Why is 5S-rRNA is different from other rRNAs in place of transcription and usage of RNA polymerase?

The three RNA polymerases (RNAPs) are very similar to each other, yet not identical. As described in this article, there are subunits that are specific for each type of polymerases.

  In addition to providing unique substrates that polymerase-specific subunits bind to give each of the RNAPs their specific functionality, the two largest subunits also shape the active site cleft of the enzymes where the transcription reaction occurs.

The results of the linked article also claim that even though the cleft loops are conserved regions, there are significant length differences between the three polymerases.

Also rRNA gene is similar to the tRNA genes and they differ from other genes in the recruitment of the polymerases. "Traditional' promoters are located upstream the start site, while 5s rRNA gene and tRNA genes have one and two boxes respectively that recruits RNAPIII.

  The 5s rRNA and tRNA genes have promoters within the coding region of the gene.

source: http://mol-biol4masters.masters.grkraj.org/html/Gene_Structure5C-Eukaryotic_Promoter_Structure_for_RNA_Polymerase_III.htm

Here are two images form the linked page:

Edit:

In this article it is described that 5s RNA genes have translocated severeal times throughout evolution, and on of the mechanisms for this could be analogous of the second class of SINE elements, that contain internal RNAP III promoters, and are derived form tRNA (this could also indicate the similar structure to tRNA genes).

From this good review Evolution of multisubunit RNA polymerases in the three domains of life
 I'd like to take one short quote that might help:

  ...The structure and function of some of these factors are conserved across the three domains, whereas some non-homologous factors show an intriguing level of structural and functional similarity, suggesting that convergent evolution has led to alternative means of facilitating the same process.


Snails are similar to amphibians in that they breathe through their skin (though they also have gills or lungs). Under dry conditions, they seek cover to combat dessication. But when it rains, they "come out," just like many amphibians.

I should qualify the first sentence to say SOME snails. There are aquatic snails and terrestrial snails (which I'm sure you're referring to). Aquatic snails generally have gills, while most terrestrial snails have a single lung (I think).

Slugs, like snails, are generally found in moist areas and can often be seen after a rain.

I don't know of a single reference that pulls it all together, but this is a good place to start...

The Living World of Molluscs


How does the Cuttlefish camouflage itself accurately despite being color-blind?

The reason why the cuttlefish is colour blind is because

  it just has one type of cone cell. Humans have three different types,
  each sensitive to a different color of light. With only one cone type,
  you couldn’t differentiate between different colors (reference).

A study was conducted in the lab of Dr Lydia M. Mäthger where two different checkerboards were used to test their colorblindness.

  1) Gray – Green. One green shade, matched to the maximum absorption
  wavelength of cuttlefish, was combined with 16 different shades of
  gray. As supposed some shades of gray couldn’t be distinguished from
  the green by the cuttlefish, which didn’t adapt the body pattern.
  Experiment one was successful.

  2) Blue – Yellow. A checkerboard of blue and yellow matching in
  intensity was used for the second experiment. The skin color of the
  test species didn’t change either and therefore experiment two was
  also successful (reference).

These experiments concluded that it was indeed colourblind.

To confirm the effectiveness of the camouflage, HyperSpectral Imaging (HSI) was used to measure the colour match between the cuttlefish and its background. Using this technology it was perceived as to how a predator would view a camouflaged cuttlefish. It was found that

  Cuttlefish can produce color-coordinated camouflage on natural
  substrates despite lacking color vision, and that the color aspect of
  cuttlefish camouflage is highly effective against fish predators. Much
  of the contrast information (which allows a predator to "pick out" a
  cuttlefish from the background environment) resides in the brightness
  (luminance) rather than in the color (chromatic) aspect of the
  reflected light. What this means is that cuttlefish camouflage
  strategies take away a tool from predators in their ability to pick
  out their prey from the background and instead leave them with only
  brightness as a method for prey identification (reference 1 and reference 2).

And now we get to the main question as to how they do it. Cuttlefish are apparently able to detect the intensity of light reflected from objects in its surroundings. It is able to perceive even a 15% change in contrast. In an experiment, it was found that

  The animals did not respond to the checkerboard pattern when placed on
  substrates whose color intensities were matched to the Sepia visual
  system, suggesting that these checkerboards appeared to their eyes as
  uniform backgrounds (reference).

In another bit of interesting research done on the ability to copy the patterns on checkerboards (reference), three inferences were drawn

  The first find was that the range (relative to the size of the
  cuttlefish ‘white square’) for the animal to exhibit disruptive skin
  patterning had to be withing a certain  narrow range. Secondly, given
  the appropriate size of checker, cuttlefish regulated their disruptive
  skin patterns according to the contrast between white and black
  squares. Third, by manipulating the number of white squares on a board to just  4
  among 316 black squares (or 1.25 %) produced disruptive patterning,
  yet increasing the number of white squares to 20, 40 or 80 did not
  increase the frequency of appearance of the cuttlefish ‘white square’,
  but only its clarity of expression.

This study shows that the number of white objects in the background significantly influence cuttlefish skin patterns further putting stress on its ability to view the polarization of light (reference).

Some cuttlefish camouflage examples


Marker validation using transcriptome and genomic sequences derived from a single cell

I think your supervisor wants to see if there is inter-cellular variation in the repeat length and if so, calculate the variation. This may be compared with inter-tissue or inter-individual variation.

Usually when you take a pool of cells for any assay, you would average out the properties of individual cells.

Using sequencing you may actually be able to find the variability in the repeat length if your reads are long enough. According to wikipedia, the SSRs are 2-5bp long motifs that are repeated 5-50 times. So the max length would be 250bp, sequencing which, is an easy task. So you would be able to know the fraction of the SSRs with a certain length from a pooled sample and obtain a length distribution. This is quite easy if you know the locus of the repeats and use specific primers for sequencing.

However, if you do not know the exact locus of your SSRs and you are doing random RNA/DNA fragmentation and total RNA/DNAseq, then you may not be able to do that so easily.

In any case I think that it is easier to determine the locus and do targeted sequencing in pooled sample, than doing single-cell RNAseq (At least if the objective is to obtain repeat length distribution).


How do traits with no negative effects get "weeded out" via evolution?

Oops I wrote a lot! This is almost a very brief introduction to some concepts of population genetics.

A little bit of terminology first

Locus

A locus (plur. loci) is a position on a chromosome.

Allele

At a specific locus, different individuals may have different variants. One individual might be ATTCTA while another might be ATTCAA for example. These variants are called "allele". The whole goal of evolutionary genetics is to understand the creation (mutation) and change in frequency of the different alleles in the population.

Heterozygosity

You probably know that in many species, we carry two copies of each chromosome. One individual can therefore carry twice the same allele at a given locus or can carry different alleles. Expected heterozygosity ($H$) at a given locus is the fraction of the population that carries two different alleles at this single locus.

Fixation

When an allele reaches a freuqency of 1 (100%), that is only this allele exists in the population (and therefore the other alleles have been wiped out), we say that it has reach fixation.

Natural Selection

The process you describe in your first paragraph is called natural selection.

Natural selection is a fitness (=a function of both reproductive success and survival) difference between different genotypes. As you said (but with other words), deleterious alleles will decrease in frequency through time and will eventually end up being weeded out from the population through natural selection.

Genetic Drift

There are other evolutionary processes than natural selection. Typically, the one we will be interested in to address your question is genetic drift.

What is genetic drift?

Genetic drift refers to the random sampling of a population in order to build up the next generation population. There are different ways to model genetic drift (Wright-Fisher model, Moran model, coalescence model) but without having to talk about the details of these mathematical models, it is important that you can conceive the role of random sampling in the change in allele frequency through time. For this, I invite you to first read Why is the strength of genetic drift inversely proportional to the population size? and when you have finished, come back to this post.

One the below figure, you can see the effect of drift through time. The below graph consider a bi-allelic locus (a locus where 2 and only 2 different alleles exist in the population) starting with an initial frequency of 0.5 (=50%). Each line is a separate simulation and shows the frequency of only one of the two alleles.

The above graph considered a population of size $N=100$ individuals. Below, the same types of simulation with a population size of $N=25$ individuals. As you can see that the genetic drift is stronger

Every single locus is subject to genetic drift whether it is under selection or not. However, if a locus is under strong selection, then genetic drift with have little power to explain what allele will get fixed in comparison to when the locus is neutral.

Genetic drift and loss of alleles

It is clear from the graph above that genetic drift also wipe variant out of the population. We just don't know for sure which variant will be wiped out. To be more accurate, the expected heterozygosity due to genetic drift is reduced by a factor $\frac{1}{2N}$ each generation. One can make plenty of calculations from basic models of genetic drift. For example the expected time to being wiped out is $\bar t(p_0)=-4N\left(\frac{p_0}{1-p_0}\right)\ln(p_0)$, where $p_0$ is the starting frequency of the allele of interest.

A interesting result is that the probability of an allele to reach fixation is equal to its frequency. If there are $N$ individuals in the populations, there are $2N$ alleles (but not $2N$ different alleles). If there are, say 235 alleles A in the population and $2n - 235$ alleles B in the population, then over the long run (so that one will necessarily fix) the probability of fixation of the allele A is $\frac{235}{2N}$ and the probability of fixation of the allele B is $\frac{2N-235}{2N}=1-\frac{235}{2N}$.

Wisdom teeth

In your question, you are interested about a supposedly purely neutral locus. You talked about wisdom teeth I suspect more as an example rather than because you are interested to this trait.

Let's assume that the presence of wisdom teeth is completely neutral. Note by the way that as a rule of thumb if $2 N s << 1$, (where $s$ is the selection coefficient on a given allele) then the allele will behave essentially as if it was a neutral allele. So, if wisdom teeth is neutral, then the probability of this trait to disappear over the long run depends on the frequency of the allele causing this trait. So far, I have assumed that we were interested in a single locus only. In reality, variation in many traits are caused by variation at several loci. In such case calculations are a little less straight forward (but still feasible). I do not know the genetic basis of wisdom teeth, so I cannot make good predictions for the evolution of this particular trait.

Other evolutionary processes

Here are a few example of interest

Gene flow

Note of course that there are other processes to consider when trying to predict the fate of a given allele or trait. For example, in a given population you might have a flux of migrants that come from a population where one allele is fixed therefore affecting the allele freuqency in the focal population. This is called Gene flow.

Hill-Robertson effects

Never forget that a locus is not alone on its chromosome. It is physically linked to other loci and selective pressures at other loci will affect the allele frequency at the focal locus. This is called Hill-Robertson effects.

Mutations

Of course, when a locus is not polymorphic (has only one allele), mutations is the ultime source of variation. When a locus is polymorphic, then it is likely the mutations will have a minor effect on the allele frequency (although it depends on the size and type of locus and depends on whether mutations can make up new functional alleles).

Pleiotropy and covariance between phenotypic traits

Phenotypic trait do not evolve independently. If wisdom teeth is a consequence of the activation of the molecular pathway for resistance to HIV (which it very probably is not), then wisdom teeth will not evolve as a neutral trait. A locus that affects several traits is said to have pleiotropic effects.


What is this insect, the bite of which is causing deaths?

You were right to suspect arachnid. Its a red clover mite. But they normally don't bite humans or cause diseases. Could you post some links to news articles talking about the disease?


The atom numbered 1 in a PDB file is the most N-terminal atom visualized by the structure determination — the most N-terminal amino acid, the co-ordinates of which are presented.
If the X-ray diffraction (or whatever technique used) does resolve the first amino acid, then it will, in fact, be the first amino acid. The following is an arbitrary example from 4LI3 (chain X):
ATOM      1  N   MET X   1     100.329 111.822  35.431  1.00 66.81           N
ATOM      2  CA  MET X   1     100.845 110.803  34.526  1.00 67.85           C
ATOM      3  C   MET X   1     101.961 111.361  33.646  1.00 71.14           C
ATOM      4  O   MET X   1     102.979 111.840  34.153  1.00 77.28           O
ATOM      5  CB  MET X   1      99.722 110.256  33.648  1.00 61.70           C
ATOM      6  CG  MET X   1      98.581 109.621  34.412  1.00 66.53           C
ATOM      7  SD  MET X   1      97.327 108.947  33.300  1.00 82.23           S
ATOM      8  CE  MET X   1      96.071 108.440  34.463  1.00 69.80           C
ATOM      9  N   ALA X   2     101.754 111.288  32.331  1.00 67.01           N

If the X-ray diffraction does not resolve the first amino acid, or if the structure is of a fragment of the protein that does not contain the first amino acid, then the co-ordinates of the first amino acid are not listed in the file and ATOM 1 is from the most N-terminal amino acid. The following is an arbitrary example from 1BTE (chain A), starting at amino acid 7:
ATOM      1  N   GLU A   7      15.888  47.505  13.150  1.00 34.63           N
ATOM      2  CA  GLU A   7      14.455  47.789  12.947  1.00 33.53           C
ATOM      3  C   GLU A   7      13.538  46.900  13.794  1.00 29.91           C
ATOM      4  O   GLU A   7      12.342  46.832  13.476  1.00 30.54           O
ATOM      5  CB  GLU A   7      14.084  47.715  11.461  1.00 37.16           C
ATOM      6  CG  GLU A   7      14.284  46.356  10.821  1.00 41.38           C
ATOM      7  CD  GLU A   7      14.124  46.366   9.313  1.00 43.82           C
ATOM      8  OE1 GLU A   7      12.959  46.323   8.849  1.00 46.10           O
ATOM      9  OE2 GLU A   7      15.151  46.420   8.600  1.00 45.51           O

(Knowledge of the first amino acid is from nucleic acid sequencing.)


Arsenic (V) Reduction to Arsenic (III) by Microorganisms

You can find a great and recent review on this topic, which is thankfully also free to access, here: https://www.sciencedirect.com/science/article/pii/S2319417016000159

Arsenic resistance is ubiquitous among bacteria, they virtually all maintain the ars operon. Among Arsenic-resistant bacteria, this is not an advantage, but Arsenic was and remains a ubiquituous substance and being resistant to it confers an advantage over those that aren't; which is why bacteria that save themselves the effort aren't abundant.

The core to your answer is in the very last summary paragraph:

  ArsM transforms inorganic arsenic into a highly toxic organoarsenical species that kills off by competing the bacterial species and may also be responsible for carcinogenesis in animals. Competing microbial species have responded to this environmental pressure by evolving detoxification mechanisms for MAs(III). Some produces ArsI that demethylates MAs(III) to less toxic inorganic As(III) while other produces ArsH that oxidizes MAs(III) to nontoxic pentavalent MAs(V). It is likely that all of these processes are taking place in environmental microbial communities as bacteria, archaea, fungi, and protozoans constantly fight for dominance.

Summarised in Figure 5: https://ars.els-cdn.com/content/image/1-s2.0-S2319417016000159-gr5.jpg

The reason why ArsC and other arsenate reductases (reducing Ars(V) to the more toxic Ars(III)) evolved in the first place, setting off this whole Arsenic methylation cycle, is that

  they are required for resistance to arsenate, which became the predominant arsenic species after oxygen appeared in the atmosphere.

Simply put: If I can make a poison that kills you but not me, why shouldn't I make it?


How does hypocalcaemia have an effect on the excitability of cell

Assuming the question is in respect to neurons..in a nutshell...resting membrane potential & excitability both depend upon sodium permeability which in turn depends on potential difference of the excitable cell....now as the sodium influx is increased the minimum voltage required to increase the conductance of sodium decreases far below its normal value...so for a small increase in membrane potential from the normal very negative level the sodium channel becomes activated elevating the resting membrane potential...

In fact, the calcium ion concentration needs to fall only 50% below normal level before spontaneous discharge of peripheral nerves occur giving rise to "tetany"...

Reference- Adapted from Guyton & Hall- Textbook of medical physiology (12E)

You can also refer to Berne & Levy's & Ganong's physiology book for further details


What are golgi?

Stacked array in the cisternae which are ought to connect vesicles and tubules
Made of >1000 different proteins
Has the ability to transform/alter in response to a cellular stimulation such as mitosis

Fragmentation of golgi during mitosis

  During interphase, the Golgi receives secretory cargo from the ER via the COP II vesicle formation pathway. Depending on their nature, secretory cargo then travel through the Golgi apparatus by a combination of vesicular transport involving COP I vesicles and cisternal maturation. A retrograde COP I vesicle pathway connects Golgi cisternae and the ER to allow recycling of Golgi enzymes and integral membrane proteins of the transport machinery such as the SNAREs. Two models have been proposed to explain the fate of the Golgi in mitosis. The first is the direct fragmentation model, where Golgi cisternae are consumed by continued COP I vesicle budding in the absence of membrane fusion, which is blocked in mitosis. This generates a pool of tubules and vesicles (Golgi haze) containing Golgi enzymes and structural proteins. The second is the ER recycling model, where forward transport into the Golgi by COP II vesicles is blocked, but COP I recycling back to the ER continues until Golgi proteins are redistributed to this compartment. Some Golgi proteins may then exit the ER via the COP II pathway, but these vesicles are unable to fuse with a Golgi compartment during mitosis, and remain in equilibrium with the ER.

A more detailed outline of the process of fragmentation of golgi apparatus can be found here and here

As I know "golgi blobs" are also referred to as "golgi haze".

Sources:

http://www.clfs.umd.edu/classroom/mocb639/Hamza_Golgi_Apr5_2005.pdf
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2175146/
http://www.cbi.pku.edu.cn/chinese/documents/cell/xibaoshengwuxuecankaowenxian/cocb/15/15-4/15-462.pdf


Does every human eye see the same visible spectrum?

Human eyes all use the same optical pigment photopsin, so they all have the same basic frequency response.

There are differences. For example cataracts will change the sensitivity of the eye to colour, and people with colour blindness have various defect to cone cells that affect colour response. However these are secondary effects.


Is setting high mismatch and gap penalties sufficient to distinguish perfectly mapping reads?

The short answer: No, setting extremely high penalties (100 or 1000) does not seem to work. I'm not sure why.

The medium answer: Since I posted the question, I did a bit of exploring, and it looks like the reads that perfectly match are the reads that are not soft clipped and that have an edit distance of zero, as indicated by the CIGAR string and NM tag, respectively.

The long answer: See https://standage.github.io/how-to-distinguish-perfectly-mapped-reads-from-a-sambam-file.html.


Are there any bacteria, virus or mold that can withstand ozone?

Bacteria resistant to ionizing  radiation (e.g., Deinobacterium chartae, Deinococcus spp., Desertibacter roseus, Geodermatophilus dictyosporus, Hymenobacter actinosclerus, Kineococcus radiotolerans, Methylobacterium radiotolerans, Microbacterium radiodurans, Paenibacillus darwinianus, Pseudomonas radiora, Rubrobacter radiotolerans, Spirosoma radiotolerans, Streptomyces radiopugnans; for links to the paper describing these species, see: Bacteria I. Names), can be expected to withstand higher doses of ozone compared to bacteria sensitive to ionizing radiation.

The sensitivity to ozone of different strains of the same bacterial species can differ markedly if the strains differ in the efficiency of DNA repair mechanisms.

Brinkman et al. (1964) Radiomimetic toxicity of ozonised air. Lancet 1: 133-136.

https://www.ncbi.nlm.nih.gov/pubmed/14074479

Hamelin & Chung (1976) Rapid test for assay of ozone sensitivity in Escherichia coli. Mol Gen Genet 145: 191-194.

  ozone resistance is probably involved with DNA repair mechanism

https://www.ncbi.nlm.nih.gov/pubmed/778585


Red and yellow insect found in kitchen in Conrad, Montana (USA)

This appears to be a stink bug in the superfamily Pentatomoidea of the true bugs (i.e., order Hemiptera).

Specifically, your specimen appears to be Perillus bioculatus or the two-spotted stink bug.

 Photo Credit: Margarethe brummermann (2008)

You can see additional photos including those demonstrating the species's various yellow vs red color morphs here.

According to the Integrated Plant Protection Center at Oregon State University [my emphasis and links]:

  Mature nymphs of the two spotted stink bug are about 8 to 9 mm long. Adults range in length from 10 to 12 mm. Nymphs may [be] pale yellow or reddishorange with a distinct black "Y-shaped" marking on the pronotum and two black spots on the thorax.

According to Wikipedia, this species is usually a beneficial predator (especially of the Colorado potato beetle), but early nymph stages feed by sucking on potato stems. The trade-off, I would guess, is worth it.

In fact, the color variation in this species (namely the shift from white/yellow to red) that my earlier link shows photos of is a result of a higher diet of potato beetles. [Source, taken from p 99 in McPherson's 1992 book The Pentatomoidea (Hemiptera) of Northeastern North America].

 Source: bugguide.net

Their range, according to bugguide.net is southern Canada, the U.S. and into Mexico.


Summary statistic that can distinguish between migration from pop2 to pop1 vs. pop1 to pop2

Yes, migrants affect patterns of genetic diveristy

Immigrants yield to higher effective population size and therefore higher genetic diversity. They will also affect the site frequency spectrum and I would expect that if the migrants are numerous enough, they would yield to positive Tajima's D.

Therefore, unidirectional migration will definitely yield to differences in patterns of genetic variance among populations (that can be measured by any summary statistic of the site frequency spectrum).

Existing methods for detecting directional selection

I have never had to do such inference so I am not able to do a good review of the existing technics.

You should probably read Slatkin and Maddison 1998 and more importantly Beerli and Felsenstein 2001. Beerli and Felsenstein 2001 has been cited 1,341 times and you should probably quickly see whether some of these papers suggest more recent methods. John Novembre has some very interesting work on how to estimate migration rate between any two populations (e.g. Novembre and Stephens 2008). He might have done something of interest to your problem.

You can always use Approximate Bayesian Computation (ABC;see for example Jeffrey Jensen's work for example of inferences with ABC in population genetics) to figure out what pattern of migration is most likely. With a simple enough model, a good ABC algorithm is not that long (with good computing ressources). The question then is what statistic(s) to use for the rejection algorithm. Again for that, you should have a look at the existing literature to come up with a set of potentially useful statistics.


Software recommendation for protein in electric field modeling?

MD
Broadly this could be attempted with Molecular Dynamics simulations. As you discovered in your search, one of the most popular softwares is free: GROMACS. This is an atomistic approach to the problem. It also has many electrostatic parameters.
I would point out that generally MD requires careful and robust methods and often an expert lending hand if the results are to be trusted. In order to do MD at the timescales for observing rotating molecules in the field, massive amount of HPC computational time will be required. This is a full blown project to get it to an appropriate level for publication.
This is computationally intensive.
Quick Electrostatics
If a HPC is not available to you then MD may not be an option. If all you want to do is visualise the location of the charge and make qualitative predictions or visualisations, PyMol and ABPS might be a quicker combo. It is also good for quantitative analysis, but obviously is a static model.


What type of white hard thing grows on lobster

These are barnacles, which are interestingly related to lobsters. See the image for comparision (from here):

They have a mobile larval stadium, but once they mature, they attach to a hard surface. They can be found on ships, surfaces in harbours, on whales and obviously on lobster shells. See here and here for some more details.


What is evolution?

In a non-biological sense, evolution means change:

  "a process of [...] change"

Biological evolution (seeing as this is Biology stack exchange) then needs to be tweaked to give a biologically specific context. Many textbooks etc. give definitions of evolution and here are a few good ones from across the history of evolutionary biology:

Charles Darwin:

  "Descent with modification".

Mark Ridley1:

  "Evolution means change, change in the form and behaviour of organisms between generations. ... When members of a population breed and produce the next generation we can imagine a lineage of populations, made up of a series of populations through time. Each population is ancestral to the descendant population in the next generation: a lineage is an ancestor-descendent series of populations. Evolution is then change between generations within a population lineage."

Brian and Deborah Charlesworth2:

  "Evolution means cumulative change over time in the characteristics of a population of living organisms. ... All evolutionary changes require initially rare genetic variants to spread among the members of a population, rising to high frequency..."

All of these have a common theme. Biological information is moving through time, descending with a degree of directionality (e.g. parent $\rightarrow$ offspring), and the information is modified with time.

Personally I would define evolution as:

  Evolution is a change in gene frequencies, resulting from four mechanisms (mutation, migration, drift, and selection) which can all affect the transmission of heritable genetic information within populations. Evolution has the potential to cause phenotypic change (when genotype affects phenotype) and has the potential to cause both adaptation (microevolution) and divergence (macroevolution).

This definition captures that biological evolution occurs through changes in heritable genetic information, the prerequisites of evolution, the mechanisms of evolution, and what the consequences of those changes can be.

I think it is important to include mutation (and drift, selection, and migration) because these explicitly state how evolution occurs. I don't think it is necessary to include copy number variation, chromosome numbers, or codon usage as they are not central to the process of evolution (though they can be important).

Whilst only the first sentence of my definition is critical, I think it useful to include the latter part (or something of a similar effect) whenever possible as it helps to clarify evolution and it's relevance.

ISBN: 978-1-4051-0345-9
ISBN: 978-0-9815-1942-5


Almost definitely not a CA native.

It looks like a coleus to me -- cultivars are pretty diverse but typically have variegated leaves with some amount of purple coloration.

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


How long does it take for memory to disperse after death?

There are multiple levels of memory, some of which would die immediately, some of which would take some time. So the answer is: it depends; some immediately, some only very slowly.

At the highest level, the current neuronal firing state of the brain encodes memory on a very short scale - working memory. The memory held on this level does not have a clear anatomical counterpart (but for the potential encoded in the synapses). It equals very short-term memory/STM sequences, such as the words you read just before you read the words you're reading right now. This memory is lost immediately when you lose consciousness, at least to some degree; as this memory is hard to even strictly distinguish from consciousness and attention (though see Jonides et al. 2008).

Other forms of short-term memory/STM are stored in a slightly different form: short-term potentation, the adaption of neuronal responses following brief and intense stimulation. Spike Frequency Adaption/SFA is at an intermediate stage between this and the previous level. Short-term potentation and SFA decay within minutes or even seconds if they are not transferred into some more durable form of memory.

Long-term memory (/LTM) stores have specific anatomical correlates; they are stored in, amongst others, the synaptic weights (i.e. the amount of influence the firing of one neuron has on another). Some forms of LTM are best located in cortical synapses, others in the hippocampus. An even more fundamental, long-term, durable storage form is the wiring itself; not just the weights, but the existence of a synapse between two points, or not. For example, an important part of early learning is synaptic pruning, where synapses which do not play a meaningful role die off, whereas those which connect functionally related brain areas remain.
This pruning instantiates one form of learning, and the non-existence of a synapse is a form of memory. Synapses are comparatively stable. Even if the corresponding neurons die, in principle, the synapses still exist - and more importantly, the nonexistence of a synapse is even more durable. This form of memory can be observed in slice preparations of animals long dead.

For a simple example, consider any experiment on the neuronal responses in slice preparations, which can be considered a form of (decontextualised) memory access.

On the most extreme end, epigenetic adaptions and large-scale brain anatomy (which shows developmental traces) can be considered a form of memory that will remain intact until the whole structure rots away.

However, the more direct answer to the question the OP is asking is that once a large amount of neurons have died (brain death), there is currently no power on earth that can access a non-trivial amount of memory. As long as this is averted, nontrivial amounts of memory can be recovered.
For the parts that are lost immediately, see the source by Jonides et al. For more durable memory, you could look at for example Purves et al, Neuroscience.


Blood circulation and blood pressure in different tissues

I'm not sure I understand your question very well-maybe try and rephrase it? As another example, low blood pressure in the kidneys is sensed by the juxtaglomerular apparatus which secretes renin into the circulation. Renin converts angiotensinogen (released by the liver) into angiotensin I. Angiotensin I is then converted into angiotensin II by angiotensin converting enzyme (this is the target of anti-hypertensives called ACE inhibitors) secreted by the lungs. Angiotensin II is a potent vasoconstrictor which directly increases the blood pressure (and hence glomerular filtration rate).  Angiotensin II also causes the release of aldosterone which acts on the kidneys to re-absorb salt and water again all facilitating an increase in blood pressure. I hope I've answered your question, if not please edit the question so it very clear.


If one is scientifically rigorous, the answer to this question is:

  Nobody knows.

If one accepts the most commonly accepted (although not proven) view of the evolution of genomes and catalysis, the answer is:

  Enzymes

Explanation

The ‘RNA world’ hypothesis, mentioned by @vkehayas, postulates that the first genome was RNA, not DNA, and the first enzymes were also RNA. DNA genomes arose later (as did protein enzymes, although the timing of that event is irrelevant to the question as originally written).

Alternative Question

If one was not aware that RNA is thought to have preceded DNA as genome, and had not been aware of catalytic RNA, then one might have asked:

  Which came first, RNA or protein?

And in fact, this question was originally asked by Francis Crick in the restricted context of  the synthesis of proteins by ribosomes on mRNA and led him to remark.

  “It is thus not impossible to imagine that the primitive machinery had
  no protein at all and consisted entirely of RNA.”

The later discovery of catalytic RNA provided a mechanistic basis for an original world in which RNA was a self-replicating genome.

(So the answer to the alternative question is that ‘RNA’ preceded protein.)

Supporting citations

I have kept this answer brief and only provide a single general reference because @vkehayas provides links to other questions about this topic on this list.


What is the relationship between Homocysteine and Norepinephrine metabolic cycles?

Norepinephrine is converted to epinephrine by phenylethanolamine N-methyltransferase (PNMT). In mammals PNMT is just one member of a large family of methyltransferases which use S-adenosylmethionine (AdoMet) as a cofactor to provide a methyl group. These methyltransferases are involved in a very diverse set of pathways including the synthesis of nucleic acids and of certain phospholipids, as well as the methylation of DNA and histones.

As you point out, these reactions generate homocysteine via S-adenosylhomocysteine. However, because AdoMet is such a critically important cofactor it is thought that cellular levels are tightly regulated. As part of this regulation, homocysteine is re-methylated to methionine via two different routes requiring either methionine synthase or betaine-homocysteine methyltransferase. Methionine synthase obtains the required methyl group from 5-methyltetrahydrofolate in a vitamin B12 (actually methylcobalamin)-dependent reaction. This latter reaction links the AdoMet-based methyl transfer system to the other part of the cellular one-carbon economy, the folate pool. This is why vitamin B12 deficiency leads to hyperhomocysteinemia.

This Figure is reproduced from Luka et al. (2009) Glycine N-methyltransferase and regulation of S-adenosylmethionine levels. J. Biol. Chem. 284:22507–22511. I show it here just to illustrate the point that there are, in fact, many gears interacting in this system. The minireview is interesting and I recommend it to you.

In conclusion, my answer to your question is that it is unlikely that stress leads to elevated levels of homocysteine as long as all of the relevant regulatory machinery is functioning correctly. If there is a problem with homocysteine recycling then yes, homocysteine levels would rise, but given that there so many AdoMet-dependent methylation reactions it is unclear how big a contribution PNMT would make to the overall homocysteine load.


You say that "only monophyletic groups are valid as species"... That is according to a certain interpretation of evolution that is not necessarily mainstream, (you wouldn't be taught that definition of species in Oxford or Yale) and which idealizes cladistics into simple trees, which don't reflect reality of hybridizing species like orchids and hominids, where simple tree like branching has been proven to not exist. Inflexible definitions of phylogeny should be taken with a pinch of salt, because pollen and other reproductive systems cause many species to be flexible. It's unwise to state that definition of species without being well aware of the mainstream one: Ernst Mayr definition.

Strict interpretations of species lead to problems, because
Darwin wrote:
No one definition of species has satisfied all naturalists; yet every naturalist knows vaguely what he means when he speaks of a species. Generally the term includes the unknown element of a distinct act of creation.

If you check the Wiki page on species, they state 11 contrasted definitions of species which are not necessarily cross compatible.   https://en.wikipedia.org/wiki/Species#Standard_definition:_Mayr.27s_Biological_Species_Concept

The definition of species that i was taught had nothing to do with the parental mechanisms that shaped the species differentiation from other species, and that it is a practical concensus to effectively group animals methodically, which doesnt actually reflect natures unmethodical reality.

Seeing as humans interbred with neanderthal and denisovan species, and orchids interbreed very commonly, the following image refers to an idealized phylogenetic model which is not applicable to all reproductive systems, and it isn't applicable to humans.


How does sodium in one's diet affect blood pressure?

The basic reason is osmosis, the tendency of solutes to move from an area of high concentration to one of low concentration across a permeable barrier. So, ingesting large amounts of salt results in a high sodium concentration in the blood stream. This in turn causes water to enter the blood vessels by osmosis. More water in the blood means a greater volume of liquid and, therefore, higher blood pressure.

This process occurs primarily in the kidneys, specifically in the part of the nephron called the loop of henle (the image below was taken from wikipedia and is originally from Grey's Anatomy):

With low salt concentrations, water exits the loop and is retained by the body. When sodium concentration is high, the opposite occurs, water enters the blood stream by osmosis and increases blood pressure.


How to calculate relative fitness from absolute fitness with recapture data?

So the dataset is this:

  id   x3 x4
   2    1  1
   3    1  1
   4    1  1
   5    1  0

Lets assume that we caught the entire population so that we know that a 0 is really a dead organism (the estimate is proportional to lifetime fitness). Furthermore, there is no density-dependent selection and the generations are non overlapping.

The survival for next year would be the fitness value of all individual. So in year x4, the absolute fitness would be W = c(1,1,1,0). Then the mean absolute  fitness would be: W_bar = (1+1+1+0)/4 = 3/4. Then to get w, the relative fitness, you divide W by W_bar. w = c(4/3, 4/3, 4/3, 0). Therefor, if you calculate mean(W/W_bar), it should give you 1.

This is as in Endler, J. A. 1986. Natural Selection in the Wild. Princeton University Press, p. 168.


So, what I was looking for, but was lacking the knowledge of, was the concept of "Thermic Effect of Food"
I really didn't know how to phrase my question well, due to the fact that I tackled the problem from the wrong angle.
Direct quote from the Wikipedia Article as it answers the question best:

The thermic effect of food is the energy required for digestion, absorption, and disposal of ingested nutrients. >Its magnitude depends on the composition of the food consumed:
Carbohydrates: 5 to 15% of the energy consumed [7]
Protein: 20 to 35% [7]
Fats: at most 5 to 15 %[8]


Why are particular laser-related skin products not recommended for darker skin tones?

The reason for laser hair removal/growth products not being safe for darker skin tones is the ability for darker skin tones to absorb more light from the laser than lighter skin does BEFORE the light is able to reach the depth at which the hair follicle is located. Light from lasers must pass through the epidermis where melanocytes are located before they reach the hair follicle.

More melanin means increased ability to absorb wavelengths as seen in the curve below. Laser products such as Theradome (678nm) and Silk'N (475-1200 nm) have shorter wavelengths, which are highly absorbed by melanin, and therefore can damage skin in darker skin tone patients. Safer products like Nd:YAG are those that have higher wavelengths at 1064nm and can penetrate the skin without over-absorption by melanin.

Disclosures: I own no stock in any of these companies.

References:

http://www.theradome.com/press-release/
http://www.amazon.com/Silkn-Flash-Removal-Device-Cartridge/dp/B0093BOR4W
http://www.nature.com/jid/journal/v122/n2/full/5602198a.html


Your question is very broad, but I'll try to address each of your points briefly.

It would be nearly impossible to edit the genes in every cell of a human being or other complex organism simply due to the number (and accessibility) of cells. A full-grown human has in the neighborhood of 30 trillion cells - 30,000,000,000,000. Cells in locations such as the brain and central nervous system are protected by the blood-brain barrier, which would keep most gene therapy vectors from accessing those cells. There are other reasons why editing each cell in the body is virtually impossible, such as vectors accumulating in the liver, but this is one of the main ones.

Cancer is indeed a risk from gene therapy in general, although DNA editing technologies like CRISPR in particular have a lower risk due to thTe circumstances surround exactly how the therapy is delivered to the nucleus of the cell where DNA resides. Other risks include potentially serious or fatal systemic inflammation due to an immune reaction to the viral vector which carries the CRISPR "machinery". Off-target effects can occur due to the wrong cells being targeted (although this risk is generally lower with CRISPR). Additionally, there is the very small but non-zero chance that the genetically-engineered vector could somehow regain its native infectious capability. Newer generations of gene therapy have significantly reduced this chance, however.

Very briefly, no. DNA is made up of "letters" (A, T, C, and G) called bases or base pairs, and typical CRISPR constructs only operate on 10-20 bases at the most — usually it's just one or a couple that are changed. A typical human chromosome has millions of base pairs encompassing hundreds to thousands of genes, so editing, adding, or removing an entire chromosome is simply out of the realm of possibility with this technology.


What is natural selection?

Natural Selection (NS) is an evolutionary process causing a directional change in both a phenotypic trait and the allele frequencies associated with particular values of this phenotypic trait whenever there is a trait that

Has a non-zero narrow-sense heritability $h_N^2$

See this post for the definition of heritability
Note that if $h_N^2 ≠ 0$, then it necessarily implies that the trait is variable in the population.

Correlate with fitness variance in the population

See this wikipedia article for the definition of correlation

You may want to have a look at this post (maybe in particular Lewontin's recipe explained in this answer) or have a look at an intro course to evolution such as Understanding Evolution by UC Berkeley if this is unclear to you.

You may also want to have a look at the post How is “selection” best defined?

Note about the environment

Note that the genotype - fitness covariance does not necessarily need to be dependent or correlated with a specific environmental variable. Many selection pressures are indeed independent of the environment. If one specific genotype is associated to heart failure, then the environment may matter little. This genotype will always be associated with lower fitness.

In other words, you do not need environmental change, or environment specific adaptations in mind to test NS.

Would evidence that what is needed for natural selection to happen does not exist falsify NS?

Mutations

I don't think that an evidence that mutations do not occur would falsify NS because while NS needs genetic variation (fuelled by mutations), the process per say does not refer to the creation of new genetic variance via mutations. Showing that mutation do not occur would not per say falsify NS (I think) but it would make the point that NS cannot happen. A bit like, the absence of energy would not falsify the theory of gravity but it would prevents any gravity to ever happen.

The theory of evolution as whole would be falsified if one were to show mutations never occur (or occur at a much lower or much higher rate than currently observed) though.

Heritability

Similarly, if one could show that $h_N^2 = 0$ for all traits (nothing is heritable), then this would also prevent any NS to ever happen

Fitness variance

Similarly, if one could show that there is no fitness variance in population or even that fitness is always independent of the gentic variance (in other words, fitness itself is not heritable), then NS would never happen.

How to falsify natural selection?

You could show that for a phenotypic trait $h_N^2 > 0$ and show that genetic variance correlates with fitness variance (fitness can be measured as the number of offsprings) and yet repeatedly fail to see any change in the phenotypic trait values (or frequency of the loci explaining variance for this trait) over time. Such observations would falsify NS.


Both.

Recent theoretical models, however, predict that convergence should be common within species-rich communities, such as species assemblages resulting from adaptive radiations. Here, we present the most extensive quantitative analysis to date of an adaptive radiation of cichlid fishes, discovering multiple instances of convergence in body and trophic morphology. ...

Independent adaptive radiations often produce convergent phenotypes
In Lake Tanganyika, convergent phenotypes evolved within a single adaptive radiation
These convergent morphologies are associated with adaptations to the same niche
Distantly related yet morphologically similar species coexist in the same habitat

--Convergent Evolution within an Adaptive Radiation of Cichlid Fishes


What is the acceleration profile of a cheetah?

According to a recent paper published on Nature, cheetahs can reach a top speed of 29ms-1 and very impressive accelerations, up to 100ms-2:

  The mean top speed was 14.9 +- 3.4ms-1 and was usually only sustained for 1–2 s. The highest speed we recorded was a stride-averaged 25.9-1

Also impressive are the lateral accelerations:

  Hunts involved considerable manoeuvring, with maximum lateral (centripetal) accelerations often exceeding 13ms-2

Here is the acceleration and speed chart:

The paper has several other charts: Locomotion dynamics of hunting in wildcheetahs


What exactly does Curare do to the peripheral nervous system?

Curare is a plant alkaloid originally used as a poison on darts and arrows used in hunting. It is a competitive antagonist for the nicotinic acetylcholine receptor, which is found in the neuromuscular junction and autonomic ganglia.  We know a lot about this receptor and it's blockade by curare, so most good basic pharmacology textbooks devote a fair amount of space to it and you'll find mention in many physiology and neuroscience textbooks. I'd refer you to Goodman and Gilman Chapter 11 for a general reference.

The basics are as follows:

Curare is a quaternary amine. This means it has a charge on it and cannot cross the blood brain barrier. This was confirmed in 1947 by Scott Smith (pubmed link), an anesthesiologist, who administered very high doses of d-tubocurarine to himself (while under mechanical ventilation), resulting in complete paralysis but no central CNS effects. It's an interesting read if you get the chance, and records very carefully details of the minute by minute response for 4 hours of a series of administrations and reversals (with an acetylcholinesterase inhibitor).

What you get, as reported by Smith and confirmed by others, is blockade of motor outflow with skeletal muscle paralysis (including respiratory muscles) and also probably some ganglionic blockade (this is supported with further research since 1947). There are no changes in sensory inflow or any central effects. The blockade of the nicotinic acetylcholine receptors is reversed with an acetylcholinesterase inhibitor by increasing the amount of acetylcholine in the cleft to the point where it overcomes the competitive inhibition by curare.


What species is this bug that appears in my bathroom?

Based on my knowledge of species found in Sweden, I think this is a species of Ptinus (Spider beetles), for instance Ptinus sexpunctatus. The general appearance, along with long antenna and long legs fits well. Species in this genus are often also found indoors. Some of the other species in the same genus can also have white/light markings on the elytra, so I'm not absolutely sure about the species. Typical of P. sexpunctatus is that is has six white marking on the wings, but the two hind ones on each wing can sometimes merge into one.

(picture of Ptinus sexpunctatus, from http://www.coleoptera.org.uk/)

(side view, from Wikipedia)


How long does the Ebola virus remain infectious on contaminated items or surfaces?

This really depends on the environment, one study (listed below as reference 1) found that the Ebola virus can survive under ideal conditions on flat surfaces in the dark for up to six days - see the figure from the same publication.

However, the virus is quite sensitive to UV radiation (see reference 2 for all the details) and most viral particles are likely to get inactivated within relatively short time. It might still be possible to get positive tests for Ebola from really sensitive PCR-based tests, but these are most likely not infectious anymore. The CDC lists common bleach (or any other routinely used disinfected) as a good way to get rid of Ebola viruses.

References:

Persistence in darkness of virulent alphaviruses, Ebola virus, and
Lassa virus deposited on solid surfaces
Sensitivity to ultraviolet radiation of Lassa, vaccinia, and Ebola
viruses dried on surfaces


Relationship between fatty acid chain and saponification number

The saponification number, or saponification value, can be described as...

  the measure of the amount of alkali required to saponify a definite weight of fat. It is expressed in milligrams of potassium hydroxide required to saponify 1g of fat.

(source: Food Analysis: Theory and Practice. Y. Pomeranz and C. E. Meloan)

Notice that, in the definition, we're talking about grams and milligrams, not mols.

Now comes the important information: in the saponification, the base reacts with the ester group, and any triglyceride, regardless its chain length, has exactly three ester groups.

Let's see this is an oversimplified example:

Suppose we have two triglycerides, A and B. A has a chain twice as long as B. So, suppose that a given number of mols of A weights around two times the weight of the same number of mols of B.

However, they have the same number of esters, and they will require the same amount of potassium hydroxide. As A has a greater weight (which is in the denominator on our equation), it will have a lower saponification number compared to B.


Why can't NMR be used on large RNA molecules?

RNA usually has pretty complex structures. What causes the problem with NMR however is that large RNAs, such as mRNAs, don't have 1 structure, they have a population of possible secondary structures, and even if small parts of the RNA always have the same local structure, the overall molecule will occupy a variety of forms. The NMR will see a population of structures and won't be able to get good signal. DNA and RNA seem like tempting targets for NMR because the phosphorus in the backbone is NMR active, potentially allowing for backbone structure determination, but this only works on short pieces of RNA that adopts a single conformation.

Unfortunately I don't have sources to cite, only a couple semesters of NMR courses and a year of in vitro transcription of mRNA.


What is the reasoning behind the Drake Equation?

Humanity has had roughly the same level of intelligence for tens of thousands of years, and as the Drake Equation estimates the number of civilizations capable of extrasolar communication - we only met that criteria ourselves within the last century.


Are more animal species edible than plants?

It is estimated by some that on earth there are

  7.77 million species (of which 953,434 have been described and cataloged) of animals
  298,000 species (of which 215,644 have been described and cataloged) of plants
  611,000 species (of which 43,271 have been described and cataloged) of fungi
  36,400 species (of which 8,118 have been described and cataloged) of protozoa.

with 6.5 million species found on land and 2.2 million (about 25 percent of the total) dwelling in the ocean depths.[1][2]

Despite the existence of toxic plants and animals, from the numbers alone it is clear that there are more animal species we can eat than plant species.

This does not take into account population or individual sizes, just species.

[1] How Many Species Are There on Earth and in the Ocean?
[2] How many species on Earth? About 8.7 million, new estimate says


If our skin is burned by the sun what causes the red color of the skin?

Sunburn causes damages in the skin which further triggers an immune reaction.
This immune reaction causes a dilation of the capillaries in the skin to allow a higher transport rate towards the inflammation site. This dilation and the higher blood flow in the area causes the "redness" of inflamed tissues. See the image for illustration (from here):

The delay in the appearance (for more severe cases also the swelling) is caused by the time it takes for the body to react and to develop an immune response. For further information you can look here and here.


Mesoderm vs Mesenchyme- what's the difference?

Mesenchyme is the meshwork of embryonic connective tissue in the mesoderm; from it are formed the connective tissues of the body as well as blood vessels and lymph vessels.
So it's a part of mesoderm


Is there a formal definition of signature of natural selection?

Here is how I would personally explain what a genetic signature is:

A genetic signature of a certain type of evolutionary history (type of selection or demography) refers to the effect that this specific type of evolutionary history has on genomic properties of populations today.

We are interested in understanding such signatures because knowing the association between a number of evolutionary histories and their genetic signature allows us to reconstruct the evolutionary history of a population just by looking at the genomics of this population.

For example, recent selective sweep, population expansion after a recent bottleneck and/or linkage to a swept gene are all causing negative Tajima's D. Balancing selection and/or sudden population contraction are causing positive Tajima's D. In this example Tajima's D is a statistics that is used to measure this so-called signature of the different process.

The above was NOT a citation. I am NOT aware of any publications defining rigorously what a genetic signature is. I think it is not so uncommon for authors to use a term without strictly defining it. As long as the unclarity of the definition does not yield to limit cases and misunderstanding, then it is totally fine.


Why do the humans become sleepy after meals?

The name used frequently for this phenomenon is "Post-lunch dip".

"The post-lunch dip is a real phenomenon that can occur even when the individual has had no lunch and is unaware of the time of day. This dip has its roots in human biology, and may be linked to the size of the 12-hour harmonic in the circadian system. It is certainly exacerbated by a high-carbohydrate lunch, and may be more likely to occur in extreme morning-type individuals."

PubMed Source

Another PubMed source
"The 'post-lunch' dip is a bi-circadian phenomenon, largely unrelated to lunch, and worsened by a disturbed prior night's sleep. Despite anecdotal claims of adverse effects of larger lunches on afternoon driving ability, there is little actual driving data to support this belief."

For other reading and research...


Can we attack viruses by attaching proteins and such to their shells?

Yes, that should be possible. And it is one of the ways antibodies work. It is already used as a treatment against rabies. There you get a dose of immunoglobulins directed against the rabies virus together with the vaccine. The immunoglobulins neutralize the virus.

The same is possible when you vaccinate against the surface proteins which a virus uses to dock to a cell. With the resulting antibodies this docking is at least hindered if not completely prevented. And there are interesting results from the Ebola research which used a small molecule inhibitor to identify the protein which is important for cell binding of the virus. It is called NPC1, when the receptor on the virus surface is blocked, no docking can take place. This will be one of the approaches to make a therapeutic. See here for more details.

And it is of course possible to design more of the molecules - the problem is to find substances which do not interfere with body functions or which stimulate other pathways.


Evolution of leukemia pluripotent short-term cells

Some background: leukemia is an immune cancer so it comes from the hematopoietic system. Thus, it would be useful to look into Hematopoietic stem cells (HSCs). Note that, in general, the (semantic) hierarchy of stem cells goes: totipotent, pluripotent, and multipotent, in order of less generality (i.e. more differentiated, or more mature as a cell in other words). Maybe reading about stem cells in general would be useful too.

HSCs have two subtypes: one which can indefinitely renew itself, and one which has a timed lifespan (i.e. it stops being capable of generating new cells of different types after awhile).  It is interesting to note that leukemias have  an analog of these, which is what is being referenced, presumably, in the paper.
See Normal and leukemic hematopoiesis: Are leukemias a stem cell disorder or a reacquisition of stem cell characteristics? for a bit more on this.
Multipotent progenitor cells (MPCs) are also capable of generating new cells, but are capable of less variety than plutipotent stem cells.
They can "choose" to become a more differentiated cell (i.e. choose a lineage).
They also cannot self-replicate (i.e. to divide and create new multipotent progenitors) indefinitely, though they can do it for some number of steps usually.
In other words, an MPC will generate a finite number of cells, whereas a true stem cell can divide indefinitely, given the resources.
The Goldie-Coldman Law (also called hypothesis) can be summarized via:

  This hypothesis predicts that the tumor cells develop resistant phenotypic variations towards chemotherapeutic agents. This resistance is independent of the chemotherapeutic agent and dependent on the number of cell divisions that occur after treatment begins. The larger the tumor size or the longer delay in initiating chemotherapy, the more resistant cells. The implication is that a regimen of alternating cycles of two different non–cross-resistant chemotherapy medicines yields a better chance of tumor eradication.
    (From here).

       In other words, it is a model for how cancers become resistant to drugs. See also Improving       Cancer Treatment via Mathematical Modeling: Surmounting the Challenges is Worth the Effort.

Ok, onto the second paragraph. I will be very informal here :)

  Let $Q$ denote the density of stem-cells population.

Within a cell population (cancer or otherwise), often there is a small subpopulation of stem cells (the rest of the cells are differentiated cells). So if there are $N$ cells in total, roughly $S=QN$ will be the number of stem cells present.

  A percentage $\eta_1$ of these ones are supposed to undergo asymmetric division with one daughter cell identical to the mother cell and the other one committed to differentiation.

Within the population of stem cells (which are a subpopulation of cells), there will be further subcategories with different reproductive behaviours.
Notice there are really only 3 options: a stem cell becomes (a) two stem cells, (b) two differentiated cells, and (c) one stem and one differentiated cell.
This sentence means that roughly $s_1 = \eta_1 S$ cells will divide in the asymmetric pattern given above.

  A percentage $\eta_2$ of the stem-like population differentiate symmetrically and go to the line of mature cells.

This means the number of symmetric divider cells is roughly $s_2 = \eta_2 S$ (both outputs will be differentiated.

  The rest of them, a percentage $p = 1−\eta_1−\eta_2$ is supposed to self-renew: both cells that result from mitosis are identical to the cell that entered to the cell cycle.

Finally, around $s_3=pS$ cells become stem cells again, i.e. division type (a).

  The same duration $\tau$ of the cell cycle is supposed for all types of division.

In order to divide, every cell has to undergo a complex process called the cell cycle. This takes time; in other words, it upper-bounds/limits the rate at which cells can divide. Presumably, different cells take different lengths of times to divide. This assumption above ignores this issue.

Edit (062018): let's take a look at the equation
$$
\tilde{r}(P) = r_1(P)\frac{x_0 - R_0}{x_0^{-p+1}} \;\text{  with  }\;
r_1(P) = \frac{P^m}{P^m + P^m_0}
$$
where $Q$ is the density of the stem cell population, $P$ is the amount of plasmatic drug, $P_0$ is the half-maximum activity concentration, $m$ is the Hill coefficient, $x_0$ is the number of infected cells, $R_0$ is the number of resistant cells, $p$ is the probability of mutation, and $q=-p\in (-1,0]$.

From a high level perspective, we need to account for three effects of treatment:
(1) the building of the cancer's resistance to that treatment,
(2) the increase in drug effect as it gets absorbed and decrease as it is excreted, and
(3) the effect of the drug on the target cells.

First, notice in the differential equations:
\begin{align}
\dot{Q} = f(Q,t) - \tilde{r}(P)Q^{q+1} \\
\dot{D} = -\lambda_0 D + K \\
\dot{P} = -vP + \lambda_0 D
\end{align}
that (2) is being handled in the equations for $D$ and $P$.
Drugs start in some compartment (like the intestines when you swallow a pill) where they are not so useful against leukemia. Here they start with some concentration $K$, and the amount of drug decreases with first-order kinetics, i.e. the first order linear differential equation that shows $D$ decreasing. See an article on pharmacokinetics for more info on this.

Once the drug is absorbed (i.e. contributes to $P$ instead of $D$), it enters the plasma and starts to have an effect on the leukemia cells. (Notice that (2) is being handled here as well, in the $-vP$ term of the differential formula for $P$, which measures how fast your body is destroying the drug.)

Naturally, only the drug concentration $P$ in the blood plasma can affect the cancer cells; hence, the term for $\tilde{r}$ only depends on $P$!

Next, we can see how the model accounts for (3) in the differential equation for $Q$. Again, we have first-order kinetics of $Q$ (by the first-order linear differential relation), modulated by $r$ and $q$. Since $q + 1 > 0$ and $\tilde{r} \geq 0$, we know that as $\tilde{r}$ increases, we are causing $Q$ to decrease faster, i.e. we are hurting the cancer more (good!). Thus we expect that as $P$ (the drug concentration) increases, $\tilde{r}$ should also increase.

Ok, so now for (1). Notice that the equation for $\tilde{r}$ breaks into 2 terms. The second term is $R_T=(x_0- R_0)/x_0^{-p+1}$. This captures the effect of resistance, as the cancer evolves via mutation to gain resistance to the drug. Notice there is no dependence on the drug itself (just as described in the Goldie-Coldman hypothesis). (Note that this may not be realistic, since the drug will induce an (un)natural selection pressure on the cells and encourage the ones that resist the drug to proliferate more easily; however it does simplify the model).
Notice that $R_T$ decreases as $R_0$ increases, meaning that as the number of resistant cells increases, the efficacy of the treatment decreases.

The first term, i.e. $r_1(P)$, describes the effectiveness of the drug as a function of its concentration via the classical Hill equation.
Simplistically speaking, drugs often act via receptor molecules on the surfaces of cells; once all these receptors are saturated, the drug cannot affect the cell anymore! Hence, the effect of a drug "levels off": as its concentration increases, it will bind more and more receptors (and thus have more and more effect, albeit at a diminishing rate), until saturation occurs and adding more drug (i.e. increasing $P$ no longer does anything). You can see this in the equation for $r_1$ since $\lim_{P\rightarrow\infty} r_1(P) = 1$ (though of course $\partial_P r_1 > 0$ still). The $m$ and the $P_0$ simply control this relationship: the Hill coefficient $m$ describes the "cooperative binding" properties of the drug (see the link above for details), i.e. whether binding accelerates further binding or not, while $P_0$ (usually denoted $K_A$, or called the dissociation constant) describes the ligand concentration at which half the target sites are occupied.
Higher $P_0$ means that occupying half the receptor sites requires a higher concentration, which means you need more drug for the same effect, i.e. the efficacy of the drug is poorer; this is why $P_0$ appears on the denominator: as it increases, the effect of the drug on the cells (given by $\tilde{r}$) will decrease.
Essentially, $m$ controls how fast the drug reaches peak efficacy (how steep the curve is), while $P_0$ controls the physical properties of molecular binding (the translation component of the curve).


bacteriophage T4 has a single chromosome (approx. 200 kb in length). The chromosomes are terminally redundant,  so the genetic map is circular, even though the physical map is linear (as I recall).
A mutation in E. coli (or its viruses) that affects two adjacent protein-coding genes is said to be 'polar'. This indicates that the two genes in question form part of an operon. A strong loss-of-function mutation in the promoter for the operon will typically affect the expression of all the genes in the operon. In your example there are two cistrons, or genes, in the rII locus of T4.

It is possible that the data for this question are taken directly from the published literature. I suggest you search PubMed for papers by Seymour Benzer, from the 1950s.


Interesting question! The cause of tears and itching is the chemicals produced by onion (Allium cepa). Lets go into some details.

Onions, coming from the family Liliaceae (also containing garlic, chives, scallions and leeks) store compounds known as amino acid sulfoxides, and the one we are talking about here is S-1-propenyl-L-cysteine sulfoxide (abbreviated as PRENCSO), also calles isoalliin (due to its similarity with alliin found in garlic). When onion is damaged (cut, chewed, etc.), an enzyme alliinase converts PRENCSO into 1-propenyl sulfenic acid. This compound is then converted into propanethial-S-oxide by an enzyme lachrymatory factor synthase (earlier this reaction was considered spontaneous). The reaction looks like this:

Propanethial-S-oxide is the major cause of the flavor and aroma of onion. However, it is a volatile compound i.e. vaporizes very quickly. When its vapors reach the eye, it causes tears because of being a lachrymator (aka tear gas) i.e. as soon as it comes in contact with cornea, it triggers a nervous response which leads to activation of lachrymal (tear) glands.

PS: when propanethial-S-oxide comes in contact with cornea, a small amount of it reacts with water to form sulfuric acid. This sulfuric acid is the cause of itching and irritation in eyes due to onion. Also, scientists are now trying to genetically either modify or stop the production of lachrymatory factor synthase enzyme to produce tearless onions. This (modification) has even been achieved to a high efficiency, as another answer discusses. However, making tearless onions could prove harmful to the crop in several ways, as discussed here.

EDIT: As asked in comments, I will add some details about how the sulfuric acid is produced from the reaction between propanethial-S-oxide and water.

The only resource I could find giving some details about this was Marta Corzo-Martínez, 2014. They summarize the complete pathway in the following diagram:

After applying some common chemistry principles, the concerned reaction turns out to be:

$\ce{4~C_3H_6SO~+~4~H_2O \rightarrow 4~C_3H_6O~+~H_2SO_4~+~3~H_2S}$

As you see, one of the products of hydrolysis of propanethial-S-oxide is hydrogen sulfide ($\ce{H_2S}$). Just like $\ce{H_2SO_4}$, $\ce{H_2S}$ also causes irritation in the eyes (its effect on eyes has been well documented, see Lambert et al, 2006 as an example). Thus, the produced $\ce{H_2S}$ only increases the irritation and itching in the eyes caused due to $\ce{H_2SO_4}$.

BONUS: Another interesting point here is runny nose. propanethial-S-oxide is actually the compound responsible for the smell and flavor of onions. But, it causes tears by exciting the lachrymal glands i.e. reflexive lachrymation. propanethial-S-oxide excites the trigeminal nerve (the fifth cranial nerve) causing activation of lachrymal glands. Interestingly, the nerve endings of trigeminal nerve are also present in the nose, along with the eyes. So, this compound can also activate the lachrymal glands from your nose, and since the lachrymal duct is joined from eyes to nose, you can also experience runny nose along with tears and irritation in eyes.

References:

Propanethial-S-oxide | University of Bristol
Alliin | Wikipedia
Tear Gas | Wikipedia
Timothy William Lambert, Verona Marie Goodwin, Dennis Stefani, Lisa Strosher, Hydrogen sulfide ($\ce{H_2S}$) and sour gas effects on the eye. A historical perspective, Science of The Total Environment, Volume 367, Issue 1, 15 August 2006, Pages 1-22, ISSN 0048-9697, https://doi.org/10.1016/j.scitotenv.2006.01.034
Encyclopedia of Perception, Volume 1 -
E. Bruce Goldstein,
SAGE, 2010
The Neurology of Lacrimation – How an Ear Infection Can Cause Dry Eye -
by Noelle La Croix, DVM, Dip. ACVO


How to design a permanent vaccine to cholera using CRISPR?

So, would it be possible to engineer a CRISPR gene editing tool to
  prevent Vibrio Cholerae from getting into our cells?

Vibrio Cholerae doesn't get into our cells.

Did you observe that your paper has no in vitro experiments?

It's going to be tough to get a cell to transcribe and translate something so small, and will the peptide work if it needs a leader sequence to be exported out of the cell?

Its much much easier to break a gene in every cell than to add a new gene and have just a small subset of cell types make large quantities of that gene product.


Why is the relative expression in qPCR so low?

It may be a particular mutation that affects expression altogether. Through qPCR you're able to tell the relative difference in mRNA levels of a particular gene between, say, a WT and a mutant. It may be that this particular mutation damages some regulatory sequence within the body of a gene (e.g. a downstream promoter element) or some regulatory sequence upstream. To me, this suggests that you're dealing with such a case here. Anyways, you'd need more data to tell for sure. You should have the mutation mapped, if you haven't already and check if the primers you used were  okay. This mutation clearly hampers expression, as long as everything was okay with the procedure.


How does entry of Ca²⁺ to the myocardiocyte make it more contractible?

The answer is a bit more complex. Calcium ions have a lot of effects in the cardiac myocyte. Apart from the increased contractility (positive inotropy), extracellular calcium concentration also alters chronicity as you mention by altering the rate of repolarisation. An attempt at a simplified picture of the inotropic effects follows:

First is to increase the contractility via directly sensitizing the tropomyosin system. Have a look here. Quoting the paper, "...In both cardiac and skeletal muscle, the force-generating molecular motors (crossbridges) are turned on by increasing the intracellular free calcium level that regulates the troponin-tropomyosin system. However, calcium activation is a two-way process in the sense that activated crossbridges also affect the troponin-tropomyosin system...An increase in Ca2+ activity causes an azimuthal shift of tropomyosin around the filament (by about 30 degrees), thereby increasing the probability of low-force crossbridge interaction, a process which by cooperative effects induces further tropomyosin movement (by an additional 10 degrees) which results in the open state of the filament characterized by forceful cross-bridge interaction...". Hence, higher the intracellular concentration of Calcium, greater is the maximum force.
Sarcomere length also affects the sensitivity to calcium. This increase in contractility is not because of calcium but is mediated by calcium. The reason has something to do with lateral filament lattice spacing decreasing, increasing the probability of cross-bridge formation, increased strain on titin alters lattice spacing and myosin packing.

As I said, this is a bit too oversimplified. There a lot of inter-regulations taking place. Have a look at these papers here.

Myofilament Calcium Sensitivity: Role in Regulation of In vivo Cardiac Contraction and Relaxation (A good review plus a bit of quantification on the topic being discussed)
The negative inotropic effect of calcium overload in cardiac Purkinje fibers (To present the complexity)


This is an interesting - and highly debated question. Generally there are two completely different directions of thinking when talking about dangerous substances (this applies to dangerous chemicals as well):

The linear no-threshold model (LNT).
The hormesis model, in our case the model of radiation
hormesis.

Summarizing the models the LNT model says that every dose has a negative response, so there is nothing like a stimulating dose and exposure should be avoided at any means. This reflects the policy in the handling of radioactive substances. If you look at the figure below, the curves a + b (supra-linear and linear) reflect the LNT model (the figure comes from here):

The radiation hormesis model says that there is a dose range in which the radiation above the background level is not only not harmful, but beneficial. High doses are (in line with the LNT model) also considered harmful. This can be seen in the curves c (linear-quadratic) and d (hormesis) in the figure above. The benefits are thought to take place through the activation of repair mechanisms (which are only activated by radiation) which protect against changes in the genome and thus also protect, once activated, against changes which are caused by other agents and reasons. See reference 1 for more details about radiation hormesis.

There are a number of studies which observe this effects in the laboratory and this is also one of the major critic points: To my knowledge it is currently unknown if these effects can also be seen outside a controlled laboratory environment.

Other critique points are low study publications (which makes studies prone to statistical errors), using wrong models (cell culture) or too high doses. See references 2 and 3.

Since our environment contains naturally radioactive substances as well as cosmic and UV radiation, we have developed pretty efficient mechanisms to deal with these problem. Additionally measurable effect of radiation on the activity repair mechanisms can be seen (and this is not debated at all), but the main question is if these effects can also have a beneficial effect. It is also not known, if all radiation ($\alpha, \beta$ and $\gamma$) have the same effect, or if some of these like $\alpha$-radiation is more dangerous.

So I think it may be possible that there is some positive effect, but until this is proven, I would rather be safe than sorry.

References:

Evidence for beneficial low level radiation effects and radiation
hormesis.
Uncertainties in studies of low statistical power
Health Risks from Exposure to Low Levels of Ionizing Radiation


Yes, they do. The ovaries produce both testosterone and estrogen. Relatively small quantities of testosterone are released into your bloodstream by the ovaries and adrenal glands. Sex hormones are involved in the growth, maintenance, and repair of reproductive tissues [1].

The serum testosterone level in women with no acne, hirsutism, or menstrual dysfunction is 14.1 +/- 0.9 ng/dL (nanograms per decilitre) [2]. An average adult man has 270-1,070 ng/dL serum testosterone [3].

Men have female sex hormones too. For a prepubescent male, estrogen levels are expected to be between 1 and 3.7 ng/dL. During puberty, normal levels fall between 2.3 and 8.4 ng/dL. Levels for an adult male should be between 2.5 and 5 ng/dL [4].

References:

WebMD, LLC. Normal Testosterone and Estrogen Levels in Women.
Ayala C, Steinberger E, Smith KD, Rodriguez-Rigau LJ, Petak SM. Serum testosterone levels and reference ranges in reproductive-age women.
Alexia Severson. Testosterone Levels by Age. Healthline Networks, Inc.
wiseGEEK.com. What Are Normal Estrogen Levels in Men? (Measurements cited in picograms per millilitre, converted to ng/dL)


What causes a polypeptide to fold into an Alpha helix over a Beta pleated sheet

All the residues in a polypeptide chain tends to configure into their lowest potential energy state. except the peptide bond all the other bonds are free to rotate, alpha helix makes optimal use of internal H bonds. The overall structure is stabilized by H bond between the hydrogen atom attached to the electronegative nitrogen atom of peptide linkage and the electronegative carbonyl oxygen atom. The arrangement of amino acids in the peptide plays a very important role in forming alpha helix. Different combination of amino acids results in different combination of dihedral angels, hence it determines alpha helix conformation.


What does "fit" mean in "survival of the fittest"?

'Survival of the fittest' has never really made sense, because it confuses the scientific (evo. biological) and colloquial definitions of the word - which some of the previous posters have also done.

Biological fitness simply refers to an individuals genetic contribution to the following generation. That is, a 'fitter' individual, in an evolutionary sense, is one whose genetic material is proportionally overrepresented in the next generation.

The mechanism by which an individual achieves this may include out-surviving competitors, but it's certainly not the only way to increase fitness. Two individuals may live for the same length of time, but one may successfully court more females, or out-compete the other for food resources, for example. So when we refer to a 'fitter' individual (or individuals), we're saying nothing about why they are so. It's not a comment on their 'fitness' in the human sense of the word (bigger, stronger, longer-living), it simply refers to how well they pass on their genetic material.

So you can see why the phrase is nonsense. If we're being precise, then 'survival of the fittest' translates to 'survival of the individual who is better able to pass on their genetic material to the next generation' - which is meaningless because it tangles up these different concepts.


Do women experience more bonding hormones than men after sex?

Does Oxytocin increase more so for women than for men after sex?

Answer: Yes, Oxytocin level shoot up for female after sexual. It is highest at orgasm, which is the main cause women could have multiple orgasm.

  Someone told me that it increases 4-fold for men and 12-fold for women
  (unconfirmed).

Answer: The level of oxytocin actually increase 5 times during sexual intercourse. Though some online article claim the male and female level as much you said, but it is not confirmed in humans.

  Is there any observable or scientific relationship between sex, Oxytocin and the desire for a monogomous relationship with a sexual partner?

Answer:

Take a look at this experiment done on people to test Bonding:

  Bonding is an important part of human romantic relationships, and
  research has suggested OT as a possible mediator of this effect. A
  2005 study by $Grewen\ et\ al^{4}$. found that couples who reported a greater
  amount of partner support showed higher baseline OT plasma levels.
  These couples also showed higher levels at 4, 7, and 10 min following
  warm partner contact. For women, OT levels increased sharply 7 min
  following warm partner contact, regardless of partner support, while
  male levels remained unchanged. This study demonstrates a
  relationship between supportive romantic bonding and OT, and shows
  that warm contact has a greater physiological effect on women than on
  men.[1]

A very famous study done on rats confirm that Vassopressin and Oxytocin is actually the reason behind monogamous relationship.

  Almost a decade ago, Thomas Insel, Director of the Center for
  Behavioral Neuroscience at Emory University, and colleagues at the
  National Institute of Mental Health and the University of Maryland
  implicated vasopressin and oxytocin in controlling the preference for
  particular partners in both male and female prairie voles. These
  investigators found that giving a male vasopressin causes it to stay
  with its mate, whereas blocking this hormone prevents a pair-bond from
  forming. The scientists saw similar effects in female prairie voles,
  with oxytocin determining the extent of pair-bonding. In contrast, the
  administration of these substances had no influence on social
  interactions in the promiscuous montane voles. Surprisingly,
  vasopressin and oxytocin are naturally found at similar levels in both
  prairie and montane voles.[5]

Source:

[1]. The role of oxytocin in mating and pregnancy

[2]. http://en.wikibooks.org/wiki/Relationships/Hormones#Oxytocin

[3]. The role of oxytocin in relation to female sexual arousal.

[4] Grewen, K.M., Girdler, S.S., Amico, J., Light, K.C., 2005. [Effects of partner support on resting oxytocin, cortisol, norepinephrine, and blood pressure before and after warm partner contact](Effects of partner support on resting oxytocin, cortisol, norepinephrine, and blood pressure before and after warm partner contact.). Psychosom. Med. 67, 531–538.

[5] http://www.smart-publications.com/articles/oxytocin-the-real-love-hormone


Why don't we speak of medial and lateral rotation of the forearm? And pronation and supination of the upper arm?

Pronation and supination involve a change in relationship between the ulna and radius.

  When you rotate your hand from palm ventrally (as in anatomical
  position) to palm facing dorsally you have moved your hand from a
  supinated position to a pronated one. This movement of supination to
  pronation occurs when the distal head of the radius rotates on the
  capitulum , the bone rotates along its long axis, and the proximal
  head of the radius flips over the ulna. (Duke Medicine)

and:

  Pronation and supination are rotational motions that exist exclusively
  in the forearm. The mechanical bases for these movements are the
  existence of two forearm bones and the presence of two coupled
  trochoid joints—the proximal and distal radioulnar joints (PRUJ and
  DRUJ). (Clinical Gate)

Image source: Wikimedia, CC licence

During medial or lateral rotation of the upper arm (without additional rotation of the forearm), the humerus rotates, but the relation between the ulna and radius does not change, so there is no pronation/supination.

It is more practical to use supination/pronation for the forearm/hand, because you can have a forearm/hand in various positions where medial/lateral or internal/external does not make sense: for example, when you rotate your forearm/hand with your arm extended toward the side. Saying that, medial/lateral and internal/external rotation of the forearm is also commonly used (search: "medial rotation of the forearm"). So, you can use any of these terns according to what's more practical and less confusing in a given context.


What causes the characteristic 'gleam' in the eye of a living being?

Not being an opthalmologist, if one happens along and gives a better/correct answer, listen to them.

Otherwise, let's take a moment to look at the eye:

What is not pictured here is the saline-like solution that keeps the conjuctiva moist. If we include the lubrication in all of the surfaces which interact with light, our list would look like this:

Lubrication
Conjuctiva
Cornea
Anterior aqueous humour
Iris
Posterior aqueous humour
Lens
Vitreous humour
Retina
Fovea

Out of that list, the Iris, Retina, and Fovea are designed to absorb light; not reflect it. The Vitreous humour merely serves as a medium for light to pass through and probably would not reflect light on its own. The same is true of both aqueous humours - they do not modify the light so much as serve the eye structurally.

That leaves us with the Lubrication, Conjuctiva, Cornea, and Lens - surfaces which also interact with light, but act to some extent to reflect or modify it as well. The Cornea is what's actually operated on when a person undergoes corrective surgery; a pattern is etched into the Cornea which redirects light similar to the person's previous prescription and giving them better vision.

Now, because you mention the difference between an excited person and presumably someone at their normal state, it's worth to note (when dealing specifically with the eye) a very common side-effect of psycho-active drugs and emotional states (particularly fear and interest/curiosity) is the change in pupil size when lighting conditions don't change:

The reflection is different depending on the size of the pupil, and I would venture to guess the pupil size difference between someone who's excited or manic (whose system is flooded with endorphins) and the person at normality is part of what you define as 'gleam.'

The other situation you draw a difference between is a dead person vs. a living person. Before rigor mortis sets in, the relaxed state of the ciliary body is to stress the suspensory ligaments - resulting in pupil dilation. In addition, and I think this is the most important distinction: dead people don't blink. The act of blinking spreads the lubrication on the surface of the conjuctiva, and can be mimicked with tear-drops for people with dry eyes. Because the lubrication acts as another surface to reflect light (similar to having a thin layer of water on a surface), the dead person's eyes will have less of a "gleam" than a living person's.

So, to sum up: The "gleam" in a person's eye is probably due to hydration and/or pupil dilation. Pupils will dilate at lower light levels, under the influence of certain drugs, or when showing interest. Hydration is constant, except when the lubrication is not produced in the quantities necessary or when the person is unable to blink ('dead' in your example).


Male grasshoppers often mate several times with multiple female, and some females will mate again after, and perhaps even before they lay their eggs. So no, they are not monogamous.

Rufous grasshoppers for example have a very special mating cycle, the male will attract other females, possibly more than one with "pursuit sounds". After copulation, he keeps her close to prevent other males from mating with her, and the females enter a defensive mode where they refuse intercourse from other males. After laying eggs however, she enters a "relaxed" mode where she is open to others for mating.

Sources:

jrank

Rufous grasshopper: inaturalist


Can men also become only bald on their legs?

Hair loss is known as alopecia, and is often associated with hair loss on the head. This type of hair loss is most noticeable, but hair loss can occur in nearly any part of the body, including the legs (source: Healthline). As an anecdote - my father in law (65+) has lost all his hair on his legs. This hair loss is referred to as anterolateral leg alopecia

About 35 percent of older men have this condition. The exact causes of anterolateral leg alopecia are unknown, but there may be a genetic component.

Age related hair loss in men is referred to as male pattern baldness, or androgenic alopecia. This type is related to hormones and certain genes.


Simple protein graphics software for stick models

This is an answer simply because I can't fit it all in a comment, or several...

To install and run PyMOL, you'll need a few extras. They are all free and open-source:

Python 2.7.10: Make sure you choose to install pip during the setup process, and also choose to add Python to your PATH, if that option is given. Also, note whether you installed the 32-bit version (x86 MSI installer) or the 64-bit one (x86_64). Which you choose depends on your operating system - if you have a 32-bit OS, you only have one choice. If you have 64-bit Windows, you can do either one - there's no real difference to the casual user. I like 64-bit, but I'm a nerd :)
The numpy+mkl package: I'd get version 1.9.2, as 1.10.0b1 is a beta version. Make sure it's not one of the "unoptimized" builds! You want the cp27 (stands for CPython 2.7) package, either 32- or 64-bit, matching your choice above.
From the same page, the PMW package (choose the py2 version).
Finally, PyMOL itself (both pymol and pymol_launcher packages for cp27).

Once you have everything downloaded and Python installed, open the command prompt by hitting WinR, typing cmd into the box, and hitting Enter. Use the cd command to change to the directory where you downloaded the .whl files (paths with spaces in them should be completely enclosed in double quotes: cd "C:\Users\John Smith\Downloads"). Next, type pip -V to ensure pip works. If it doesn't, just use the whole path: C:\Python27\Scripts\pip -V. Once you get the version statement, you're good to go. For each filename, type pip install really_long_filename.whl to install it. Remember that you can start typing a long name, then hit Tab to complete it. Do this for all four wheels - numpy+mkl, pmw, pymol, and pymol_launcher - in that order.

Once you do that, you should be all set. I'm not on Windows at the moment, so I can't tell you whether you'll get an icon or not, but if you don't, then open Windows Explorer and browse to the C:\Python27\Scripts directory - there may be a PyMOL script there you can run.

If you have any questions, please ask on Stack Overflow, tagging the question with [python] and [pymol]. People are generally very quick with comments and/or answers, so please stick around on the question's page for 5 or 10 minutes to assist those who would help you.

Good luck!


Does the most common definition of "allele" include a change in phenotype?

Yes, allele is an alternative form of the same gene which can be produced through any variations/mutations of a gene, such as deletion, segmental duplications, inversions, insertions through transposons, even a SNP or point mutation (http://en.wikipedia.org/wiki/Allele) and as correctly stated many alleles do not produce any observable/discernable phenotypic variation. A gene can have many alleles in a given population, but do not confuse allele with gene homologues (which I suspect what you were alluding to above in the second paragraph), which are similar versions of a gene such as RIN1, RIN2 and RIN3 (http://homepage.usask.ca/~ctl271/857/def_homolog.shtml).


Self-replication in the genome in the seed

DNA in cells in general replicates when cell division occurs (unless it is a cell that contains many nuclei or multiple copies of its own genome, in which case DNA would replicate as copies are made. Multinucleate cells include things like the mycelium of fungi, and here is an example of a bacterium with thousands of copies of its own genome).
As long as a plant embryo is developing, then the cells are dividing and the DNA is replicated. You might be thinking of the stage of seed dormancy; insofar as during this stage the embryo is no longer growing, cells aren't dividing and therefore DNA is indeed not replicated. I don't know whether we could say the genome is "turned off" however, DNA's role isn't just being replicated, more importantly its role is to be transcribed into RNA which leads to the proteins the cell needs to function being created. I couldn't find whether DNA transcription happens during cell dormancy but it's plausible enough that it is at least slowed down as well. The cells presumably don't have much to do during this period and you wouldn't want them to do much, to conserve energy.
Seeds contain nutrients that can feed the embryo until it can feed itself (for plants that is the moment when they germinate enough to photosynthesize). That is where flour comes from!


What is the deepest place in the crust that has been found to harbor life?

The deepest living animal:

That award goes to the "Devil Worm" (Halicephalobus mephisto), a nematode that has been found living at 3.6 km below the surface!!

Halicephalobus mephisto is tiny (only 0.5mm long), and represents the deepest multicellular organism ever found.

The original paper can be found here: Borgonie et al. (2011)

I should note, that the paper found definitive Halicephalobus mephisto at 1.3km depth, but found rRNA gene sequence belonging to a specimen of Monhysteridae at the deep 3.6km depth.

Do these microbe abundances and diversity change with depth?

According to  Inagaki et al (2015), microbe density is very low at low depths:

  By counting the cells of these microbes, they also conclude that it is a small community, with just one cell in a cubic centimetre of sediment in some sections of the sediment


Is it possible to have multiple stop codons in one exon?

An exon can have multiple stop codons but the first codon will terminate the ORF. The remainder of the exon will be a part of the 3'UTR.

However, there are some cases in which stop codon readthrough happens [1]. In these cases an internal stop codon does not terminate the translation and the ribosome reads through it. During this process an aminoacyl-tRNA successfully competes with the release factor. This is quite evident in the case of selenocysteine and pyrollysine- tRNAs which bind to the UAG (amber) stop codon in certain organisms [2,3] (this is also referred to as amber suppression). The exact mechanisms that affect stop codon readthrough are not elucidated but features in the mRNAs are likely to play a role in this. In case of amber suppression, the relative rarity of the UAG stop codon and lower concentrations of release factor-1, can be major factors.

I don't know what you mean by "beginning of the exon" but there are short ORFs (< 100 codons) which can code for small peptides [4]. Small peptide as small as 6 amino acid residues has been reported but most of the known small peptides are ~30-100 residues long.

References:
[1] Loughran, Gary, et al. "Evidence of efficient stop codon readthrough in four mammalian genes." Nucleic acids research 42.14 (2014): 8928-8938.
[2] Agafonov, Dmitry E., et al. "Efficient suppression of the amber codon in E. coli in vitro translation system." FEBS letters 579.10 (2005): 2156-2160.
[3] Wikipedia: Expanded genetic code
[4] Andrews, Shea J., and Joseph A. Rothnagel. "Emerging evidence for functional peptides encoded by short open reading frames." Nature Reviews Genetics 15.3 (2014): 193-204.