalogram.

$\alpha$ waves:

Awake but resting position.
Frequency: 8-13 Hz.
They originate from occipital region

$\beta$ waves:

Alert wide awake person.
They originate from frontal region.
Frequency about 14-30 Hz.

$\theta$ waves:

They occur under stress and in case one is drowsy.
Frequency about 4-7 Hz.

$\delta$ waves:

These originate when person is in deep sleep.
Frequency about 1-3 Hz.

does the lower frequency correspond to lower ionic activity by all neurons, or the same ionic activity per neuron, but fewer active neurons; ie, if I'm at a football game and everybody is screaming, decibel levels are high, but everybody talking at once might have the same lower decibel leval as 90% of people completely quiet and 10% of the people screaming.


text:
Causes of Misophonia
Whether it's snacking on chips, munching on salad, or simply chewing gum, when I hear someone do it within an earshot, it drives me completely bonkers!
It doesn't matter if it's my girlfriend, my mom, someone sitting next to me at the office, or random stranger on the train, it bothers me just as much. The "mouth open" chewing type makes me want to get violent, and I often find myself in a blind rage. I also notice the slower, and more "deliberate" the chewing/munching is, the more I get tense and more it bothers me.
Sometimes I feel like they are doing it on purpose, and completely fake, sort of like a commercial where they exaggerate the act of eating.
I want to know more about Misophonia or "Hatred of Sound"?

Misophonia

Misophonia is a relatively unexplored chronic condition in which a
person experiences autonomic arousal (analogous to an involuntary
“fight-or-flight” response) to certain innocuous or repetitive sounds
such as chewing, pen clicking, and lip smacking. Misophonics report
anxiety, panic, and rage when exposed to trigger sounds, compromising
their ability to complete everyday tasks and engage in healthy and
normal social interactions.1

Physiology
The auditory pathways may be functioning normally, but there is an abnormally strong reaction of the limbic (emotional system) and autonomic nervous system (body control system) to which the auditory system is intimately connected.
Several definitions are listed for the disorder, including:

“Abnormally strong negative reactions of the autonomic and limbic systems to specific sounds resulting from enhanced functional connections between the auditory and limbic systems for these sounds.  The auditory system works in a normal manner, without abnormally high activation.  At the behavioral level, sounds specific for a given patient evoke strong negative reactions.  This situation may cause general negative attitude to sound as well.  When fear is dominant emotion (patient is afraid of sound) phonophobia occurs (phobia – fear).  Phonophobia is a specific case of misophonia.”

“Selective sound sensitivity should be considered a type of misophonia, where soft sounds (typically eating and breathing sounds made by emotional attachment figures) are the focus, and the quality of those sounds causes annoyance and rage in the listener.”

“Pre-puberty seems to be a very common age of onset for the majority of those with misophonia, with lifetime persistence for most cases, and there appears to be a genetic component.”

“Misophonia can be considered abnormally strong connections between the autonomic and limbic resulting from enhanced connections between the auditory and limbic systems.  These connections encompass both a high level of cortical level loop with involvement with cognition as well as subconscious connections, most probably involving the link between the medial geniculate body and the amygdale. The functions of these connections are governed by the principles of conditioned reflexes.”

(source: wordpress.com)

(source: wordpress.com)

source:
1 Misophonia: physiological investigations and case descriptions
[2] MISOPHONIA 4S Provider Network USA
Great Site: http://lifewithmisophonia.wordpress.com/

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


text:
Cross section of actin network in neurites
for a simulation I am developing I would like to know how the actin network in neurites is distributed.
Is actin confined to the periphery or is the whole neurite shaft containing actin with a rather constant density?
If you have any papers backing up the one or the other view don't hesitate to pass the link.
Thanks for answering.

does this help? (http://www.neuraldevelopment.com/content/pdf/1749-8104-6-27.pdf)

on first sight this paper only gives a 2D distribution of actin over the whole neuron or? I would like to know what you would see if you cut a neurite and subsequently look "into" the cross section. Is the actin only found on the outer part of the cross section or evenly distributed across the circle?

Just look at papers doing confocal microscopy/imaging of actin with z-stacking (z refers to the axis) since thats the main approach people use for 3D imaging and people also use delta vision microscope with z-stacking and deconvolution.

Actin is required for the neurite architecture and is present throughout the shaft (along the direction of the neurite process)
See these images.

                                        [Source]

                                             [Source]
These are not from research papers but the sources are trustworthy.

From those images I would not deduce that the neurite shaft has a substantial actin skeleton but rather a small amount of "misguided" filaments. Is that right?

Why would you assume some misguided filaments? The region indicated as meshwork is essential for the structure.

In the second picture actin and tubulin are labeled. I cannot see any actin along the shaft except of growth cone areas. So there is no substantial amount of actin concentrated along the shaft. Or?

OK I didnt understand what you meant by shaft. I thought you were referring to the filopodial region. Yes actin is not abundant in the axonal regions


text:
Microbial Fuel Cell Reaction
I found a formula online which explained the reaction which occurred in the anode chamber of a microbial fuel cell but there was a typo
$\small NADH + Ferredoxin_{(ox)} (NADH-Ferredoxin\ Oxidoreductase) \longrightarrow NAD^+ + Ferredoxin_{(red)}\ \
Ferredoxin_{(red)} (Hydrogenase)\#61614;Ferredoxin_{(ox)} + 2H^+ + 2e^-$
I attempted to correct it but I'm not sure if I'm right could you check this and see if it's correct?
$\small NADH-Ferredoxin\ Oxidoreductase \longrightarrow NAD^+ + Ferredoxin_{(red)}$
$\small Ferredoxin_{(red)} \longrightarrow Hydrogenase + Ferredoxin_{(ox)} + 2H^+ + 2e^-$

This the page? http://www.altenergymag.com/emagazine.php?issue_number=07.04.01&article=haldia

Anode reaction,
$\small Glucose + 2NAD^+ (Embden-Meyerhof pathway) \leftrightharpoons 2 Pyruvate + 2NADH$
$\small Pyruvate + Ferredoxin_{(ox)} (Pyruvate-ferredoxin Oxidoreductase) \leftrightharpoons Acetyl-CoA + CO_2 + Ferredoxin_{(red)}$
$\small NADH + Ferredoxin _{(ox)} (NADH-Ferredoxin Oxidoreductase) \leftrightharpoons NAD^+ + Ferredoxin_{(red)}$
$Ferredoxin_{(red)} (Hydrogenase)\leftrightharpoons Ferredoxin_{(ox)} + 2H^+ + 2e^-$
[Last one: http://en.wikipedia.org/wiki/Ferredoxin_hydrogenase]
Cathode reaction,
$4 H^+  + 4e^- + O_2 \leftrightharpoons H_2O$
$C_6H_{12}O_6 + 6O_2 \leftrightharpoons 6 CO_2 + 6 H_2O, DG° = - 2870 kj$
Full paper: http://www.altenergymag.com/emagazine.php?issue_number=07.04.01&article=haldia


text:
How do mushrooms react to being grown in a microgravity environment?
I'll use Agaricus Bisporus as an example mushroom. If cultured in potato dextrose yeast extract agar, will the resulting growth grow in a normal pattern? Will the sporocarps emerge from the surface (assuming there is one) properly? Will they develop inside the agar, or emerge an an angle?
Will the plant develop at a normal rate, and to normal proportions?

There were some experiments done in microgravity in longer space shuttle missions. The reports show that the fungi develop relatively normal but grow in random orientations instead of orientating upwards. See this images:

The upper image shows fungi grown on earth which are subjected to normal gravity. The lower image shows fungi (actually only the fruiting bodies) which are grown during 7 day on the Spacelab D2 mission. The fungi obviously have a way of detecting gravity to let their fruiting body grow upwards. The image is from here, the article contains more information about this.
There is also a publication in this topic:

Mushrooms in microgravity - Mycology at the final frontier

Thank you Chris. I guess I didn't search long enough.


text:
Is it possible to genetically modify a plant at home?
Would I be able to genetically modify a plant at home? What equipment will be necessary? I think it might be a fun change from the 'norm' of regular hybridisation, to try some inter-family gene insertion, instead of staying within a genus. Are some plants easier to modify than others?

You might also have to consider any regulations that might exist in your country. In some countries genetic modified organisms can only be handled in designated laboratories.

@MadScientist Do you know of any such regulations in Pennsylvania, United States?

The USA regulates the product of genetic engineering, not the process, so there are no federal regulations (some state/county laws may be different) to prohibit you. Most likely you cannot just release the plant into the wild though as it may require USDA approval (depending on the genes inserted and method of inserting them).

This q. is a follow-up to the the above problem....can't it be simply done by creating a hybrid??...I mean that too is a genetic mix-up & will show features diff. from the parents..

@souvik But you cannot add genes from out of the genus this way, so not the same. I've hybridized plenty of plants in my time, including some quite nice roses.

Oh...I get it...so try something like this- http://biohaxlab.site90.com/lib/Gene%20Expressing/Luciferase%20Gene%20in%20Plant%20Cells.pdf ...it's cool..

Well, that depends on your home. ;) I think it is not an easy process.
There are two main methods that are used to genetically modify plants:
Using the bacterium, Agrobacterium tumifaciens, as a vector for the DNA. Agrobacterium has the ability to infect plants and insert DNA into a plant's genome. It causes crown gall tumours in natural infections. This method has mainly been used to modify broad leaved plants, such as sugar beet and oilseed rape, but is now also being applied to monocot species, such as maize and rice
Particle bombardment or biolistics where the DNA to be inserted is coated on minute gold particles and fired into plants cells. This approach is used for monocot plants such as maize and rice
Here I found simple step by step article, but lil bit old. may be there are new methods for this process.
How To Genetically Modify a Seed, Step By Step

What equipment might I need?

With agrobacterium, a usual practice is to dip the flowers in the bacterial suspension (Floral dip). You would need the bacteria, culture media and your gene inserted in the agrobacterium Ti-plasmid.

Meh add elctroporation or suffer the pains of a -1 ;p

Yes it is. The easiest plant to transform would be Arabidopsis, which can be transformed by agrobacterium using the floral dip method. The process would be as follows:
1. Design a gene sequence you wish to insert into the plant
2. Synthesize (or otherwise acquire the DNA)
3. Insert the DNA into your agrobacterium, at home you would use a cold snap transformation process described here: https://www.youtube.com/watch?v=PvkfIECvyqs This can be done at home using a dry ice bath.
4. Then use the floral dip method to insert the dna into the plant. This involves growing a plant to just the right age when it is flowering and dipping the Arabidopsis flowers into a solution of the agrobacterium.
5. Then grow the flowers to seed and grow the seeds on a suitable select able marker (which you designed into your DNA plasmid).
The specific experimental conditions needed to do all this are too long for this answer, but you can look them up online as all the procedures are standard.
Plants which result from this process would not be legal to release into the wild due to USDA regulations.
Engineering other plants, depending on the species, can be more complex but could possibly also done at home. There are even designs online for an open source gene gun if you didn't want to use agrobacterium.

genetic modification can be done with mutations. A mutation is a permanent change in the sequence of DNA. In order to obtain an observable effect, mutations must occur in gene exons, or regulatory elements. Changes in the non-coding regions of DNA (introns and junk DNA) generally do not affect function.
Mutations can be caused by:

external (exogenous) factors, such as chemicals and radiation

or

endogenous (native) factors

Mutations can be advantageous and lead to an evolutionary advantage of a certain genotype..this will be a solution for your plant modification..
A mutagen is a physical or chemical agent that changes the genetic material, usually DNA, of an organism and thus increases the frequency of mutations above the natural background level.
chemical mutagens:

Bromine
Sodium azide
Psoralen
Benzene

long term treatment plant with mutagens caused mutations some might be advantage
then select advantage ..
 As many mutations cause cancer, mutagens are therefore also likely to be carcinogens!

Yes, It is.
An Indian Company IndieBB can help you get one.
IndieBB: a DNA system designed to help you and your friends to explore genetic engineering and synthetic biology by making fluorescent bacteria at home.

That's pretty cool! How about plants?

I haven't watched the youtube video completely, but I think they are pretty good.

Do you mind expanding to the other points I asked about?

How fresh do the hair follicles have to be?

@J.Musser: I haven't tried it myself. but I think it had to be fresh. PS; I don't know how you will get it with follicles??

That's a Mimosa pudica, or "touch-me-not". This won't work.

@DevashishDas Thank you for removing the reference to the hoax video, however this refers to bacteria, not plants, and links to a defunct indiegogo campaign.

@user137 I can't delete the answer till it is unselected as the correct answer.

Not to forget that simple cross breeding your plants the Mendelian way also modifies their genetic make up, as @souvik bhattacharya indicates in his comment. No equipment necessary, no chemicals, no ethical issues.

But you cannot add genes from out of the genus this way, so not the same. I've hybridized plenty of plants in my time, including some quite nice roses.

@J.Musser: you're right, but across-species gene insertion is not mentioned in the question anywhere - I'm just answering the question

My bad, I edited my question to clarify.


text:
What causes morning wood?
Sometimes men wake up with an erection in the morning. Why does this happen?

Sometimes men wake up with an erection in the morning. Why does this happen?
Shortly speaking: REM (Rapid Eye Movement) is one phase of sleep. During this phase, we dream and some of our neurotransmitters are shut off. This include norepinephrine, which is involved in controlling erections. Norepinephrine prevents blood from entering the penis (preventing the erection). In absence of norepinephrine—during REM phase norepinephrine is absent—blood enters the penis, leading to an erection. This phenomenon is called nocturnal penile tumescence. Such erections typically occur 3 to 5 times a night. A related question concerning similar erections in women can be found here.
High pressure in the bladder may also lead to a "reflex erection". This erection allows for preventing uncontrolled urination. The drawback is that when in the morning one has an erection and can't wait to pee it might get hard to accurately target the toilets!
This video is also a nice and easy source of information on the subject.
Is it bad?
(Reading my "note" below, you have edited your post to get rid of this question, thank you)
It is perfectly healthy you don't have to worry about that. These erections are even thought of as contributing to penile health. At the opposite end of the spectrum, the absence of erections during the nights are an index of Erectile Dysfunction (E.D.).
Note
Be aware that medical questions are often considered off-topic on this site. Asking "is it bad?" turns your question into a medical one. Health-related questions (but not personal health) should be asked on health.SE


text:
Why are watermelons sweeter in the center?
Today I had a slice of watermelon and when I reached the outer parts of the pulp I wondered why those are less sweet.
Whether or not the sugar occurs in crystalline form in watermelons is still an open question, but a quick search on the internet did not yield acceptably thorough answers.
The options I found are as follows (in descending order of personal preference):

Watermelons ripen from the center outwards.
If this is the case, then watermelons wouldn't grow during the ripening, right? So they would need to achieve their final size before the ripening sets in. Or maybe it's the other way around: They ripen as they grow, and as such the center has the highest concentration of sugar.
The sugar is needed by the new seedlings to grow. (Although I think this hypothesis has been disproven with apples.)

Has any of this been proven, has there been research done on this matter?

I think the cells are smaller in the center, so higher concentration of everything but water. The outside cells have a lot more space and are more watery without so much sugar, etc.


text:
Does a presence of ants on a plant mean that the plant has been infested by aphids?
Ants protect aphids from their predators (such as ladybirds):

Aphids and other hemipteran insects secrete a sweet liquid called honeydew, when they feed on plant sap. The sugars in honeydew are a high-energy food source, which many ant species collect. In some cases, the aphids secrete the honeydew in response to ants tapping them with their antennae. The ants in turn keep predators away from the aphids and will move them from one feeding location to another. (source: wiki: Ant)

Does a presence of a large amount of ants on a plant in my garden (especially fruit trees, willow trees, flowers, vegetables) mean that the plant has been infested by aphids?
It's easier to spot the ants rather than the relatively smaller aphids so I am wondering if I may use this as a trigger for using an anti-aphid pesticide before the aphids start causing visible damage to the plants.

On the last paragraph, never treat for pests unless you know they are there. Ie, wait until you see aphids or actual damage. Ants do not necessarily mean aphids.

When I see the actual damage it's already too late. And also for early fruits I must not apply the pesticides too close to the harvest time. So any early clue gets useful.

@J.Musser perhaps you should post that as an answer. presence of ants does not mean presence of aphids.

Simple answer is no:
$Ants \neq Aphids$
However, they could be used as evidence that aphids are there depending on the reliability of the coexistence. Ants and aphids are independent entities and do not rely on each other so can exist in non-overlapping populations. Applying this idea to the correct species of ant and aphid is, of course, important for it to work as an indicator - it will only be true in those combinations where this "aphid protection" occurs.
I can't find any information on the reliability of the relationship, especially not knowing which species you are looking at. If there was a high positive correlation of ant density and aphid density then one would expect the presence of ants to be a good indicator to the presence of aphids. If the correlation is low there is a higher chance of a false positive (where a false positive = when you see ants, conclude there must be aphids, and there are no aphids).

What are the other possible reasons why you may observe a lot of ants on a plant/twigs?

@HonzaZidek Probably means some resource (food, water source, etc.) the ants "want" is on, or accessed by moving along, the plant you are observing - can't say more without knowing very specific details about the ants, plants, and aphids you are seeing, maybe watch some of the ants (follow individuals and see where they go).


text:
Dark veil when getting up too fast
I was asking myself this weird question.
When you get up or stand up too fast, sometimes, you see something like a dark veil, and you aren't able to see anything distinctly for 2 or 3 seconds, then it come back to normal.
Do you know what causes this weird phenomenon (biologically speaking), or am i the only weird person feeling this sometimes?

If your interest is academic then you may wish to look further into orthostatic hypotension. I don't know why this causes visual disturbances however.

the eyes can lose vision easily when they don't get enough oxygen or are otherwise impaired.  I'm reminded of diabetic retinopathy - temporary eyesight loss happens when blood flow to the eyes are interrupted.  this can be a sign that the cardiovascular system isn't as efficient as it should be!

»[…] or am i the only weird person feeling this sometimes?« Nope, definitely not.

It's caused by a sudden shift in the pressure needed to circulate blood to your brain which your body fails to respond to sufficiently quickly. This results in a sudden loss of blood pressure termed Orthostatic Hypotension which, in term, results in a transitory reduction in the blood supply necessary for brain function. You experience a momentary loss of vision for the same reason that you would if someone strangles you.

wow!! Never knew this exists. Can you add some more references?

Are other brain functions also affected when this happens?

Other brain functions may indeed also be affected. Dizziness is another possible effect, as one example.

I would describe it more as a fading of colors and peripheral vision.


text:
How many different protein coding genes are in the Human Biome?
There are approximately 20k protein-coding genes found in the human genome. This number is presumably very small when considering all the genomes found in the diverse microbes associated with the human body.
Is there an estimate for the total number of protein-coding genes found in human microbiome?

What is the relation between microbiome and human genome?

Sorry, I mean only the human microbiome.

Still?? Microbiome is the micor-organisms in human body. http://en.wikipedia.org/wiki/Microbiome

Yes, I'm asking how many different genes are associated with a human and its resident symbionts, i.e. the number of protein-coding genes in the human genome + the number of protein-coding genes in the human microbiota.

The Human Microbiome Project collected samples as shown in the image below from healthy volunteers:

They give an estimate of about 8 Million genes in the human microbiome, which is about 360x the number of genes in the human genome. See here for their press release with a lot of information. Additionally these two articles are as well interesting, if you want to dive deeper into the stuff:

A framework for human microbiome research
Structure, function and diversity of the healthy human microbiome

Human Microbiome Project
According to Published data on HMP website:

The human microbiome consists of all the microorganisms that reside in or on the human body.
They may cause illness but some are necessary for good health.
There total count is 10 times more than Human cells.
~800 genomes had been sequenced.
~5000 Human sample had been used.
Include 14 disease project samples.
Total data stored on the DACC resource is 14 terabytes.
Total protein(~8 million) coding genes found to be 360x of number of human genes

Source:
[1] http://en.wikipedia.org/wiki/Human_Microbiome_Project
[2] http://commonfund.nih.gov/hmp/index

These look like numbers for the human genome only.

If I had to guess, I'd estimate there are at least hundreds of thousands of different protein-coding genes associated with a human.

I know. Can you edit the question, it is actually confusing? You need to know the number of genes in human Microbiome which have an effect in human genome?

Thanks @Devashish I tried to clarify the question. I hope it makes more sense. And no, the genes do not have to be known to affect the human genome; they just need to be resident.

"360x more abundant than human genes" looks like a good answer. So, probably millions of genes.

Would you consider exactly same genes from different microbes as different genes? By gene do you mean the genes in the genome or gene products?

The main text of your answer is entirely copied from a Wikipedia article. While you mentioned the source at the end of your post, you didn't mark the text as a quote. This is still plagiarism and not allowed on this site. You have to make clear any place where you quote a source verbatim. Answers should also not be taken entirely from external sources, they should be in your own words and quotes should be only for support.

@WYSIWYG I think I would consider the same gene found in two different microbe species to be different as they operate within a different genomic environment. But I'm not sure. I imagine that there is a lot of mutualistic sharing of gene products between microbes, and probably some horizontal gene transfer as well. The answer I'm most looking for is some quantification of genetic and molecular information.


text:
Where can I find a list of common enzyme cofactors and/or co-enzymes?
Where can I find a list of enzyme cofactors and/or co-enzymes, ordered by how common they are?
For example, $O_2$, $H_2O$, $ATP$, $ADP$, $NAD$, should be ranked in the first places, because they participate in most reactions.

$H_2O$ is not a cofactor for any enzyme.

Also oxygen cannot be called a cofactor. It is just an electron acceptor- in a way a co-enzyme.

@WYSIWYG I have edited to include co-enzymes.

Check this out. This resource lists organic cofactors and the associated enzymes.
See the wikipedia page also.
Many metals also serve as prosthetic groups in enzymes. They include- Magnesium, Manganese, Iron, Cobalt, Nickel, Copper, Zinc, Molybdenum.
FeS clusters are also an important part in many important enzymes in mitochondria and plastids.

Cofactor:
coenzymes are organic molecules that are required by certain enzymes to carry out catalysis.
Database:
CoFactor - The organic enzyme cofactor database of EBI
Examples:


text:
Re-solidify disturbed agar plates
I am stuck in trouble while pouring LB agar onto my petri dishes. I had to add kanamycin to my plates just before it started to solidify, out of forgetfulness, which I tried to mix using the tip. The plate was such a disaster! Is there a way to melt the agar in the plate and re-solidify it evenly.
I use falcon sterile plastic petri dish.

Yes. It is quite simple actually. Do this inside a clean laminar hood:

Take a clean sterile scalpel blade or any other sterile long object. 1ml pipette tip would also do.
Cut the agar on your plate. Scrape off cleanly.
Put it in a sterile glass bottle.
Heat in microwave
Add kanamycin
Pour back

Another solution is to coat the agar surface with kanamycin just like spread plating. Check the appropriate concentrations.

If the agar has solidified with a nice surface, I would prefer the spreading technique. Works pretty nice and is definitely much less hassle (and contains less contamination problems) than removing and remelting. Before spreading, dry the plates open so they can take up the liquid.


text:
Why do we feel cold on having fever?
Why do we feel terribly cold on catching fever of any sort, however our body becomes hotter?
Why is it that a rise in temperature makes the sufferer feel colder? Also, sweating symbolises betterment of the conditions. Why?
{This question has been asked with reference to personal experiences}

Body temperature results from a balance between the heat generated by our cells and the heat “lost” to the environment. Heat created by our cells comes from the energy used to keep us alive. Heat is lost through our skin and the air we breathe out. Human beings have an average temperature of 98.6 degrees Fahrenheit. The brain monitors body temperature and controls our bodies to keep our temperature within the normal range.
If you get a fever when you’re sick, it’s because your brain has told your body to get hotter. It directs the body to make a number of changes to correct the imbalance. Those changes include increasing heat production within the body (by shivering, for example) and reducing heat loss to the environment. Heat loss is reduced by decreasing blood flow to the skin.

Why are some fevers also accompanied by chills and shivers...like, the malarial fever...?

@Shamayeta: same reason, body try to heat up by shivering.

@Devasish Sir: My bio book refers to HAEMOZOIN that is responsible for the shiver during malaria. How does haemozoin work to raise the body heat?

@Shamayeta: Can you ask this as a separate question, it's long answer.

@Devasish Sir: I shall be doing it.


text:
Gender and age-specific mutation rate in plants
Background
General concept
According to Cochran and Harpending (2013), mothers transmits on average a number $x$ of new mutations to their offspring. This number $x$ is independent of the age of the Mother. Fathers, however transmit a number of new mutations to their offsprings that is very much dependent on the age of the father for developmental reasons. In short (and probably poorly stated due to my lack of knowledge in physiology), spermatogenesis is a continuous process that occurs during the lifetime of the individual while the creation of ovules occurs once and are then stocked.
Human example
According to Kong et al.(2012), in humans the mother transmit on average $15$ new mutations and the father transmit on average $25 + 2(g-20)\space\space$ new mutations, where $g$ is the age of the father. For example, a 30-year-old father transmits $25 + 2(30-20) = 45\space\space$ new mutations. (This approximation holds only for men older than 20 years).
Question: How about plants?

Do you think that in plants too, male and female organs (or individuals for (gyno/andro)diocious species and eventually sequential hermophroditic species) transmit a different number of new mutations for similar developmental reasons?
Do you think that in plants the number of new mutations is age-dependent in males but not in females alike in humans?
Do we have any estimate of the sex and age-specific number of new mutations transmitted in plants?

The age dependency for males is because of continuous spermatogenesis (older spermatogonia might acquire more mutations). Oogenesis however, happens quite early in development and oocytes are locked at metaphase. Female age also matters and is evident in case of aneuploidies. I dont know the mutation rates in plant germline but I suppose it is higher in pollens because they are more exposed to sunlight and other environmental factors.

Why would age matter in females in case of aneuploidy? It is not evident to me. I didn't think of external factor such as sunlight, that's interesting. So, does pollen go through continuous spermatogenesis in plants too but not ovules just like in animals so that we could expect the same pattern than in animals even increased by the sunlight. @WYSIWYG Thank you

female age correlates with non-disjunction of chromatids- leading to aneuploidy. See this.. Usually in many plants flowering happens throughout life (both gametes produced). Some plants however flower only once per lifetime. For some it is periodic. So depending on the flowering pattern, the spontaneous mutation rates may vary.

@Remi.b: Have a look at these: http://jxb.oxfordjournals.org/content/57/9/1847.full and http://web.udl.es/usuaris/e4650869/docencia/segoncicle/genclin98/recursos_classe_(pdf)/revisionsPDF/mut%26variat.pdf

From Whittle and Johnston (2006):

Specifically, human epidemiological data and/or nucleotide substitution rates of selectively neutral DNA (which equals the mutation rate, Kimura, 1983; Miyata et al., 1987) have shown that more mutations occur in the male than in the female germ line for numerous animal taxa (e.g. humans, mice, chickens, and sheep) and in older rather than younger human males, patterns that each agree with the cell-division hypothesis (i.e. more DNA replications in males and in particular older males; Penrose, 1955; Risch et al., 1987; Becker et al., 1996; Moloney et al., 1996; Li, 1997; Green et al., 1999; Crow, 2000; Li et al., 2002; Makova and Li, 2002). Other data, however, have indicated that the mutation bias reported relative to gender and male age are not generally well correlated with the number of germ cell divisions and that other factors could explain these trends, such as methylation patterns, differential repair, metabolic rates, and preferential transmission of mutations to pro- geny from older males (Risch et al., 1987; Martin and Palumbi, 1993; Drost and Lee, 1995; Bromham et al., 1996; Hurst and Ellegren, 1998; Martin, 1999; Crow, 2000; Huttley et al., 2000; McVean, 2000; Sommer et al., 2001;Hebert et al., 2002; Hurst and Ellegren, 2002; Kumar and Subramanian, 2002; Li et al., 2002; Bartosch-Harlid et al., 2003).

…so basically we don't really know whether difference in gametogenesis between males and females lead to more sex and age-specific mutation rate!
However, Whittle and Johnston (2006) in reviewing many articles also show that old seeds are more likely to carry chromosomal aberration and that old individuals are more likely because of the instability of their metabolism to transmit more mutations but that would be sex independent and would not result in different gametogenesis as I was expecting in asking this question. Also the kind of mutations that become more frequent with all parents are chromosomal abnormalities or important deletion but not so much substitutions (which was also what I was interested in when asking).
Thanks @DevashishDas for finding this article. This other one was interesting as well.

authors: حنين فوزي عبد الحليم


text:
Why does crying lead to a running nose and reddened nose tip?
Why do we have a running nose for quite some time after crying? It persists even after we stop crying. Why is it so? I have faced this always. Also, why does our nose redden on crying for long?

When you cry, you produce tears, which come out of your tear ducts. These are not only open to the eyes but also have a connection to your nose, see the image below:

A part of your tears runs through this connection and mixes with the mucus which is present in your nasal system making it thinner and allow it to flow more easily. If the tear flow is prolonged, the nose will produce more mucus and make your nose running for a longer time. The nose appears redder because the blood flow is increased. This is partly due to the production of more mucus and also because you repeatedly touch the nose when using a handkerchief.

Thank you for the explanatory answer. The diagram proved to be of immense help.


text:
What does hemozoin do?
My bio book refers to HEMOZOIN that is responsible for the shiver during malaria. How does hemozoin work to raise the body heat?

That is correct. When plasmodium infects red blood cells, it consumes the hemoglobin in the cell, leaving the heme behind, which they can not metabolize (heme is a heterocyclic porphyrine ring with an iron atom coordinated in the center). Since the heme (or $\alpha$-hematin) causes the production of reactive oxygen species and thus oxidative stress, it has to be removed from the cell. This is done by the conversion into the insoluble and inactive hemozoin (or $\beta$-hematin). This crystalizes in the cell and is not causing any harm to the parasite. See here for more details.
When the parasite finishes this development step, the cells burst and set their interior free into the blood stream. Among the substances released in this step are hemozoin and also glucose phosphate isomerase which stimulate macrophages to secrete cytokines and other factors which then cause the fever and the shivering observed in malaria.
See here for more details:

Hemozoin Induces Macrophage Chemokine Expression through Oxidative
Stress-Dependent and -Independent Mechanisms
Malarial pigment hemozoin and the innate inflammatory response.
Effect of malaria components on blood mononuclear cells involved in
immune response.


text:
What is the female equivalent of the morning erection that some men experience?
There was question about what causes "morning wood." It was answered that the erection in the morning is caused by decline of norepinephrine during REM sleep. Which in part allows to prevent uncontrolled urination.
My question is: How does the decline in norepinephrine affect women? They obviously don't get erection.

This question is protected to prevent "thanks!", "me too!"... - that's quite funny protection :)

Women have erections too! These erections are called clitoral erection. Clitoral erections are usually accompanied with vaginal lubrification.
Just like men (see here), the absence of norepinephrine during the REM phase of the sleep causes erections. In women, this phenomenon is called Nocturnal clitoral tumescence while it is called Nocturnal penile tumescence in men. In women, not only the clitoris get engorged with blood but the vagina too.

You sure? Because I have only had 1 typical sign of a female orgasm and only once. And I haven't been sexually active in my life. What I felt was a vaginal contraction. For a few seconds it felt like I could control menstrual flow. I myself have never had a clitoral erection though I have had noticeable vaginal discharge increase related to my menstrual cycle.

@Caters It is not a sign of orgasm just like discharge isn't. Both can be signs of arousal. Clitoral (and vaginal) erection possibly results in outer (closer to the entrance) vaginal tightening and as far as I am aware (I don't have a vagina, so I can only rely to womens' reports) if one touches clitoris when there is no erection it is not as pleasant (or even unpleasant) feeling than when there is an erection. But it might be the case that not every woman has these.


text:
What limits the speed of human perception?
I'm writing a novel in which the main character's perception and thought processes are sped up considerably, in essence slowing down the world around him. To others, it seems like his reactions are far faster than normal. Of course, there's a fantasy explanation for this in the story, but it led me to wonder exactly what limits the speed of human perception and reasoning in the real world.
From what I know, the speed at which we perceive events appears to be a constant. What exactly determines that rate? Is it possible to change it? Is it possible that different people perceive things at different speeds?

Actually there is a movie on this concept- Limitless..
You can check this post. You may find it useful.

The vertebrate photoreceptors may have a certain speed threshold, so you can give him mutant fly photoreceptors. Chimpanzees can see 10 different objects on a screen and choose one of them much faster than a human, perhaps it's to do with peripheral vision. you can have mutant connections between the old and new areas of the brain which can learn reflexes perfectly.

Flicker Fusion Threshold:
The wikipedia definition:

It is defined as the frequency at which an intermittent light stimulus appears to be completely steady to the average human observer.

Background
In 1824, Peter Mark Roget (who also wrote the famous Thesaurus) first presented the concept of "persistence of vision" to the Royal Society of London, as the ability of the retina to retain an image of an object for $\frac{1}{20}$ to $\frac{1}{5}$ second after its removal from the field of vision.
A second principle - the $\phi\ phenomenon$ or stroboscopic effect is closely related to flicker fusion. It was first studied by Max Wertheimer and Hugo Munsterberg between 1912-16. Wertheimer and Munsterberg found that subjects can perceptually bridge the temporal gap between two consecutive displays, so that a series of static images appear as continuous movement. The discovery of flicker fusion became the perceptual basis for moving pictures, television, and all media based on stroboscopic presentation of stimuli.
The minimal frequency at which flickering stimuli appear continuous is called the critical flicker frequency.

Perceptual factors affecting the critical flicker fusion threshold
This critical flicker fusion threshold depends on the stimulus’

Luminance (the Ferry-Porter law),
Size (the Granit-Harper law),
Color,
Retinal eccentricity,
Background Luminance, and other factors.

Biology Behind it:

Physiological evidence in humans and monkeys shows that flicker rates
  above the perceptual critical flicker frequency threshold can
  nevertheless generate cortical and subcortical visual responses.  Thus
  the temporal integration underlying flicker fusion does not occur at
  the level of the retina,  but must take place later in the visual
  hierarchy. Single-unit recordings in the primary visual cortex of
  primates suggests that,  for two brief-duration targets presented in
  close succession, the after-discharge to the first  target interferes
  with the onset-response to the second target (Macknik, 2006) (see
  Figure 5). The onset-response to the second flash is absent for
  inter-stimuli intervals of 30 msec or shorter (equivalent to 17 Hz
  periodic). If the flashes are separated by more than 30 ms, the
  after-discharge to the first flash and the onset-response to the
  second flash begin to recover (i.e. equivalent to <17 Hz flicker).
  These intervals roughly coincide with the critical flicker fusion
  threshold in humans for 100% contrast stimuli in the fovea .
This suggests that perceptual flicker fusion may be due to the lack of
  robust transient responses to the flickering stimulus.

http://images.scholarpedia.org/w/images/thumb/8/8b/Flicker_fusion_fig5.png/360px-Flicker_fusion_fig5.png

Source:

Bartley (1939). Some effects of intermittent photic stimulation. Journal of Experimental Psychology 25, 462-480.
Bloch, A. M. (1885). Experience sur la vision. Comptes Rendus de Seances de la Societe de Biologie, Paris 37, 493-495.
Brücke, E. (1864). Über den Nutzeffect intermittierender Netzhautreizungen. Sitzungsber k Akad Wissensch Math-naturw Cl, Wien 49, 128-153.
Di Lollo, V., and Bischof, W. F. (1995). Inverse-intensity effect in duration of visible persistence. Psychol Bull 118, 223-237.
Ferry, E. (1892). Persistence of vision. Amer J Sci 44, 192-207.
Fukuda, T. (1979). Relation between flicker fusion threshold and retinal positions. Percept Mot Skills 49, 3-17.
Flicker Fusion

What is the Different speeds of Visual Perception?

First-order motion
Experiment: A moving sinusoidal grating with bright peaks and dark troughs is seen through a window.
Result: Even when its velocity is so high that 30 of its bright peaks pass each location per second (30 Hz), observers still perceive its direction of
motion.

Depth from binocular disparity
Experiment: Two identical gratings, one in each eye, are viewed through identical windows.
Result: One is spatially shifted relative to the other, introducing a binocular disparity that is perceived as depth.
Even when they move at a 30 Hz rate, the depth is still perceived.
If the input to depth mechanisms were blurred at a >30 ms timescale, detecting the depth would be impossible at this rate.
Edges and texture boundaries
Experiment: Against a gray background, a field of white dots is adjacent to a field of black dots.
Result: Both fields are set in rapid alternation between white and black, but out of phase – when
one is white, the other is black. The conspicuous boundary between them is perceived even at fast
rates of 30 Hz, whereas at faster rates the black and white are averaged by the brain into the same color as the background.
http://ak.picdn.net/shutterstock/videos/3139525/preview/stock-footage-retro-geometric-dot-background-in-black-gray-and-white.jpg
Binding of color and orientation sharing a spatial location
Experiment & Result: If a red, right-tilted patch is alternated with a green, left tilted patch,
it is easy to distinguish from the complementary pairing of red left alternating with green right, even at
fast 20 Hz rates.
Binding of form and color across space
Alternating color-shape pairings can only be reported at rates below ~3 Hz.

source: http://www.psych.usyd.edu.au/staff/colinc/HTML/dynamics.htm
Binding of global form with color
Two specially constructed dot patterns that form distinct shapes alternate, with all the dots of one red and all the
dots of the other green.
At alternation rates faster than several a second it is very difficult to determine the shape color pairing even though the shapes and colors themselves
are easily identified.
Direction change and acceleration perception
A moving stimulus alternates between two speeds (acceleration) or two directions. When the alternation occurs
faster than several per second, these changes are unperceivable.
Its limit is 8-10 Hz.
Word perception
Certain pairs of words (such as ‘jump’ and ‘pink’), when alternated in the same location, cannot be distinguished
from another matched pair at rapid rates as one perceives only the sum, which is the same for both pairs.
They can be distinguished only at rates slower than several items per second.

Source: http://www.psych.usyd.edu.au/staff/alexh/research/words/
Source:

Holcombe AO (2009) Seeing slow and seeing fast: two limits on perception. Trends Cogn Sci 13:216 –221.
http://www.psych.usyd.edu.au/staff/colinc/HTML/dynamics.htm

Hi, nice response! but I'm still wondering which part in your response shows the limiting factors/reasons behind the human perception speed limitation. You have a very nice list of perception/cognitive limitations but not the underlying reason. Are there explanations for these limitations that can be elaborated through neurophysiology or molecular biology perhaps?

Definitely some interesting material that you've shared here, Devashish Das, but I also would be interested in the underlying reasons that the human perception rate is limited. You don't seem to have talked about that too much here--looking forward to hearing more from you.

@Bez: Oh Sorry!! You were asking about Flicker fusion threshold!!!

The limitations are of several natures: cognitive once the signal has arrived in the brain, but also physical within the eye e.g. for vision.
For vision, the crucial bit is to transform changes of incoming light into an electrical signal. It is not completely elucidated. Recent research shows e.g. that for some flies, there may be a mechanical intermediate stage: the light-sensing cells react by contracting, and this would modify the electric resistance of their membrane. I don't think it is known whether the human, who have less need for a fast response but want more detail of what they're looking at, have the same mechanism or not: maybe your hero has something of the fly that we don't have?

Here's a paper on the link between perception and reaction time. The general theme in biology is that the greater number of neurons an animal has in series, the more latency that animal will have in that pathway. This can partially account for organisms which have tiny nervous systems and very quick reflexes.
In our own body, we have reflex pathways which entirely circumvent our brain. These help us maintain our posture and remain upright. These are muscle spindles and spinal reflexes. They are among the quickest response mechanisms.
You might want to look up synaptic pruning and synesthesia. These are two phenomena on opposite ends of the spectrum of synapse count. Synesthesia is an excess of sensory pathways in the brain and synaptic pruning is the natural deletion of pathways in the maturing brain.
Most of our movements are variations on muscle memories, mediated by the cerebellum. You can start your research on muscle memory here. Developing muscle memory is a rigorous process, but is a fundamental learning tool for musicians and those in martial arts.


text:
How can flies sense mirrors?
I've noted that flies in my house have no problem landing on even perfectly clean mirrors. Why don't they fly straight into them? Can they sense that there is a surface there, even though they can't see it?

I think it should be glass rather than mirrors

@casey Yes, but flies will often fly into a window, while the same fly will land on a mirror.

Maybe fly vision isn't very good, but good enough to see the outside through the window, while a mirror reflects the wall across from it, so it looks like a wall. Try to put a mirror across from a window and see if flies treat it like a window.

@user137 Hmm, interesting theory, but if the fly has any depth perception, wouldn't it see the wall (if it can) as far away? It has no reason that I can see to know there is a surface at that point

@J.Musser, That's why it's an experiment, I don't know anything about the visual acuity of flies. Maybe the mirror reflects more glare from the lights around it, while a window appears to have less reflection because any reflection would have to compete with sunlight behind it.

IDK what is your mirror, but flies definitely bump into my room's mirror constantly.

It might be pretty straightforward. Common window/mirror glass is opaque to UV, so as far as the fly is concerned mirrors are just translucent surfaces.
This of course leads to the question of why flies can't see window glass. Maybe the large amount of light passing through at visible frequencies makes it look like a tinted fog to the housefly? Maybe they're trying to fly through mirrors too, but land on their feet and just roll with it?

First link doesn't appear useful anymore.


text:
Is there some genetic variance underlying music appreciation?
Is there any research done on the genetic variance for Music appreciation?
If not, why is there no genetic variance for this trait?

It is important to understand what genetic reason behind .. means. It usually makes much more sense to ask Is there some genetic variance underlying music appreciation?. You may want to have a look to this and/or this post. You may, then eventually want to edit your question.

@Remi.b: Sounds better!

I wouldn't vote to close but I think your question deserves a little editing. Is there some genetic variance underlying music appreciation? Not gene variance. Is there any research done on the gene responsible for Music appreciation? This assumes there is only one gene. I'd suggest to stick to the formulation using genetic variance. I consider it is a detail but that might be important to you given that someone voted to close! What do you mean If not, is there any reason its impossible to predict? Does it mean If not, why is there no genetic variance for this trait??

Yes, it looks much better to me! Well.. I personally have no idea! The only think I can say is that such studies in humans are likely to be biased due to the culture and assortative mating.

One can perhaps look at extremes: compare Beethoven (or any other musical genius) with lets say a great mathematician who has no appreciation for music. (That way you have normalized for basic intelligence). But these are just opinions.

Or otherwise if it is just about sound patterns (harmonics), their production and perception then the genomes of a songbird and a chicken can be compared.

@WYSIWYG: Mathematician and Music is actually kind of wrong as both need same region of brain might have some correlation: http://www.ucl.ac.uk/news/news-articles/0214/13022014-Mathematical-beauty-activates-same-brain-region-as-great-art-Zeki

So wouldn't that just mean that music appreciation is correlated with general IQ ??

@WYSIWYG: I don't think so. Still I found this http://www.psmag.com/navigation/books-and-culture/classical-music-linked-to-high-intelligence-27959/

See that is what I was saying. There are no conclusive studies and this question is tending to "primarily opinion based". Did you consider the option of comparing songbird and chicken?

Yeah, this is definitely on topic.

In 2013,
Dr. Liisa Ukkola-Vuoti, University of Helsinki, Finland, done a detailed GWCNV(Genome-Wide Copy Number Variation) Analysis of certain group of people for musical creativity and aptitude.
Genome-Wide Copy Number Variation Analysis in Extended Families and Unrelated Individuals Characterized for Musical Aptitude and Creativity in Music

They did a Genome Wide Copy Number Variations (CNVs) in five extended
pedigrees and in 172 unrelated subjects characterized for musical
aptitude and creative functions in music
Muscial Aptitude is taken as Sum of Scores of Auditory structuring ability, Seashores test for pitch and for time. Along with data on creativity in music was surveyed using a web-based questionnaire.
Several CNVRs containing genes that affect neurodevelopment, learning
and memory were detected.
A deletion at 5q31.1 covering the protocadherin-α gene cluster (Pcdha 1-9) was found co-segregating with low music test scores (COMB) in both sample sets. Pcdha is involved in neural migration, differentiation and synaptogenesis.
Creativity in music was found to co-segregate with a duplication covering glucose mutarotase gene (GALM) at 2p22. GALM has influence on serotonin
release and membrane trafficking of the human serotonin transporter.
Genes related to serotonergic systems have been shown to associate not only with psychiatric disorders but also with creativity and music perception.
Both, Pcdha and GALM, are related to the serotonergic systems influencing cognitive and motor functions, important for music perception and practice.
A 1.3 Mb duplication was identified in a subject with low COMB scores in the region previously linked with absolute pitch (AP) at 8q24.
No differences in the CNV burden was detected among the high/low music test scores or creative/non-creative groups.

In summary, CNVs and genes found in this study are related to
  cognitive functions. Our result suggests new candidate genes for music
  perception related traits and supports the previous results from AP
  study.

Source:
[1] Genome-Wide Copy Number Variation Analysis in Extended Families and Unrelated Individuals Characterized for Musical Aptitude and Creativity in Music
[2] Musical Aptitude Is Associated with AVPR1A-Haplotypes

Interesting study, thank you! It is worth noting that probably these two traits (creativity and aptitude) may be highly correlated with IQ.

@Remi.b: Yes they are. Thanks for not closing this question.

@Remi.b no those traits would correlate more strongly to expertise in a specific field rather than general intelligence. iq measures not genius which is what these genes could potentially spawn with others of course


text:
Hypersensitivity Simultaneously in Ear canals
I got experimental data where hypersensitivity (i.e. tonic pain when touching ear canal) was recognised for about 100 minutes.
I do not know which type of hypersensitivity is this one.
IgM can reach ear canal, I think (not sure) - it is just in the limit.
If IgM cannot reach ear canal, then the hypersensitivity must be caused by

humoral immune system

which is responding slowly to the trigger.
It is proposed that this cannot be contact dermatitis because

the reaction happened simultaneously in both ear canals

after irritating ear canals with plastic the subject is not allergic.
Irritation was also a selected signal which resulted in the dynamic cycle of bass music by Beats earphones.
It was studied the effect of the specific signal with bass music on the movement on the inner membrane on the subject with problem in maintaining the inner physiology of ear itself (also repeated cycle of ear infections during childhood).
Can IgM reach ear canal?
The hypersensitivity was simultaneous in both ear canals.
I did not know before that you can get hypersensitivity reaction in ear canals and also simultaneously.
I think hypersensitivity is not in normal condition.
There must be some etiological factors (probably neuronal) that can cause it.
There are other organs which can have hypersensitivity too.
So I started to think what is the trigger of hypersensitivity.
My conjecture is about Secreted substances of endothelium (EDRF, EDCF).
There are three types of substances secreted by the endothelium

NO
Endothelium hyperpolarising factors
Endothelins

NO is the most important one.
But what is its role in the hypersensitivity of ear canal is unknown to me.
What is the mechanism of hypersensitivity of our body and particularly in the ear canal?

What happened before the hypersensitivity was noticed?

@Chris I answered to your comment. Any allergic reaction caused by the plastic material was minimised. So contact dermatitis not probably.

But you must have a reason to think into the direction of the immune system.

This answer is based on embryological studies and is limited.
I will extend it later when understand better.
Sensory areas

maculae acusticae - walls of utricle and saccule (this most probable area)
cristae acusticae - change in body position

Nerve

vestibular fibers of cranial nerve VIII (TODO each branchial arch has a nerve - how these differentiate between different arches?)

Embryonal Ganglion

statoacoustic (spinal) ganglion (19.5 C Fig)

Embryonal ganglion splits into two

cochlear portion
vestibular portion

which supply sensory cells of organ of Corti, and those of the saccule, utricle and semicircular canals, respectively
Branchial Arches
Each arch has a vessel, cartilage and nerve.
The task is to understand which part of embryonal ear is able to start hypersensitivity reaction.
Middle ear
Tympanic Cavity and Auditory Tube

origin endoderm (1st pharyngeal pouch) - malleus and incus
malleus - 2nd a.a.a.

Eardrum or Tympanic Membrane

ectodermal epithelial lining at bottom of auditory meatus
endodermal epithelial lining of the tympanic cavity
intermediate layer of connective tissue (See Langmans' Fig 19.9B). TODO this part is superficially covered in Langmans.

Auricle

6 mesenchymal proliferations at dorsal ends of 1-2 a.a.a.

TODO I must look again embryonal slides of ear to see where the nerves occur first and how they develop.
Sources

Langmans Medical Embryology, 12th ed, 2011
My notes of Embryology classes, Spring 2014 (I did not have all my notes now so must study these things again after holiday)

Can you be a bit more explanatory? Actually this answer gives a lot of facts without connecting them.

@Chris It is just overview. I will clarify it when I can answer the TODOs. At the moment, I cannot do it.


text:
Does documentation exist that shows the evolutionary connection between common horses and the okapi?
I'm trying to put together some documentation on the relation between the common (modern) horse and the okapi. I've found a tree that shows that connection but it has no references. I'm hoping that someone has documented this connection somehow.

Can you add a link to the tree?

Okapi is like a giraffe right... so you have to go back to a pretty basal ungulate.

I have started to recreate the tree image that I found in Google Docs as a Drawing. Here is the link: https://docs.google.com/drawings/d/19NuQ0BgnUKuYqhabovdEI-UG6Tj3OfcEOb8h23UThIk/edit?usp=sharing

tolweb.org is your friend!
Because the okapi and the horse are not so closely related you will probably find several articles on the subject. Okapi belongs to the order of artiodactyla while the horse belongs to the order of perissodactyla. They are both mammals, eutheria, ungalata (superorder).
Here is the tree of the eutheria (within the mammals) from tolweb. You have approximatively 150 references. You can click on perissodactyla and artiodactyla and you will find 100 more references.
These two references may help you (I only read the titles)

Graur, D., M. Gouy, and L. Duret. 1997. Evolutionary affinities of the order Perissodactyla and the phylogenetic status of the superordinal taxa Ungulata and Altungulata. Molecular Phylogenetics and Evolution 7:195-200
Xu, X. F., A. Janke, and U. Arnason. 1996. The complete mitochondrial DNA sequence of the greater Indian rhinoceros, Rhinoceros unicornis, and the phylogenetic relationship among Carnivora, Perissodactyla, and Artiodactyla (plus Cetacea). Molecular Biology and Evolution 13:1167-1173

My name is Casey and I approve of this message +1


text:
Why do Mangoes have a single large seed, and not multiple small ones?
I was just thinking about this, wouldn't it make more sense for a mango to have multiple seeds, as it would allow more seed propagation?

It is an interesting question and it applies to other fruits with big seeds as the avocado as well. It is very likely that these fruits evolved to be spread by large animals (like big birds or large mamals) which existed for a relatively long time, but are extinct today. These animals swallowed whole fruits and excreted the seeds afterwards (most of these seeds are slighty laxative) together with dung to support the growth.
They are called "evolutionary anachronisms" and there is a very interesting book about them, called "The ghosts of evolution: nonsensical fruit, missing partners, and other ecological anachronisms." (which can be found as a PDF online)
Two interesting articles about this phenomenon can be found here:

The Trees That Miss The Mammoths
Anachronistic Fruits and the Ghosts Who Haunt Them


text:
Any relevant knowledge/studies about voluntary goose bumps
I'm not entirely sure how normal this is, but since I was a child, I've been able to produce myself voluntarily a "chill" sensation that seems to start on my head and traverse the rest of my body, being least intense in the feet. Looking around the internet and forums, looks like other people but not everybody also describe this ability. However, unlike other people's reports, I don't see "goose bumps" on my skin, at least there aren't any visibly; it's just the sensation.
Does anybody know if there are any relevant studies or knowledge out there about "voluntary goose bumps"? Is there even a proper name for that?

Related question: Getting goosebumps at will

Recent studies prove that this involuntary phenomenon must be untrue. Obviously this is false, in order for research like this to take place people need to spend money. It would be interesting if we could create a crowd sourcing account maybe on kick starter to find ways to bring money into the research. I wish I had more information for you, I've been able to do it as long as. When you go to the dentist, just curious, you don't happen to have two bones underneath your tongue that is an anomaly as well? I've been trying to think of correlations for years. I can get the medical terms, if you like. Find me on Facebook Chris Azzy

What you wrote is much more of a comment than an actual answer. Your statement of "Recent studies..." should reference the studies.


text:
Can neurotransmitter depletion cause short-term drug tolerance?
I'm curious to know if neurotransmitter degradation factors into drug tolerance and neural conduction and, if so, to what extent. As I recall from textbooks I read as an undergrad, one mechanism of drug tolerance works by increasing the necessary thresh-hold at a synapse such that larger concentrations of neurotransmitter or more-frequent action potentials in the upstream axon were required to depolarize the membrane and propagate the signal. It seems to me that the same effect would occur if there were fewer available molecules of the required neurotransmitter.
Does over-stimulation of a neural pathway (through the use of a drug or other stimuli that up-regulates a given neurotransmitter) shorten the half-life of the neurotransmitters it uses?
Could a diet which is poor for necessary precursor nutrients cause a person's neurotransmitter concentrations to drop and reduce signaling along specific neural pathways?
Could lack of sleep or other physiological stressors have a similar effect?
I am not a neuroscientist so please correct (and forgive) me if I'm using any terms incorrectly or am flat-out wrong in any of my assumptions.

I don't think the mechanism by which the body no long responds to psychoactive drugs has been found.

But that's just my understanding perhaps someone else will have a better idea

Have a look at this article. Is this the direction you are thinking about?

As I recall from textbooks I read as an undergrad, one mechanism of drug tolerance works by increasing the necessary thresh-hold at a synapse such that larger concentrations of neurotransmitter or more-frequent action potentials in the upstream axon were required to depolarize the membrane and propagate the signal.

Yes - usually through a reduced expression of receptors on the surface. Increasing the drug dosage merely increases the probability that one of the molecules will find the receptor. Chronic exposure of increasingly large doses can dramatically reduce receptor expression. In time, sans the drug, the receptor count will climb back up.
This is why a common cause of chronic drug addicts who have just gone through rehab is overdose: After months in rehab or free of a drug they immediately go back to the amount of drug they were doing before rehab - with some severe side-effects at the least, death at the worst.

Does over-stimulation of a neural pathway (through the use of a drug or other stimuli that up-regulates a given neurotransmitter) shorten the half-life of the neurotransmitters it uses?

No. The half-life of a neurotransmitters is not a major concern; your body will construct them from stored resources if necessary, and healthy neurons have a significant store of neurotransmitters to prepare for multiple firings.
A neuron can be artificially over-stimulated and the neurotransmitter pool emptied (or all the neurotransmitters is bound to its receptor) - but only for Ach receptors at neuromuscular junctions. It hasn't been observed naturally, and not for other types of synapses. This does not result in the muscle no longer responding, but rather it will not respond any faster.

Could a diet which is poor for necessary precursor nutrients cause a person's neurotransmitter concentrations to drop and reduce signaling along specific neural pathways?

Yes, but by that point you're not in good shape, if not courting death. Neurotransmitters are either very common in the diet - like ions - or are constructed from very common constituents of a normal diet - like Glutamine, the most common amino acid.
It would not be a therapy to treat drug addiction.

Could lack of sleep or other physiological stressors have a similar effect?

You would die of lack of sleep first. Your body generally keeps a 30 day supply of absolutely essential vitamins and minerals, and will easily digest itself for precursors to construct neurotransmitters out of.
I have not heard of any physical or mental stress which has reduced the amount of neurotransmitters released into the synapse beyond absolute starvation or artificial scarcity.

No the ttl of neurotransmitters are very important

Your last paragraph makes no sense


text:
Why doesn't Clopyralid damage cool season lawn grasses?
I use Clopyralid (3,6-dichloro-2-pyridinecarboxilic acid) to kill broad leaved weeds in lawns. From my understanding, it works by mimicking an auxin which affects plant growth. Naturally this pulls the chemical to the growing points (stems, roots) of the plant and disrupts the growth, killing the plant.

My question is: Why doesn't this affect cool season lawn grasses (Winter rye, fescues, bluegrass)? It is also considered safe to use on some warm season grasses, but in my experience the results are not always good.

Auxins are a class of phytohormones involved in plant growth and behavior. Auxinic herbicides, such as clopyralid, induce an overinduction of the auxin response in susceptible plants (kelly & Riechers, 2007). From the Kelly & Riechers 2007 article I quote:

[Auxinic herbicides] cause various growth abnormalities in sensitive dicots, ranging from leaf epinasty and/or cupping and stem twisting, to thickening of stems and roots, and ultimately chlorosis and necrosis [...]. Lack of phytotoxicity in grasses has been attributed to several factors, including anatomical differences in vascular structure and differences in ability to metabolize the herbicide [...]

Hence, grasses seem to be protected due to anatomical and metabolic differences. Specifically, auxinic herbicides seem to kill dicots and spare monocots (Song, 2014). Song explains, and I quote:

However, the underlying molecular mechanism of how auxinic herbicides selectively kill dicots and spare monocots is not understood yet [...]. Early research has
  proposed that the selectivity of auxinic herbicide is because of either limited translocation or rapid degradation of exogenous auxin, altered vascular anatomy, or altered perception of auxin in monocots [...] The difference in vascular tissue structure between dicots and monocots may contribute to the selectivity of auxinic herbicides. In monocot stems, the vascular tissues (the phloem and xylem) are scattered in bundles, and lack a vascular cambium; in dicot stems, the vascular tissues are formed in rings and possess a cambium.

So in all, the exact mechanism of specificity between monocots and dicots is unclear, but may be related to structural and/or metabolical (pharmacokinetical) and/or different pharmacodynamical differences between monocots and dicots in general. Dicots are susceptible to auxin herbicides, while grasses, being monocots, are protected.
The complexity of the auxin hormonal system (Song, 2014) may explain why differences exist between grass species, but this is speculative.
References
Kelly & Riechers, Pesticide Biochem Physiol 2007;89:1–11
Song, J Integr Plant Biol 2014; 56:106–13


text:
How does MSMA kill crabgrass with only minimal damage to lawn grasses?
I use MSMA (Monosodium methyl arsenate) to kill crabgrass in lawns. I am not certain of the mode of action.

How does this chemical work? How does it target the annual grassy weeds, without damaging the lawns much?

Please consider this a sort of comment — I tried looking up for articles related to MSMA mode of action but almost all the articles are about its toxicity in mammals.
By what I understand, trivalent arsenates act as phosphate analogs and therefore interfere in phosphorylation reactions including DNA synthesis [Ref].
The weed is affected perhaps because of its relatively higher growth rate. Also the already established lawn grasses would have good population size to regrow out of the damage.