Does red light preserve your night vision?

This is a very good question.  Red light is routinely used by scientific laboratories to do low light dissections of retinas, and of course it is used in other low light contexts such as printing plate development.

In both of the above contexts, you have a clear subject: the retina being dissected or the printing plate being developed.  In the case of the printing plate the film has been designed to be specifically non-reactive to red light, so red light is used because your eyes can see it, but the film doesn't react to it.  Similarly in some scientific settings it makes sense to use red light during dissections.  Mice lack a long wavelength opsin, and therefore using a dim red light allows the experimenter to have a relative sight advantage compared to the mouse when keeping the mouse dark adapted.

But in the case you're asking about, there is no film or animal to serve as a second party.  So is there any intrinsic advantage to using red light?  As it turns out, there is.  The fovea, which is in the center of our eye and used for high acuity vision, has no rods and primarily L- or red sensitive cones.  Note the high density center area which lacks blue sensitive cones and has 2:1 red to green cones.

So by having red light present, you stimulate this area.  But red light is present in white light, too, why not just use that?  Leonardo's answer comes the closest, but it's a little off.  Red light is used because it preferentially stimulates L cones more than rods, but you are definitely not able to preserve night vision by using red light.  Why not?  Well it may look like it is possible to exclusively stimulate cones from the chromatic sensitivity figure

But that figure is 1) normalized and 2) not indicative of synaptic signal processing.  1000's of rods can converge onto a single ganglion cell, where cone convergence in the fovea can be on the order of a single cone per ganglion cell.  When it comes to perception, in order to compare the black rod line above with the red L-cone line you'd have to magnify it dramatically in size.  Practically speaking, it is nearly impossible to stimulate cone pathways without stimulating rod pathways when using a relatively broad spectrum LED that you're powering with a battery.  Maybe with a high power infrared laser.

So the purpose of using red light is to attempt to balance the activation of high sensitivity (red insensitive) rods with that of the low sensitivity (but red sensitive) cones in the fovea.  While using a similar level of rod activation with blue light, you would perceive a "blind spot" where your fovea is.

Finally, instrinsically photosensitive cells (the melanopsin cells brought up) do not factor into this processing.  These cells are activated only with extraordinarily bright levels of light, and the therefore do not enter into conversations dealing with night vision.


Why don't electric eels shock themselves?

Short answer, no one knows, there is some minor evidence they are do shock themselves but are resistant to it, (they react far stronger in air than in water to their own discharge), but it is not a high priority for research so no one has really tested it.


Can we apply NGS (next generation sequencing) on DNA extracted from formalin fixed paraffin embedded tissues (FFPE)?

It's a little hard to tell based on your question, but it seems that you want to do Illumina sequencing of FFPE tissue samples. This is quite routine, Illumina sells kits for it.
I do not know how the FFPE process affects microbial cells, but people have published recently on doing metagenomic analysis of FFPE tissue samples. This suggests to me that it is possible.
If "any contamination" is a problem, then maybe there are additional roadblocks; low-level contamination is a routine problem in metagenomics, which is exacerbated by complicated, old, or low-input sample types. I would suggest treating it the way you would treat any other metagenomic sample, and try to exclude the possibility of contamination through methods and account for it in data analysis.


even though they exist inside the bacteria cell cytoplasm

Plasma has several meanings in biology.  Cytoplasm is a type of plasma.

A quick trip to Wikipedia tells us that the term plasmid was first used by Joshua Lederberg in Cell Genetics and Hereditary Symbiosis.  It seems that he coined the term plasmid to reconcile the many terms used to describe extrachromosomal DNA, at the time.

  These discussions have left a plethora of terms adrift: pangenes, bioblasts,
  plasmagenes, plastogenes, chondriogenes, cytogenes and proviruses, which have lost
  their original utility owing to the accretion of vague or contradictory connotations. At the risk of adding to this list, I propose plasmid as a generic term for any extrachromosomal hereditary determinant. The plasmid itself may be genetically simple or complex. On occasion, the nuclear reference of the general term gene will be emphasized as chromogene...


Eyebrows function to protect the eyes from perspiration and provide shade.
Eyelids function to protect the eyes from foreign objects and sunlight.
Eyelashes function to protect the eyes from foreign objects, produce sebum (a lubriant that the eyelids) and acts as protection for the eyes from tears [1].

The above seems to be backed up by health how stuff works and the anatomy of the eye from emedicinehealth.
However, note that biologist dont have any concrete reasons for the eyebrow. This is just what many of them agree on I suppose. Here is another resource from sciencefocus.


Can you identify the bird in this photo?

Looks like Butastur indicus, the grey-faced buzzard. The spotted breast and the greyish chin fit well.

A nice picture can for example be seen here


How did the cardiovascular system evolve?

While others have addressed the big picture aspects of your question, I think it would be useful to look at the specifics.

Have a look at the heart (or more accurately, the hearts) of the earthworm:

They're nothing more than veins with some pumping muscles wrapped around them. It seems almost a stretch to call them hearts, they are shaped so different from what we think of as a heart proper.

Also, note the earthworm's lungs, or rather, lack of them. It doesn't have any! Why not? It doesn't need them. It gets enough oxygen through its skin via osmosis. It's only larger organisms that need dedicated systems to concentrate oxygen from the surrounding environment.

So, the worm has a simpler system (no chambered heart, no lungs) that works.

All vertebrates descended from a common ancestor that was very similar to this earthworm. It had simple hearts, and no lungs. You can follow the evolution of the human heart through fish heart:

which is a more sophisticated pumping vessel with two chambers.

Amphibians evolved from fish, reptiles from amphibians, and mammals from reptiles. In this diagram, you will find that the heart becomes more sophisticated and efficient in each:

So, this should give you a good idea of the evolution of the human heart from simpler, working system. I won't take the time to draw out the evolution of blood vessels or lungs; maybe someone else will, or you can google them yourself, the information is readily out there. But they all follow the same pattern: gradual, incremental improvements on working, simpler systems.


The term neural computation is basically synonymous with computational neuroscience.  It is the science of studying how the brain processes information by creating realistic mathematical models. Unlike general study of artificial neural networks (ANNs), neural computation heavily relies on biological accurateness. However, it may use models from ANN research, and vice versa.

Also see this course description of the PhD level course "Neural Computation" at Carnegie Mellon University  (CMU) :

  Neural Computation is an area of interdisciplinary study that seeks to
  understand how the brain computes to achieve natural intelligence. It
  seeks to understand the computational principles and mechanisms of
  intelligent behaviors and mental abilities -- such as perception,
  language, motor control, and learning -- by building artificial
  systems and computational models with the same capabilities. This
  course explores how neurons encode and process information, adapt and
  learn, communicate and compute at the individual level as well as at
  the levels of networks and systems. It will cover basic concepts in
  computational and neuronal modeling, information theory and coding,
  neural networks and learning, neural data analysis and decoding,
  signal processing and system analysis, statistical learning and
  probabilistic inference.

(Emphasis mine)


Those voltages refer to the difference between the inside and outside of the cell (i.e., -70mV means the cell is 70mV more negative than the outside).

You can't possibly measure that potential difference from outside of a cell. When you do extracellular recording, you are measuring spatial differences in ion concentrations that occur due to ions flowing in and out of cells. For example, when a cell fires an action potential, lots of positive ions flow into the cell; this makes the area just around the cell slightly more negative than an area further away. The magnitude of this potential as measured depends greatly on your recording configuration, the type of signal you are recording (i.e., population activity or just a single cell; synaptic currents versus action potentials), how close your electrode is to the signal you are recording, and where your ground is (or position of both of your electrodes if you are doing a bipolar recording).

Although it varies, in most cases the signals you record extracellularly are on the order of microvolts to a couple of millivolts.


A little help understanding DNA supercoiling

After studying this topic a bit more I came to the conclusion that supercoiling itself does not overwound/underwound the DNA any further that it already is. Supercoiling just relieves the stress introduced after DNA gets further twisted in the first place, it relaxes the DNA by decreasing the twist back to normal (10.4bp per turn just like normal relaxed B-DNA) (in case of positive sueprcoiling and vice versa for negative) and the extra tension that made the DNA twisted in the first place now increases/decreases the writhe for positive and negative supercoiling respectively. The authors might have considered a DNA molecule with higher writhe value also a more wounded form of DNA that's why they used the term 'overwound'

Please correct me if I am wrong


How do trees manage to grow equally in all directions?

There are some other good answers which provide part of the picture, but I think there is a fundamental organising principle which has been missed. Konrad has touched on it in his answer.

The reason trees, and most plants, tend to grow equally in all directions is that they have iteratively generated branching and radial symmetry which is controlled in a feedback loop of the growth promoting hormone auxin and auxin-sensitive auxin transporters. This is an elegant biological algorithm which explains all branching growth.

The things Konrad identifies (phototropism, gravitropism, etc.) serve as orientation cues which help the plant determine which axes to grow along, but fundamentally the process is about auxin gradients. There are exceptions, as others have pointed out in their answers, and they usually result from severe imbalances in the orientation cues.

I'll try to explain the growth process clearly (and it gives me an opportunity to try my hand at diagramming again ^_^)...

Auxin is a plant hormone (actually a class of hormones, but mostly when people say auxin, they mean indole-3-acetic acid) which promotes cell elongation and division. The basic principle which allows auxin to act in the organising way it does is that auxin is produced inside cells, and proteins which export auxin from a cell develop on the side of the cell which has the highest auxin concentration (see figure below).

So auxin gets transported up the concentration gradient of auxin! Thus if you get an area of high auxin concentration developing somehow, more auxin is then transported towards that area. An area of high auxin concentration relative to the surrounding tissue is called an auxin maximum (plural 'maxima').

For most of the life of the plant, auxin is produced pretty much equally in most cells. However, at the very early stages of embryo development, it gets produced preferentially along the embryonic axis (see figure below, part 1). That creates a meristem - a group of cells where cell division is taking place - at the auxin maximum at each end of the embryo. Since this particular meristem is at the apex of the plant, it is called the apical meristem, and it is usually the strongest one in the plant.

So by having a meristem at each end, the embryo then elongates as cell division is only taking place at those points. This leads to part 2 of the image above, where the two meristems get so far apart that the auxin gradient is so weak as to no longer have its organising effect (area in the red square). When that happens, the auxin produced in cells in that area concentrates in a chaotic way for a short time until another center of transport is created. This happens, as the first one did, when a particular area of the tissue has a slightly higher concentration of auxin, and so auxin in the surrounding tissue is transported towards it. This leads to part 3 of the figure, in which two new meristems are created on the sides of the plant (called lateral meristems).

Lateral meristems are where branches occur on plants. If you then imagine this process continuing to iterate over and over, you will see that the branches, as they elongate, will develop meristems at the tips and along the sides. The main stem will also continue elongating, and develop more lateral stems. The root will begin to branch, and those branches will branch, etc. If you can understand how this elegant system works, you understand how plants grow, and why they grow in repeating units as opposed to in a body plan like animals.

It also explains why, if you cut off the tip of a stem, it promotes branching. By removing the apical meristem, you get rid of the auxin gradient and enable the creating of multiple smaller meristems which each develop into branches.

So far I've explained regular branching, but the same system causes the radial symmetry which makes trees (usually) grow in all directions equally...

Imagine taking a cross section through a stem and looking down all the way through it (as depicted crudely above). Just as auxin gradients act to coordinate growth along the length of the plant, they also coordinate it radially, as the maxima will tend to space themselves out as far from one another as possible. That leads to branches growing in all directions equally (on average).

I welcome comments on this answer, as I think its so important to understanding plant growth that I'd like to hone my answer to make it as good as possible.


Is it possible to estimate how much variation in common phenotypes is predicted by genetics?

Height

This is just a single example, but "height" has received a lot of GWAS (genome-wide association study) attention, and last year the GIANT consortium published results of an analysis on 250,000 people looking at the genetic influences of height [1].

Using just 2,000 genetic variants they could statistically account for 20% of the phenotypic variation in height. Using 9,500 genetic variants this rose to 29%.

What this emphasises is that common traits (such as height) are highly polygenic; there is no "height gene" that controls it - instead it is the combination of many small-effect variants that cumulatively give rise to an individuals final phenotype (height, in this case).

Pigmentation

Pigmentation (of eyes, skin and hair) on the other hand is not nearly as polygenic. A 2013 review [2] discussed the known genetic variation for these traits. Prediction of eye colour using genetics, for instance, requires only six genetic variants "to be suitable to predict blue, intermediate, and brown colors with an overall accuracy of 0.91, 0.72, and 0.93, respectively".

So in contrast to height where even with 9,500 variants measured you would still only have 29% accuracy, you can be 91% sure that someone will have blue eyes if you know the individuals genotype at only 6 positions.

So in short the quote you reference is incorrect - we can predict many common traits with reasonable accuracy - although for some phenotypes the individual predictive capability of a specific genotype may be around 0.01% (e.g. some of the height variants).

Wood, A. R. et al. (2014) Defining the role of common variation in the genomic and biological architecture of adult human height. Nat Genet 46, 1173-1186, doi:10.1038/ng.3097
Liu, F., Wen, B. & Kayser, M. (2013) Colorful DNA polymorphisms in humans. Seminars in Cell & Developmental Biology 24, 562-575


In vitro transcription, contamination problem

DNase treatment is actually one of the optional steps if you want to get rid of the original DNA template: https://www.neb.com/protocols/2013/04/02/standard-rna-synthesis-e2050

If you know, your the contamination happened after the transcription, DNase treatment should obviously help.

Concerning the aliquots: your stock is 200 times more concentrated than the aliquots (so to get equal amounts of RNA as in 1 µl of the stock, you'd need to take 200 µl of the 1 ng/µl aliquot). I don't think it's worth mixing them (and the efficiency of RNA precipitation will likely be decreased), otherwise just make another transcription.


Estimation of cases with dominant inheritance

It depends on the genotype of P (parents). If only one parent carries the dominant allele, F1 will have the allele 50%.

D = dominant allele, d = recessive allele

P: dd x Dd

F1: Dd 50%, dd 50%


What percent of e coli genes are necessary for survival?

About 10% in rich media.

There are lots of papers that try to answer this question. The basic way you do it is you knock out one gene at a time, either in parallel experiments or (more common nowadays) in a pooled experiment, and figure out which knockouts survive and which don't.

The most recent study counts 358 essential genes (out of about 4000 genes in E. coli). http://mbio.asm.org/content/9/1/e02096-17.full . Figure 2 compares a few other papers.

The exact answer will depend on the exact conditions you grow the cells in (if you have fewer nutrients or other stressful conditions, more genes will be essential).


Are all known germs benign in small enough quantities? i.e. Why do we wash our hands?

There is a Wikipedia page  which gives some typical values for infectious doses of bacteria. I suspect that lot of these have been taken from this slideshow which confirms the values on the Wikipedia page, gives more interesting details of how they have been arrived at, and also mentions a few viruses.

It seems from the slideshow that infectious dose isn't estimated in the way that the OP envisages - "What is the probability of infection if I ingest one cell?".

What is clear is that the infectious doses for some bacteria can be less than 10 cells (e.g. Shigella flexneri, E. coli O157:H7). Conversely for many other pathogens such as other strains of E. coli the estimate is >106 cells, so standard hygiene precautions will always offer some protection.


Seeds are spread by many mechanisms

Wind dispersal: When air currents used to spread seeds. Often these plants have evolved features to facilitate wind catching, for example dandelions. Aka, anemochory.

Propulsion & bursting: When seeds are propelled from the plant in an such as in these videos. This is called Ballochory.

Water: Similarly to wind dispersal plants can spread seeds by water movement/currents, aka Hydrochory. This is used by many algae and water living plants.

Sticky Seeds: There are many ways a seed can attach to the outside of an animal - by using hooks, barbs, sticky excretions, hairs. Seeds then get carried by an animal and fall off later. This is epizoochory.

Fruiting: Plants can use seed-bearing fruit to encourage animals to eat the seeds. They will then be spread when the waste is excreted after digestion. This is a process of endozoochory.

More than one way to spread a seed

From above you can see there are many ways to spread a seed. This means that many plants (those that do not use fruit) will want (from an evolutionary perspective) to avoid being eaten at all costs, and therefore evolve poison/taste cues that reduce the frequency of this. However, if investing in producing fruit bears a net benefit, ie many seeds are spread and successfully propagate, then the cost of fruit production is not a risk. A fruiting plant can minimize the risk by limiting reward (making fruit taste good and be nutritious) to only the right spatiotemporal moment when the seeds are primed for dispersal, if the fruit is eaten before the seeds are ready/present in the fruit then there will be no benefit of producing the fruit. (I expect this is why unripe fruit doesn't tend to taste so nice - it doesn't taste nice unless it's ripe because those where mutations made fruit taste good before the seeds were ready had no offspring, and those that time the ripening well were much more successful).

Producing an edible fruit is not necessarily the best way but is the way many plant species have evolved to spread their seeds. Evolution works by random mutation and selection, which can only work with the variation it has available - only if a mutation to produce fruit arises in a species and it improves fitness is it then likely to spread. It appears that endozoochory could be a very good methods of long distance dispersal.

Some interesting stuff

Interestingly, according to this blog post, unripe fruits taste bitter because they are full of tanins. Cranberries are an odd fruit because they taste bitter which means they are unattractive to animals, but they do float - which is a good dispersal method - because of an air-pocket inside the fruit that evolved. It could be the case then that once a mutation arrived for the air-pocket the fruit could just float away on water to a new location, and then using resources to make the fruit sweet and tasty became an unnecessary cost so was lost (to some degree).

This article contains this text:

  Like many species of plants native to North America, the cranberry is specially adapted to wetlands -- water-soaked areas that create transition points between dry land and open water. But cranberries do not grow directly in the water. Instead, they typically lay their roots at its edge, taking advantage of the rich soils created by alternating layers of peat, sand, clay and rock.
  Other fruits are dependent on hungry creatures to spread their seed,
  so sweetness can help their chance of being eaten and transported
  elsewhere. Not cranberries. Because of their little air pockets, the
  fruit falls from the plant's long vines when ripe and lets the water
  transport it to distant beds.

  This advantage dictated the fruit we eat today.

  Blueberries and cranberries are close cousins and are in fact not
  berries at all; they belong instead to a class of fruits known as
  epigynous or false berries. Unlike a true berry, the fruit grows from
  beneath the rest of the flower parts and as the fruit ripens the
  flower stays attached and ripens as well.

  Vorsa believes that at some point during the last ice age there were
  fewer animals to eat the fruits, and this might have driven the two
  species to diverge. The cranberries developed an acidity level five
  times higher than blueberries because it came to rely on water for
  seed dispersal. Cranberries did not need to produce large amounts of
  sugar that their blue-colored relatives required to entice consumption
  by animals in order to spread their seeds.


Clarification on RefSeq Genes track on IGV

The thinnest blue line is intron, so not in your transcript.  The medium thickness segment is untranslated exon, the thickest blue segment is translated.


Endosymbiosis leads to an irreversible loss of independence of the endosymbiont and the host.
For example, all members of the insect superfamily Aphidoidea (aphids) have an obligatory association with bacteria, commonly called primary endosymbionts (Munson et al., 1991; emphasis mine):

The primary endosymbionts are found in specialized organs, the
mycetomes, which consist of cells (mycetocytes) containing the
endosymbionts. The endosymbionts are enclosed within vesicles which
are derived from the cell membranes of the mycetocytes.
None of the [primary] endosymbionts has been successfully cultivated in
bacteriological media or in tissue culture. [These] organisms are essential
for the life of the aphids since the removal of the endosymbionts by
antibiotics leads to aphid sterility.
The endosymbionts are  maternally transmitted, and
there are complex mechanisms which assure that the progeny are
infected.

Munson et al. (1991) Buchnera gen. nov. and Buchnera aphidicola sp. nov., a taxon consisting of the mycetocyte-associated, primary endosymbionts of aphids. Int J Syst Bacteriol 41: 566--568.


Why is glucose used in oral rehydration therapy?

Oral Rehydration Therapy uses electrolyte solution containing some glucose. It is because, the absorption of electrolytes is more efficient when glucose is added. Sodium uptake from intestine is carried out by sodium glucose co-transporters.


While Ankur's answer is correct, it must be noted that not all non-coding RNAs are introns.

An intron must be excised from an mRNA, which therefore means that any non-coding RNA that is not part of an mRNA cannot be an intron.

For example, rRNA and tRNA are all examples of non-coding RNAs that are not introns, since they are not part of mRNA. miRNA may in some instances be produced from introns, but when transcribed separately, they are not introns.

mRNA translation depends on many factors that bind to processed mRNA (a very long process). Other RNA do not undergo this process, and therefore are not reconised by ribosomes and are not translated.


How does a protein reach its substrate within the cell?

The protein doesn't move towards anything. It just randomly diffuses (bounces around) in the cell until it sticks to something. The particular chemical structure (the shape) of the protein and whatever it hits will determine how tightly they stick together and whether or not a chemical reaction occurs.

A way to imagine this is to think of a jar filled with a lot of glass marbles (water), 1 marble shaped magnet (the protein), and 1 metal marble (the substrate). Put the magnet at the bottom, fill the jar most of the way full with glass marbles, and then put the metal marble on top. Then close the jar and shake it. Eventually, after colliding with a lot of glass marbles, the magnet and the metal marble will collide and stick to each other. That's how it works in cells also. In cells, the speed at which the molecules move is proportional to temperature.

Here's a cool video that shows how proteins with a very specific shape bouncing around randomly can assemble into a complex structure.

To get a sense of just how quickly molecules move in a cell, think of a bacterial cell. An E. coli cell is about 1 micrometer in diameter. In a cell of that size with no sub-cellular compartments, every molecule will collide with every other molecule in the cell about once every second (if we make some assumptions such as no binding to other molecules). So if the cell contains just one unit of a certain enzyme, and just one molecule of its substrate, they will still collide fairly frequently (about once every second).

This rate decreases dramatically as radius of the cell increases. For example a cell with double the diameter (2 micrometers) has a volume eight times larger, so collisions between any two molecules take 8 times ($2^3$) as long to occur (in other words, it takes molecules 8 times longer to "find" each other). This is one reason why there is a kind of upper limit on the size of an individual cell. Bigger organisms are bigger because they have more cells, not because they have larger cells.

The field of biology concerned with how likely it is for a reaction to occur is called enzyme kinetics. A related field, which deals with how frequently molecules collide is called statistical mechanics.


Ambiguity about the relation between membrane potential and concentration gradient in neuron cells

I interpret your question to be roughly: "the equilibrium potential is based on a concentration difference, but as ions move to create the electric potential, the concentration difference is changing. Why doesn't this in turn change the equilibrium potential such that the concentrations become equal and the potential becomes zero?"

If I'm correct...

The answer to your paradox is that very few ions have to move.

The number of potassium ions that would have to move across the membrane to establish the resting membrane potential is tiny. Electrical forces are very very strong. The imbalance in ions doesn't affect the concentrations inside and out appreciably.

  For a typical cell, 1 microcoulomb of charge (6 × 10^12 monovalent ions) per square centimeter of membrane, transferred from one side of the membrane to the other, changes the membrane potential by roughly 1 V. This means, for example, that in a spherical cell of diameter 10 μm, the number of K+ ions that have to flow out to alter the membrane potential by 100 mV is only about 1/100,000 of the total number of K+ ions in the cytosol.

from Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K., & Walter, P. (2002). Ion channels and the electrical properties of membranes.

However, because membranes are also a little permeant to sodium, and because action potentials and synaptic transmission allow some additional ions to flow across the membrane, if you gave infinite time, eventually the ion concentrations inside and out would equalize, and the membrane potential would eventually be zero. The sodium-potassium pump solves this problem by continuing to keep potassium high and sodium low inside the cell.


I found some reports on it (like reference 1) but there is an oddly little amount of publications on this topic. then I found this review in Mucosal Immunology (reference 2, interesting to read) which doubts this activation. It says:

  Interaction with complement

  IgA lacks the residues identified in the Fc regions of IgG or IgM that
  bind to C1q, and consequently IgA does not activate the classical
  complement pathway. Although several papers have reported activation
  of the alternate pathway by heat-aggregated, denatured, or
  recombinantly generated IgA, this seems to be essentially artifactual,
  and intact native IgA antibodies complexed with antigen inhibit
  complement activation induced by IgG or IgM antibodies. This
  effect is also replicated by Fabα fragments generated by cleavage of
  IgA1 antibodies with IgA1 protease. It is telling that mixed
  aggregates of heat-denatured IgG and IgA activate the alternate
  pathway in proportion to the content of IgG, and that C3b becomes
  covalently linked to the IgG heavy chains, not to IgA. Intriguing
  reports that IgA antibodies promote complement-dependent lysis or
  opsonization of encapsulated bacteria probably also arise from
  facilitation of alternate pathway activation by bacterial
  polysaccharides

It names three papers to underline this (which are number 45-47 in the reference list of the article), which can be found as references 3-5. So the question here is not only how the mechanism looks like, but also if this is real or an artefact.

References:

Activation of complement by human serum IgA, secretory IgA and IgA1
fragments.
Structure and function relationships in IgA
Anti-inflammatory activity of human IgA antibodies and their Fabα
fragments: inhibition of IgG-mediated complement activation
IgA blocks IgM and IgG-initiated immune lysis by separate molecular
mechanisms.
Activity of human IgG and IgA subclasses in immune defense against
Neisseria meningitidis serogroup B.


At what saltiness will water simply pass through us?

"Unaffected" is impossible. If you meant homeostasis, where fluid ingested = fluid excreted, well that happens all the time, and all "output" is not through urine. Sweat, respiration, fluid in feces, etc. are fluid loss. The body constantly needs water. Fluid regulation is a highly complex system managed by the body through a variety of osmotic gradients in the body and hormones which is not driven solely on the osmolarity of the fluid ingested. Under no circumstances would fluid ingested pass through the stomach, small and large intestine, and colon without absorption. Once absorbed from the GI tract to the bloodstream, our kidneys regulate fluid balance. For more reading, reference the renin–angiotensin–aldosterone system.


What portion of the electromagnetic spectrum do cats see?

Short answer
Spectral sensitivity of cats indeed ventures into the UV, but not beyond ~320 nm. Their maximum is likely similar to ours, i.e., ~750 nm.

Background
The spectral sensitivity of blue cones (photoreceptors detecting low wavelengths) of many species, including humans and cats, extends into the UV range (Fig. 1).

Fig. 1. Human cone absorption spectra. Source: University of Kentucky

However, the various structures in the eye, most notably the lens, filter out UV in humans (Fig. 2). Indeed, surgical removal of the lens in humans results in enhanced sensitivity to UV light below 420 nm (Griswold & Stark, 1992).

Fig. 2. Human transmission spectra. Source: Columbia University

In the cat, however, the lens transmits a large portion of the UV light in the range of 320 - 400 nm, while primates transmit virtually no light of these wavelengths. Figure 3 shows the lens transmission spectra of various species. At 50% transmission the second (dotted) line from the left is the cat (50% transmission at ~340 nm), while a primate (squirrel monkey, species representative for humans and other primates) in this graph is line number 7 from the left with (50% transmission at ~410 nm). Hence, cat lenses absorb less light in the UV region, but transmission is virtually nil at 320 nm (Fig. 3). Given that their cones, just like humans, are sensitive to UV, we can reasonably expect that cats can see in the UV region including wavelengths of 320 nm and up. Cats also have the 560 nm (red) cones, like we do, so their maximum wavelength is expectedly similar to ours (~750 nm).

Fig. 3. Lens transmission spectra of various species. Source: Douglas & Jeffery, 2014

References
- Douglas & Jeffery, Proc R Soc B (2014); 281: 20132995
- Griswold & Stark, Vis Res (1992); 32(9): 1739-43


Why is thymidine incorporation (DPM) normalized to per mg protein content while testing for cell proliferation?

I'm not sure that there is a strongly disciplined reason for the mg protein content as the normalization, but there is obviously a need for some normalization for different amounts of tissue- if you use 10X as much tissue, you should expect DPM to be 10X as high!
For example, in this somewhat old paper, They normalize not to protein content but to wet tissue mass or to intestinal crypt count (as they are looking at incorporation in intestinal crypts). So the normalization that you observe is not universal (or more likely, is a more recent innovation). They observe that the cruder measure of wet mass provides a poor normalization:

Instead there was a positive intercept of dpm/mg tissue which represented about
25-30% of the maximal tritium content of the intestine. (abstract)

That is a good reason to use a more precise normalization! They find that the more precise normalization of dpm/crypt works better, presumably because the crypt is the incorporating tissue.
I would suspect that the dpm/mg protein is simply a more precise method for normalization.
A yet more precise method would be the one used in this 1987 paper, in which thymidine incorporation is estimated as dpm / microgram DNA- here, you are actually directly comparing to the mass of the DNA, which is where thymidine is incorporated. That is a more obvious normalization than protein content.
However, for crude tissue extracts I suspect that it is more straightforward to estimate protein content than DNA content. So protein content is used as a "good enough" normalization.


What determines whether the maternal or paternal allele is expressed?

Except in the case of X inactivation in females, and genes on the Y chromosome in males, generally speaking both alleles are expressed in cells.

A good example is the ABO blood type marker system. If the mother is type AA, she will pass on an A allele, which codes for the A antigen. If the father is type BB, he will pass on a B allele, coding for the B antigen. Therefore, any children will be type AB, as the maternal chromosome 9 will express the A form, and the paternal chromosome 9 will express B.


DNA extraction from oil-containing seeds

The paper "Modified method for combined DNA and RNA isolation from peanut and other oil seeds." has a nice protocol for isolating DNA and RNA (which later can either be differentially digested or precipitated) from oil seeds for PCR. You can find the complete paper in the link above, the materials and methods sections says the following for the extraction method:

  RNA and DNA isolation

  Approximately 1–1.2 g of dried seed of each genotype was utilized in
  extraction. Seeds were frozen with liquid nitrogen and pulverized by
  grinding with mortar and pestle until a fine powder. Tissue was placed
  into 10 mL solution I (100 mM Tris, 150 mM LiCl, 50 mM EDTA, 1.5 %
  SDS, 2 % PVP-40, 1.5 % b-mercaptoethanol) buffer, pH 7.5, and mixed
  thoroughly by vortexing or inversion.

  To the homogenized tissue, a 5
  mL acid phenol, pH 4.3 (Fisher Scientific, Pittsburg, PA) was added
  and tissue was mixed thorough for 5 min, followed by the addition of 5
  mL chloroform:isoamyl alcohol (24:1) and mixed for an additional 5
  min. The homogenate was centrifuged for 10 min and the upper aqueous
  layer (around 9 mL) was transferred to a fresh 40 mL tube containing 9
  mL of solution II (2 M guanidinium thiocyanate, 0.5 M sodium citrate,
  1.5 M ammonium acetate, 1 % N-lauroylsarcosine) buffer, pH 5.2, mixed by gentle inversion, and allowed to incubate for 10 min at room
  temperature.

  After incubation, a 4.5 mL phenol:chloroform:isoamyl
  alcohol (25:24:1), pH 6.7 was added, mixed thoroughly for 5 min,
  centrifuged for 10 min at 13,000g, and the aqueous layer (around 16
  mL) was transferred to a new 40 mL tube.

  To the transferred solution,
  9 mL 1.2 M NaCl and 9 mL isopropanol were added, mixed, placed on ice
  for at least 1 h, and centrifuged for 15 min at 13,000g. The liquid
  was discarded and the resulting pellet was washed with 2 mL cold 70 %
  ethanol, dried, and resuspended in 4 mL RNase-free water.

  4 mL 4 M
  LiCl was added, mixed, placed on ice in the refrigerator for at least
  1 h, and centrifuged for 15 min at 4°C at 13,000g. The supernatant
  (around 8 mL) was transferred to a new 40 mL tube for DNA isolation
  and the pellet was retained for RNA isolation. For RNA isolation, the
  pellet was washed with 2 mL ice-cold 70 % ethanol, dried, and
  resuspended in 750 lL RNase-free water.

  For DNA isolation, 8 mL
  isopropanol was added to the transferred supernatant tube, mixed well,
  centrifuged for 5 min, discarded the liquid, washed pellet with 2 mL
  ice-cold 70 % ethanol, dried, and resulting pellet was resuspended in
  500 lL 10 mMTris, pH7.5. The amount of DNA or RNA was determined using
  Nanodrop 2000c spectrophotometer (Thermo Scientific, Wilmington, DE).


What is the highest pressure at which plants can survive?

See Effect of very high pressure on life of plants and animals (2012).

Judging from the fact that all the living creatures we have examined, both animals (tardigrades and Artemia) and plants (Ptychomitrium, Venturiella and white clover) were alive after exposure to 7.5 GPa, it was suggested that most of the proteins of those creatures which unfolded at the early stage of the compression remain principally unchanged after exposure to the very high pressure of 7.5 GPa. It was also suggested that the unfolding of proteins was completely reversible up to 7.5 GPa.
The maximum hydrostatic pressure applied to all the living specimens investigated in the present experiments corresponds to that in the upper mantle, at the depth of 180 km from the surface of the earth.

So survival of plants at 75,000 times atmospheric pressure is possible. In this experiment the exposure times were 30 minutes and 1 hour for the plants and 13 hours for the animals.


In what fluid does the sperm swim in the oviduct?

Specifically in the fallopian tubes, the fluid is called tubal fluid, and is produced by the innermost mucosal layer of the tubes (specifically, the peg cells in the epitelium)

In the follicles, there is the follicular fluid, liquor folliculi.
In the uterus, the endometrial fluid.
In the cervix, cervical fluid.

I don't know about the color. For what it's worth, cervical fluid varies from white to yellowish, but it's transparent when it's best for spermatozoa to swim.


First bump is called P point, middle is QRS wave (as in Q-down, R-up, S-down), and last bump is T. Every feature is representation of electrical activity in certain region of heart. E.g. P bump is contraction of atrium. See more here. Bumps are P/QRS/T.

The reason why you see so many different recordings is that it was taken with many-lead ECG. Heart has very distinct shape, its atrium is on top of ventricle, it is a bit tilted to the right, etc. Your recording is a projection of electrical activity vector onto vector that connects two leads used for given recording. Pick two other electrodes and you will have different picture just because axis of projection changed.

via NIH

It seems to me that recording you show are from different pairs of electrodes, but it shouldn't matter. As you can see, different pairs of electrodes will "pick up" some processes better that the other.

Now, because ECG is electrical activity recording, heart rate is least useful information to extract from it. Measuring pulse will be less of a hassle and as accurate. But what you can do is estimate biophysicals properties of given heart. For example, distance between P and QRS (PR interval) complexes is time that it takes for heart to contract ventricle after atrial contraction. Any abnormalities will cause lengthening of PR or other change. Lengthening of PR interval often indicates 1st degree AV block (AV node is not conducting as usual).

There is bunch of information out there on ECG and abnormalities, you can find useful this page from U Utah with examples of many severe conduction abnormalities.


What elements are a possible basis for life?

This is an interesting question, particularly considered in the context that Cairns-Smith (1985) even suggested that clays (silicates in solution) may have had some sort of early selection acting on them due to their surface chemistries.

However, there are a number of major problems with Silicon. Some are chemical and some are astrophysical in nature. For example:

Silicon has a lower electronegativity than carbon and a longer bond length. Silicon can polymerize, but many conformations (such as rings) are highly reactive or unstable.
Silicon lacks chirality. Since biochemical reactions are very specific this may present a fundamental problem for alien biochemistries.
We don't see silicon macromolecules in nature. Large carbon molecules are seen in space such a polycyclic aromatic hydrocarbon rings. The largest silicon molecule seen in space is a chain of SiC_3 (and maybe SiC_4).
On reacting with oxygen (which it does readily) silicon likes to form solids like sand.
Silicon is much less common than Carbon in the Universe. The Solar abundance of silicon is 1/10 that of carbon, and supernova yields suggest that the silicon abundance may be as low as 1/100 that of carbon during nucleosynthesis in low/intermediate mass stars.

To form complex silicon molecules we would probably need to keep it in an oxygen-free environment and somehow maintain it in solution. One possibility would be to hold it at high pressure and temperature such as in the interiors of planets (think deep hot biosphere theory) but this presents another host of problems for conceivable biochmistries and is very speculative.

Apponi, A.J., McCarthy, M.C., Gottlieb, C.A., & Thaddeus, P. 1999, Journal of Chemical Physics, 111, 3911

Cairns-Smith, A. G. (1985) Seven Clues to the Origin of Life  Cambridge University Press, New York, ISBN 0-521-27522-9.

Woosley, S.E., & Weaver, T.A. 1995, Astrophysical Journal Supplement, 101, 181


Yes that's how it works as far as I know

Because the theory part is pretty straightforward.of the genes are on the Same chromosome, the chance of them being separated in segregation during meiosis is lower

Consider a simple example

---------A--b--------------c----d-e---------------------------------f

Let this be a rope with 6 point a b c d e f
If I were to make a random cut anywhere here, the chance that a,b will get separated is much lower than a,f....because a and f are so far apart that any cut in the middle will ensure them to be separated.
If u look at it again...the chance of d,e to be separated is EXTREMELY low

This is the principle of LINKAGE

Now let me say gene a stands for tall, b for blue and f for bushy...(don't judge the characters)

Now if this is a part of a chromosome on the parent, and meiosis is taking place
We all know that crossing over too is a phenomenon involved here

Now during crossing over.....a and f are bound to get separated for sure, so they will be independently assorted, obeying the law of Mendel

But when we talk about a and b, they may or may not get separated in the various gametes

The closer they are, the lesser chance of them being separated and thereby, higher chance of them occurring in the same gamete and therefore, higher chance of them being expressed in the same offspring(assuming they are dominant)

lets assume we cross blue tall(dominant) with green dwarf(recessive)
As you know f1 will be blue tall(no incomplete or co dominance please)

Now if I take this blue tall and cross it with parental green dwarf

You will have very high number of blue tall and green dwarf(remember, there are alleles of SAME GENE....AND OCCUPY SAME LOCI)(therefore.....high chance of both occurring together in the same gamete)

Therefore the number of recombinant you get will be very low(blue dwarf and green tall........as the chance of these characters entering different gametes is very low)

Therefore we can conclude that higher the number of recombination....higher the chance of the genes segregating which implies a greater distance between the genes)

Therefore a higher recombination frequency implies a higher distance between the 2 linked genes

I hope u have understood the concept and are not struggling to byheart it as a force
Thanks


How is it known that Homo sapiens and Homo neanderthalensis interbred?

Although this question makes some false assumptions, it is fundamentally interesting as the methodology used is neither simple or easy to understand. It is not my area, but I have found it especially interesting to read the long 2010 Science paper by Green et al.. One really needs to read it for oneself (it is free view), but it is not a trivial undertaking.

False assumptions / misconceptions in the question

The main misconception in the question are:

That it is necessary to know anything about the genome of H. erectus to make these conclusions. The methods used do not require this. (Although comparison with chimpanzee is sometimes used to give an indication of whether a genetic change occured in humans or Neanderthals.)
That the similarities and differences under discussion relate to differences in complete genes — “but gene B was not already present in H. sapiens…”. They do not, which makes the analysis more complex to follow.

Towards an explanation

Let me start by addressing the question “What distinguishes those genes (purported to have been acquired by H. sapiens from Neanderthals) from genes that both species inherited from a common ancestor?”. The answer relates to the absence of such genes from modern humans of African origin, and the fact that we know the general evolutionary relationship between neanderthals and modern humans (African and non-African) from a wealth of non-sequence paleontological evidence. This is shown in the diagram below, modified from a recent and recommended review by Nielsen et al. in Nature (2017).

Clearly any gene present in the common ancestor to humans and Neanderthals should be present in both African and European populations, unless it had been lost from the African population.

So if the analysis is not done by detecting gain/loss of individual genes, how is it done? Certainly not by overall percentage sequence similarity, because of the high overall similarity and the population variation. It is done by studying SNPs — single nucleotide polymorphisms — in particular genes.

For example, consider a gene that has only a single haplotype in Neanderthals, and originally had a single but different haplotype in humans. (This might determine something like eye colour, although this is not an actual example.)  If the other haplotype were acquired by humans as a result of interbreeding, then the modern human population would contain both alleles. When you compared the relationship of the SNPs for this gene between different humans and between humans and Neanderthals you would find different results from those for a gene the variant of which had not been acquired by interbreeding. The acquired gene in humans would be more related to that in Neanderthals than non-acquired genes, but less related to that  in other humans (because of its more recent appearance in the population and time for homogenization, I believe).

The African/non-African aspect is explained in the Science paper cited in my introduction, but there is a good visual diagram in a 2014 Nature paper by Sankararaman et al., the manuscript of which can be viewed freely in PMC through the US HHS.

(1) Sites where a panel of sub-Saharan Africans carries the ancestral allele and where the sequenced Neanderthal and the test haplotype (marked non-African) carry the derived allele are likely to be derived from Neanderthal gene flow; (2) Haplotype divergence patterns. Genomic segments where the divergence of the test haplotype to the sequenced Neanderthal is low while the divergence to a panel of sub-Saharan Africans is high are likely to be introgressed.

These papers contain a wide range of controls, including comparisons of different non-African population groups, and detailed discussion of alternative possibilities.

A final point of interest is that Sankararaman et al. examined some of the genes in which these SNPS suggest Neanderthal origin. They write:

  “…genes involved in keratin filament formation and some other
  biological pathways are significantly enriched in Neanderthal
  ancestry in European populations, east-Asian populations, or both
  …. Thus,
  Neanderthal alleles that affect skin and hair may have helped modern
  humans to adapt to non-African environments.”

Coda

It would be scientifically dishonest not to mention some oddities. One is that the Green et al. paper suggested that gene flow had been uni-directional: from Neanderthals to humans, which is apparently unusual in interbreeding. However a more recent study (Kuhlwilm et al., 2016) shows some human gene flow into Eastern Neanderthals, although not into European Neanderthals. (Thanks to @iayork for pointing this out.). The other is that modern Asians appear to have more Neanderthal DNA than modern Europeans. (This is discussed in the paper already mentioned by Green et al.)


How many cells are in prophase on this onion root tip slide?

Hard call on early prophase versus interphase, especially since these are not natural distinctions with discrete boundaries but are used to articulate a continous process.

I'd say you're pretty close, I count six for sure. That includes the one in the top row on the far left that is partially clipped in the photo. One iffy possibility is in the third row just left of the obvious anaphase on the left.

Unless your teacher is far more particular than I was with students, I think you're good to go.


The frequency fluctuations will be determined by a standard model of selection as found in any basic population genetics text. In this scenario they take a very basic form: during each long period $i$ the frequency of $A_1$ increases from $f_i$ to $f_i\cdot (1+s_1)^{n_1}$ and during each short period $j$ the frequency of $A_1$ decreases from $f_j$ to $f_j\cdot (1/(1+s_2))^{n_2}.$ Thus over each pair of periods the frequency of $A_1$ changes by $(1+s_1)^{n_1}/(1+s_2)^{n_2}$. If this quantity exceeds 1, $A_1$ goes to fixation; if it is less than one $A_2$ goes to fixation.

More generally, for an infinite population in a fluctuating environment, the allele with the higher geometric mean fitness will go to fixation. Early discussions of these results are due to Dempster (1955; Cold Spring Harbor Symp. Quant. Biol.), Haldane and Jayakar (1963; J. Genetics), and Lewontin and Cohen (1969; PNAS).


Why is mRNA needed in the Protein translation?

One reason is that an intermediate like mRNA allows for higher amounts of protein expression. You can have multiple mRNA molecules that are translated simultaneously. If you read directly from DNA you can have at most two translations in parallel.

I'm not sure about this, but I would imagine that having to unwind the DNA double strand every time for translation could be a drawback to directly reading from DNA as well. The mRNA is also subject to various forms of regulation, which might be an advantage as well for the added intermediary.


Generally spoken, "host cellular factors" are proteins, receptors etc. of the host cell. In this case, they are important for the HIV infection. The authors write:

  Recently, a genome-wide siRNA analysis revealed over 250 host cellular
  factors that influence HIV-1 infection.

This means gene silencing techniques where used to identify the host cellular factors which are important for the infection, you can find these results here: "Identification of host proteins required for HIV infection through a functional genomic screen."
The overall goal is to identify proteins which are important for the function and infection of HIV to understand the interaction between virus and host cell better.


I suspect that the question reveals an incomplete understanding of enzymic catalysis and could more generally be rephrased as "If enzymes just speed up biological reactions, what makes the reactions proceed in the first place." The simple answer to this is the fact that the thermodynamics of the reaction are favourable, i.e. the reaction involves a negative change in (Gibbs) free energy.

So what is stopping the reaction proceeding at a reasonable rate without catalysis? The fact that the thermodynamic path of reactions involves an activated state with a higher free energy. In most cases this is sufficiently large that it acts as a barrier to spontaneous reaction. You can get over the activation barrier by e.g. supplying heat (i.e. supplying activation energy) but this is not possible in living organisms. Enzymes act by lowering the activation energy (energy barrier) or raising the ground state (which in effect decreases the activation energy).

One should realize that "just speeding up the reaction" is generally increasing the reaction rate from being negligible to biologically sufficient. So what makes the reaction go is a combination of the reactants being there with a favourable chemistry and the enzyme being there in the right place to deal with them.

If you are unfamiliar with this basic reaction chemistry see:

http://www.ncbi.nlm.nih.gov/books/NBK22384/#A1100

and the image below from Wikipedia.


Is there any advantage of having mitochondria for aerobic respiration?

From the evolutionary point of view, the eukaryotes acquired these metabolisms (except glycolysis) from their prokaryotic endosymbionts. Not all prokaryotes have the ETC. The free living ancestor of mitohondria is supposed to be the alpha-proteobacterium.

Now, glycolysis is a common pathway in lot of lifeforms perhaps because of abundance of glucose. TCA cycle is coupled with ETC at certain steps which makes it essentially a part of aerobic metabolism.

The reason for having a dedicated organelle for respiration

ATP synthesis is a membrane process. Imagine a large prokaryotic cell- as big as an animal cell. Such a cell cannot take care of its energetic demands which primarily consists of protein synthesis with the given area of membrane i.e it needs much more ATP-synthases than it can have to cope up with the energy demands of maintaining such a huge cell (this index is approximated based on surface to volume ratio). Therefore it is wise to harbor multiple efficient organelles i.e. mitochondria which themselves have just a small essential genome and proteome to maintain.

For a better understanding, please read this article. I just loved it.
There is also a book by the same author about mitochondria called Power, Sex, Suicide.


Generate full dimer from monomer with C2 symmetry?

This article will probably be informative for you:
Looking at Structures: Introduction to Biological Assemblies and the PDB Archive

The PDB file contains the asymmetric unit found in a particular crystallographic study. The biological assembly is the quaternary structure known or predicted to be found in living systems. For many proteins (but not 2PJY), the biological assembly can be downloaded directly from RCSB. For other proteins, the PDB file may contain the transformation matrix used to create the biological assembly from the asymmetric unit. If you look at the file in a text editor, this information is found under remark 350:

REMARK 350 BIOMOLECULE: 1
REMARK 350 AUTHOR DETERMINED BIOLOGICAL UNIT: HEXAMERIC
REMARK 350 SOFTWARE DETERMINED QUATERNARY STRUCTURE: HEXAMERIC
REMARK 350 SOFTWARE USED: PISA
REMARK 350 TOTAL BURIED SURFACE AREA: 8880 ANGSTROM**2
REMARK 350 APPLY THE FOLLOWING TO CHAINS: A, B, C
REMARK 350   BIOMT1   1  1.000000  0.000000  0.000000        0.00000
REMARK 350   BIOMT2   1  0.000000  1.000000  0.000000        0.00000
REMARK 350   BIOMT3   1  0.000000  0.000000  1.000000        0.00000
REMARK 350   BIOMT1   2  1.000000  0.000000  0.000000        0.00000
REMARK 350   BIOMT2   2  0.000000 -1.000000  0.000000        0.00000
REMARK 350   BIOMT3   2  0.000000  0.000000 -1.000000        0.00000

Note that the actual biological assembly of 2PJY is a hexamer and the asymmetric unit in the PDB file is a trimer. You can see that the first matrix is identity (ie keeps the original asymmetric unit). The second matrix transforms the assymmetric unit to create the full hexamer. This matrix is both author and PISA predicted. You can actually go to the PISA website and have it predict the biological assembly of a particular PDB file, and it will spit out the coordinates of the hexamer (and other predicted assemblies) which you can then load into PyMOL.

PDB files may also contain a CRYST1 record, which gives information about the unit cell and space group of the crystal. Via the symexp command, PyMOL can use this information to recreate neighboring asymmetric units. By limiting the cut-off distance (and this requires trial-and-error), the biological assembly can be recreated. This script, for example, will generate the hexamer:

fetch 2PJY
symexp 2PJY, 2PJY, 2PJY, 2.5
hide everything
show cartoon


How to selectively filter BLAST results for an endogenous retroviral LTR to retrieve members of the same ERV family?

I don't think there is a definite answer to this problem, but here are a few things that might help you, apart from a simple length filter for the hits:

Filter for regions: since LTRs are repeats you might get multiple BLAST results from the same repeat region/locus (especially if your input sequence is smaller than said region). You probably want to keep only one hit per region
Check for a conserved (sub)sequence: hopefully your specific LTR sequence has a 'core' that needs to be present, so that it can be considered part of your familiy. You only want to keep BLAST hits that have an absolute match for this 'core'.


Are human teeth only diphyodont or both diphyodont and monodont?

The definitions from the Oxford Dictionary of Dentistry:

Diphyodont

  Describing the development of two successive dentitions, one primary
  and another secondary (permanent), as found in most mammals including
  humans.

Monophyodont

  Possessing only one generation of teeth. It is a characteristic of
  some mammals, including the manatee, seal, and walrus.

As you can see, the term diphyodont is generally not used to refer to the individual teeth, but rather to the whole animal (i.e. the sets of teeth). A monophyodont is an animal that has only one set of teeth.


What's inside the males body in the space where females have the ovaries and the uterus?

Wider hips in females is not contributed because of large volume of organs.

Broadening of the hip bones happens as a feature of the female pubertal process, and estrogens (the overwhelming sex hormones in females) cause an enlarging of the pelvis as a piece of sexual separation. Consequently females for the most part have more extensive hips, allowing labor.

However, I found this article from International Business Times that states >>

  Women have not evolved wider pelvises despite it being difficult and
  dangerous to give birth – yet they may have developed some physical
  features that help during labour.

  Barbara Fischer, from the University of Oslo, has found a link between
  pelvis shape and statue and head circumference of both baby and
  mother.

There was, however, no sufficient evidence to back this article, but it is quite an interesting approach otherwise.

Males are not needed to have any extra organs, but females have just more space in the pelvis region. That space can be linked to idea of uterus expanding to hold the fetus during gestation as mentioned by @BryanKrause.


The issues of global ocean acidification and global warming are two symptoms of the same disease, too much carbon in the atmosphere. And they have 1 solution, put less carbon into the atmosphere. It doesn't really matter which aspect is the more harmful one, you can't treat one without treating the other.

If reducing carbon output were simple, we would have done it by now. However, it will most likely require radical changes to our energy infrastructure, with moves away from coal, oil, and natural gas and towards solar, wind, and nuclear power. It will probably require changes to our agricultural practices, and you should really watch Allan Savory's TED Talk for how those changes should be implemented.

People are very slow to change their habits, and short term profit is a powerful motivator against change, but I believe these we can and must solve these problems if humanity is to continue to thrive on Earth.


This thin waist is called petiole (aka.  wasp‐waist).

How many times did the petiole evolve?

  Why did a lot of common insects evolve such a thin waist?

Reading this question make it feel that you are assuming that several lineages evolved this petiole independently. It would be wrong. The petiole evolved once only and all the species that are having a petiole today (ants, bees, wasps, ...) are descendent of this lineage that evolved this petiole.

The taxon of all these species having a petiole is called Apocrita, which is a suborder of hymenoptera. You can learn much more about the phylogeny of these taxons in Rasnttsyn and Haichun (2010).

Why did it evolve?

The early lineage who evolved this trait where parasites (or even parasitoids at that time, I am not sure). This lineage was laying their eggs in tree trunk (or maybe already in other insects larvea if they were already parasitoids). The constriction that is the petiole allowed these individuals to have greater maneuverability for depositing their eggs accurately (Peters et al., 2017; Wilhelmsen et al., 2010).

The evolution of this petiole greatly affected the future evolution and diversification of Apocrita as things like stings and even maybe eusociality. From Peters et al., (2017)

  The evolution of the wasp waist, a constriction between the first and the second abdominal segment greatly improving the maneuverability of the abdomen’s rear section, including the ovipositor, was a major innovation in the evolution of Hymenoptera that undoubtedly contributed to the rapid diversification of Apocrita


What's the smallest organism that can produce voice?

I will go with lesser water boatman(Micronecta scholtzi).

The loudest of everything as well as small.

Size: 0.07-inch (2-millimeter)

Produces the highest sound by size ratio.
It's sound is almost equivalent to pounding jackhammer at two feet distance.

http://www.plosone.org/article/fetchObject.action?uri=info:doi/10.1371/journal.pone.0021089.g001&representation=PNG_L

Source and Image Courtesy:

So Small, So Loud: Extremely High Sound Pressure Level from a Pygmy Aquatic Insect (Corixidae, Micronectinae)

Youtube: https://www.youtube.com/watch?v=i7-hREXmMFM

Update:

If we consider voice, I will go with Paedophryne amauensis

Smallest frog an known vertebrate
size: 7.7 mm (0.30 in)


What is the biological significance of finding palindromes in DNA sequence?

My knowledge of biology is extremely limited, but this is what I know of palindromic sequences:

Palindromic sequences are their own reverse complements. I have seen many restriction sites be palindromic. Also, some Transcription Factor Binding sites are palindromic. The canonical E-box site, for example, can be expressed as CANNTG.

Also, these palindromes, when occurring in pairs with a sequence between the occurrences, can double back and bind to each other (when the DNA is transcribed to RNA, say), and this would result in the RNA stem and loop structure.


Edit: I am only addressing aneuploidies as those are the examples given. Other classes of mutation have distinct mechanisms, so I would split those out into another question if you are interested.
Chromosomal abnormalities occur more frequently when it is hard for cells to do meiosis and mitosis properly with a chromosome, or when the chromosome is more prone to "break" for some other reason.
The cell relies on certain architectural features (centromeres) to segregate chromosomes properly during mitosis. When segregation goes wrong, then you find aneuploidy much of the time. Chromosomes have other features such as telomeres and satellite DNA that can lead to chromosome fusion errors by different mechanisms. For example, yeast cells that have aberrant telomeres lead to high rates of aneuploidy.
Different chromosomes of the same genome have some variation in structure, repeat content, and other features that may predispose to aneuploidy formation or otherwise. These can include the quality and functionality of features such as centromeres and telomeres; these can vary even for the same chromosome across the lifespan of an organism.
For example in yeast, people have observed quite dramatic differences in the occurrence of spontaneous aneuploidy between different chromosomes (see figure 1). Yeast cells are much more robust to chromosomal variation than humans as they do not have a complex developmental cycle. However, aneuploidy of chromosomes with certain genes does seem to be selected against in that paper. There also appear to be dependencies in which the aneuploidy tolerance of one chromosome depends on the karyotype state of some other chromosome. "In other words, CIN [chromosomal instability] does not appear to be caused by some general property of being aneuploid per se but rather by determinants associated with specific aneuploid karyotypes."

Figure 1.
Experiments in the muntjac (a mammal) seem to show that the different chromosomes segregate more or less effectively based on centromere size (Figure 2).

Figure 2.
Human chromosomes have quite different rates of aneuploidy formation (see Table 1), so yes there is a bias. This is most markedly a bias in which acrocentric chromosomes and the shorter chromosomes have a somewhat elevated rate of aneuploidy (Table 2, same paper). So having an acrocentric architecture may make a chromosome more difficult to segregate.
When you ask about trisomy 21, note that chromosome 21 is acrocentric in humans. Thus, aneuploidies occur for chr21 at a somewhat higher rate.
However, commenter @MikeyC has a good point that there is a bit of ascertainment bias in how we find aneuploidies. Many aneuploidies are embryonic lethal and spontaneously abort; chr21 trisomy on the other hand yields living babies with noticeable features of their aneuploidy, so we know a lot about it and see it a lot. This seems to agree with the yeast data.
So there are multiple contributing factors. There is some variation in how chromosomes give rise to aneuploidy, but we also need to consider the means by which we observe aneuploidies in evaluating those molecular mechanisms.


How to interpret Percent identity matrix created by Clustal Omega?

Gene-1   Gene-2    Gene-3
Gene-1  100.00    16.18     20.35
Gene-2  16.18    100.00     29.66
Gene-3  20.35     29.66    100.00

Gene-1 and Gene-1 have 100% similarity (and all the other diagonal elements). Gene-1 and Gene-2 have 16.15% similarity, and so on. Therefore the matrix is symmetric M(i,j) = M(j,i).

You can also show just the upper triangular part of this matrix and that would be sufficient.

        Gene-1   Gene-2    Gene-3
Gene-1  100.00    16.18     20.35
Gene-2           100.00     29.66
Gene-3                     100.00

The colours basically denote the type (molecular nature) of residue. Have a look at this and this.


Can anyone identify this species of spider?

Based on your area and this pest control site I believe that the bugs in your picture are not spiders, they are clover mites. I have found that some clover mites are a darker brown color and also slightly larger. This image gives a better view of the features of a clover mite, including the longer pair of front legs and oval shaped body:  Clover mites don't pose a threat to people or animals as they live off of either plants or fungi, but smashing them can leave stains on furniture and clothing.


Semantics Question: epigenetic mark on a person's DNA?

We may restrict your definition of epigenetics as heritable changes in an organism's phenotype that occur without a change in the sequence of DNA bases. That is, changes to the DNA molecule itself is permitted, as long as the sequence of ATCGs are not affected.

In this sense, it would not be wrong to refer to an "epigenetic mark on a person's DNA". For example, a mechanism of epigenetics that does directly change the DNA molecule would be something like DNA methylation.


There is no requirement that DNA should have a whole number of base pairs per turn. As a thought experiment, say you have a helix of dsDNA with 10 base pairs that completes one helical turn (ie it has 10 bp/turn). Now, twist that DNA along its axis so that it completes 1.5 turns. There is still only 10 bp and thus 6.67 bp/turn (which you should notice is a decimal).


SNPs in DNase hypersensitive and histone marks sites

First off let's define some concepts.

DNAse hypersensitive regions are DNA regions which are in an open chromatin conformation (i.e. euchromatin). This means that those regions are more active at the genomic level (i.e. higher gene expression, gene regulation and higher TF binding) and are less prone to form nucleosomes.
Histone mark sites are DNA regions known to bind certain type of histones and therefore also influences the chromatin conformation leading to the same effects described previously. The critical point is that the histones you are listing do not primarily bind a specific DNA sequence (as described by @mdperry) but rather DNA sequence marked by epigenetic modifications such as methylation and acetylation.

Now for your first questions, SNPs in DNAse hypersensitive regions might influence the chromatin state and therefore yes might influence gene expression and gene regulation. Will those SNPs also influence TF binding? Well they might indirectly via chromatin modifications. They will not directly act on TF binding if not located in a sequence known to bind TFs (TFBS). DNAse hypersensitivity is not a synonym for transcription factor binding regions/sequences.

For your second question, SNPs in histone mark sites are a little bit more difficult to interpret. They might, or might not, provoke chromatin changes by influencing the binding of histones but not in a direct way. CpG islands are, for example, DNA regions known to be greatly under the influence of epigenetic marks and therefore mutations in those specific regions (e.g. a C -> T mutation) might influence the relative methylation/acetylation state and therefore the binding of histones. SNPs might therefore influence gene expression via chromatin changes which leads to higher/lower TF binding but again not in a direct way. Here again a SNP would influence TF binding directly only if the mutation is located in a TFBS.

As you can see my answer is full of "might" and the reason is that it is very difficult, at the current state-of-the-art, to determine the exact impact of a SNP on the 3D conformation of the chromatin and therefore predict the effect on specific gene expressions.

An advice would be to try to co-localize your SNPs with known TFBS either predicted In-silico or measured via CHiP-SEQ experiments and merge that with the information about DNAse hyperactivity and histone marks you already gathered. For example a SNP in a TFBS in a DNAse hyperactive region is very likely to have a greater impact than a SNP in a TFBS in a non active region.

I am sorry I cannot be more specific but this is a very active research area in genetics and there is still a lot to understand, especially for the interactions between all the players influencing the chromatin conformation.


Carbon Monoxide "CO" would definitely inhibit aerobic respiration. This is in fact the mechanism of the toxicity of compounds such as carbon monoxide and cyanide, namely, carbon monoxide binds (coordinates) with an affinity several orders of magnitude greater than oxygen to the heme group of mitochrondrial cytochrome oxidase, thus inhibiting the enzyme. When the respiratory electron chain is no longer drawn by the reduction of molecular oxygen, the hydrogen ion gradient across the mitochrondrial inner membrane is depleted, and ATP production halts.

Carbon dioxide would not effect the electron transport chain directly, but is rather involved in the reactions of the citric acid cycle, although, in all likelihood, the cell would die of acidosis before CO₂ concentrations became great enough to reverse the citric acid cycle. Cytochromes and flavoproteins are complex molecules that if the cell were to endocytize them, it would simply digest them.

I do not know your degree of experience in biochemistry, but if you wish, search on the internet for protein structural images of cytochrome oxidase or hemoglobin bound to oxygen and carbon monoxide. Oxygen binds the iron of the heme group at an angle, while carbon monoxide binds directly perpendicular to the heme ring. This difference in geometry is partially responsible for the differential affinity of the two species for heme.


Do all organs of our body secrete hormones?

Good question! The major and most common endocrine glands in the human body include pituitary, thyroid, parathyroid, thymus, adrenal, pancreas, gonads and pineal gland, along with neuroendocrinol glands like hypothalamus. Some other, not-so-common, examples include heart (Anti-Natriuretic Factor), GI tract organs (gastrin, secretin, etc.), placenta (estrogen, progesterone, etc.), kidneys (erythropoietin, renin), skin (cholecalciferol) and adipose tissue (leptin)1. Even the lungs are known to secrete calcitonin2.

In spite of this, I can think of quite a few examples of organs which do not act as endocrine glands. That is because there is a difference between the organs secreting hormones and endocrine glands. The definition of endocrine glands is as follows1, 5, 6, 7, 8:

  Endocrine glands are glands of the endocrine system that secrete their products, hormones, directly into the blood rather than through a duct.

So, if these organs don't directly secrete the hormones into the bloodstream, then they are not endocrine glands. Leading this way, emotional tears are known to consist of hormones such as prolactin, ACTH and leucine-enkephalin3, 4. Thus, though eyes do secrete hormones, they are not endocrine glands. Also, not sure about this, but lungs still do not seem to fit in the category of endocrine glands.

In short, all the organs of the body might secreted hormones, but they all cannot be considered as endocrine glands.

References:

Endocrine gland - Wikipedia
[Hormone expression and opioid receptors in fetal and adult lung]
Gómez-Román JJ, Cifrián Martínez JM, Fernández Rozas S, Fernando Val-Bernal J.
Frey W. H., DeSota-Johnson D., Hoffman C., McCall J. T. (1981). Effect of stimulus on the chemical composition of human tears. Am. J. Ophthalmol. 92 559–567. 10.1016/0002-9394(81)90651-6
What biological functions does crying serve? - Biology Stack Exchange


What do the variants on the PolyT sequence mean?

I haven't read too far into this, but from what I understand the variant PolyT sequence is the number of thymine bases in a short sequence within one of the introns of the CFTR gene. Introns and exons are both parts of a gene structure, but introns are spliced out of the final transcript before its converted to protein (for more information see this article on RNA splicing).   Studies have shown that the presence of a 5T sequence in this region may increasethe skipping of exon 9 in the CFTR gene (there is a nice picture showing what I mean here).  This exon skipping will alter the final protein product translated from the spliced RNA species.

I could not find a lot of information about the 6T allele that your son has, however, I found one short article about a patient with 6T and F508 in the European Journal of Genetics. It references another paper that talks about the length of an additional repeat sequence of GT bases and its affect on individuals the the 5T variant.


Does playing music during sleep actually suppress rather than rouse the brain?

This is a very interesting but difficult to answer question. That is because scientists are still debating about the various stages of consciousness. As it stands, there is evidence that people can learn even though they are asleep indicating that it is likely that sensory channels are open and information is being processed even when asleep. That likely means the brain is behaving as if it were awake at certain times during sleep. In this article they interpret the lack of blood flow seen by fMRI as less active which is mostly correct. Playing audio during REM is a tricky question because as you know dreaming does not require sensory input so that channel(hearing) may be free to receive information although your guess may also be true if if the music was loud enough to interfere with other cognitive processes.


How does inorganic phosphate inhibit alkaline phosphatase?

When alkaline phosphatase dephosphorylates a substrate one of the intermediates in the reaction pathway is a phosphorylated form of the enzyme in which the phosphate from the substrate has been transferred to the enzyme. This phosphate is subsequently lost by hydrolysis. Under certain conditions alkaline phosphatase will actually catalyse a reverse reaction - the addition of inorganic phosphate on to alcohol substrates, and this also proceeds via the phospho-enzyme intermediate, but proceeds in the opposite direction.

This means that phosphate will inhibit the enzyme as a phosphatase via the formation of the phospho-enzyme, thus blocking the active site to substrates for dephosphorylation.

  Reaction mechanism of alkaline phosphatase based on crystal structures: Two-metal ion catalysis
  Kim, EE &  Harold W. Wyckoff, HW 1991 Reaction mechanism of alkaline phosphatase based on crystal structures: Two-metal ion catalysis. J Mol Biol. 218: 449-464


Interpretation of agarose gel electrophoresis of a plasmid

The closed plasmid comes in three different forms: nicked-relaxed, supercoiled and circular single-stranded. All three forms have a different tertiary structure and thus they run differently on the gel. This should look like this (image from here, there you also find a more detailed explanation):

When you digest the vector you linearize all the forms and they all have the same tertiary form.


Why would low complexity regions be linked with relaxed selection?

Low complexity regions have repeats in nucleotides ( or amino acids ).  E.g.  PPCDPPPPPKDKKKKDDGPP or AAATAAAAAAAATAAAAAAT.  This 2011 article compares 14 individual Plasmodium falciparum genomes and finds that these repeats are highly variable between individuals - some may be short AAAATAAAA  others may be longer AAAATAAAAAAAAATAAAAAAATAAAATAAAA....AATAA even to scores of bases.

I think its not clear what these sequences do, but the mere fact that they can vary so much from one viable individual to another indicates that they are not strongly selective.  *If they were subject to selection, you would be able to see the difference in the variation in the health, fitness, and reproduction that these significant genetic changes have, but in this case the change in sequence would not change the properties of the sequence much if at all. *

I think these are also related to copy number variable (CNV) regions.  which expand and contract in the genome easily even between identical twins.  (sorry for the indirect reference - like many SDN stories, the reference is totally wrong), but I remember this work...


Autosomal Recessive Trait when skipping one generation

What you are saying is very similar to the statement that:

  Absence of evidence is not evidence of absence

Suppose you have an autosomic gene A, which has a mutant allele a, causing an illness (or any other phenotype, for that matters). The particular nature of a makes its associated phenotype recessive.

You have three possibilities:

AA -> no illness
Aa (or aA) -> carrier, with no illness
aa -> ill

Now, let's take an aa individual (ill) and cross it with a sane AA individual:

aa x AA

All of the individuals of the first generation (F1) will be carriers (Aa) because the father will always give a and the mother always A.

Now if we breed them together

aA x aA

both parents have 1/2 probability of giving a and 1/2 of giving A. We will then have a proportion of:

1/4 aa
1/2 Aa (1/4 A from mother and a from father, 1/4 vice-versa)
1/4 AA

But this is just down to statistics. You have only 1/4 chances of seeing the trait reappearing, so you are much less likely to see it if they have 1 offspring then if they have 20.
Moreover, you have Aa offsprings in the progeny... this means that these could pass the mutant allele to the third or fourth generation.

Another important thing is that all we said is true if the first cross is

aa * AA

If it was

aa * aa

or

aa * Aa

The trait will (surely in the first case, and with 1/2 chance in the second) appear directly in the first generation.


Same as @bpedit but stated a little bit differently.

  You are heterozygous at locus A. Both of your alleles, A1 and A2, have a 10% allele frequency in the population. If you are one of 22 people in a room, how many people do you expect to share a locus A allele with?

There are 5 possible genotypes that could share at least one allele with "you" A1|A1, A1|A2, A2|A2, A1|A3 and A2|A3, where A3 is the allele (or set of alleles) which frequency is $0.8$. Under Hardy-Weinberg assumptions, the frequencies of each of these genotypes are

$f(A1|A1) = 0.1^2$
$f(A1|A2) = 2 \cdot 0.1^2$
$f(A2|A2) = 0.1^2$
$f(A1|A3) = 2\cdot 0.1\cdot 0.8$
$f(A2|A3) = 2\cdot 0.1\cdot 0.8$

which sums to $4\cdot(0.1^2) + 2(2\cdot 0.1\cdot 0.8)=0.36$.

As the frequencies of both A1 and A2 are $0.1$, the frequencies of each of the three mentioned genotypes are all $0.1^2$. Therefore, the expected number of individuals that share at least one allele with "you" at this locus is $21\cdot 0.36 = 7.56$ people.

Why did we need Hardy-Weinberg assumption to make this calculation?

This section comes in reaction to @Atwo comment below.

To give you the intuition for why you need H-W for this calculation. Imagine all A1 where in heterozygous A1|A2 (and therefore same for A2), then the only other genotype that would share an allele with you are A1|A2 genotypes that would be present at frequency $0.2$. And therefore the expected number of people the share at least one allele with you in the room would be $21\cdot 0.2 = 4.2$ people.

For exercise, I would like to invite the reader you to repeat the same calculation for a case where all A1 and A2 alleles are only found in heterozygous A1|A3 and A2|A3.


How does the brain's energy consumption depend on mental activity?

The energy consumption doesn't vary that much between resting and performing tasks, as discussed in a review by Marcus Raichle and Mark A. Mintun:

In the average adult human, the brain represents approximately 2% of
the total body weight but approximately 20% of the energy consumed
(Clark & Sokoloff 1999), 10 times that predicted by its weight alone.
Relative to this high rate of ongoing or “basal” metabolism (usually
measured while resting quietly awake with eyes closed), the amount
dedicated to task-evoked regional imaging signals is remarkably small.
The regional increases in absolute blood flow associated with imaging
signals as measured with PET are rarely more than 5%–10% of the
resting blood flow of the brain. These are modest modulations in
ongoing circulatory activity that rarely affect the overall rate of
brain blood flow during even the most arousing perceptual and vigorous
motor activity (Fox et al. 1987, Friston et al. 1990, Lennox 1931,
Madsen et al. 1995, Roland et al. 1987, Sokoloff et al. 1955).
[...]
From knowledge of these relationships, one can estimate that if blood flow and glucose utilization increase by 10%, but oxygen consumption does not, the local energy consumption increase owing to a typical task-related response could be as little as 1%. It becomes clear, then, that the brain continuously expends a considerable amount of energy even in the absence of a particular task (i.e., when a subject is awake and at rest).

Techniques like fMRI measure relatively small differences, their existence does not contradict the claim that the energy consumption of the brain doesn't change a lot between the resting state and performing an activity.

1. Raichle ME, Mintun MA. BRAIN WORK AND BRAIN IMAGING. Annual Review of Neuroscience 2006 Jul;29(1):449-476.


What is the modern state of the theory of evolution?

My friend Brightblades is right in one thing.  It seems your teacher was working off a caricature of what the theory of evolution actually says.  First of all, you should read Sklivvz's excellent answer at this question.  Now to address the elephant in the room, the accident at Chernobyl only happened in 1986.  That was only 26 years ago.  In that timeframe, noticeable effects in an animal population really would not be at all noticeable.  Furthermore, the paper cited by Marta Cz-C actually shows that there have been some changes (in fungi though, not animals).

  fungi seem to interact with the ionizing radiation differently from other Earth’s inhabitants. Recent data show that melanized fungal species like those from Chernobyl’s reactor respond to ionizing radiation with enhanced growth. Fungi colonize space stations and adapt morphologically to extreme conditions. Radiation exposure causes upregulation of many key genes, and an inducible microhomology-mediated recombination pathway could be a potential mechanism of adaptive evolution in eukaryotes.

Read the rest of the paper for more information on how there have been some other slight changes to fungi at Chernobyl as well as other locations throughout the world.

Now I am going to repeat a bunch of stuff from one of my web pages that talks about evolution.  This web page is set up mostly to deal with creationist arguments, however, the caricature is so severe as to warrant this.  As I said earlier, evolution is a population phenomenon.

Evolution acts upon heritable variation of characteristics, and you can only have variation of this sort within a population. A single individual organism, at least if its a multicellular eukaryote, has a fixed genome. It can't change what it has inherited. But a large number of organisms can all have different genomes, and can disseminate variation via inheritance to the next generation. It is upon the population as a whole that evolution acts, with various mechanisms coming into play to remove some variations from the population, and propel other variations to numerical dominance within the population. The organisms in question remain part of that population, and within a generation, those organisms don't change. But the moment a new generation is produced, dissemination of variation can result in the appearance of a new feature in one or more members of that population. If that new feature leads to greater reproductive success for the organism possessing it, that feature spreads through the population, as more and more future offspring inherit it. Over time, the population changes, and more and more organisms with new features appear within that population.

Understanding inheritance basics and mechanisms for changes (genes), we have all that is needed for the appearance of cladogenesis events. Split a decent sized population of living organisms into two, and let's call these new, separate populations A and B. Now let a barrier be erected between population A and population B, so that individuals from one cannot reproduce with individuals from the other. This barrier can be an insurmountable physical obstacle, for example, but this need not be the only form such a barrier can take. Now, first of all, there is no reason whatsoever to think that population A and population B will start off in identical states to begin with. After all, those two populations were derived from an original population comprising lots of organisms with different genomes, and the likelihood of population A and population B being identical at the start of this process is vanishingly small. Then, once our barrier is erected, and our populations are allowed to reproduce separately from that point on, there is no reason to think that those populations will move in the same direction in the long term. Indeed, it is far more likely that they will be subject to different environmental and ecosystem influences, and those different environmental and ecosystem influences will shape the long term heredity of those populations. Indeed, that's all that natural selection IS - it's a single, concise term used to encapsulate all of those environmental and ecosystem influences succinctly, and additionally to encapsulate the fact that those influences affect the inheritance of characteristics within a population over the long term.

As a consequence, any two separated populations of living organisms, that originated from a single population, will diverge from each other. If the extant influences on those two populations are sufficiently different, that divergence will take place more rapidly. Eventually, we will arrive at a point where those two populations become sufficiently diverged from each other that individuals from population A can no longer produce viable offspring with individuals from population B, and vice versa. When this happens, we have a speciation event. Indeed, this has been observed taking place in the wild AND in the laboratory, and has been documented in the relevant scientific papers. So, if anyone wishes to assert that there are 'magic barriers' to speciation or other cladogenesis events, then reality doesn't agree.

You will not have any animals giving birth to any radically different animals as a result of radiation.  Most changed sue to radiation will not provide any particular advantage to an animal anyway.  Also, a change may also be dependent on a previous change and require many generations to fully manifest.  All this was demonstrated by the long term evolution experiment led by Richard Lenski at Michigan State University.

So in essence, your teacher was just plain wrong.  As for the findings of the past 20 years, we are always learning more and more.  For instance, there has been an explosive capability in DNA analysis and sequencing, which has only provided more support for the theory of evolution.  A mechanism that Charles Darwin could not have had any idea about in his day and age, yet it perfectly supports his conclusions.  Again, read the answer provided at Skeptics.


I believe it is for this reason: the female body plan is the default one. Males are a variation upon that, in humans at least. Nipples are part of the basic body plan. For a man to not have them, he would need to actively evolve something that would prevent nipples from developing. There is no selective pressure for the development of such a thing, so it hasn't happened. Keep in mind that the code for the general body plan is shared between males and females. The Y chromosome modifies the development of that body plan so the person becomes male.


Why don't antiseptic agents kill 100% germs?

This is actually an interesting question! Let me answer both the parts separately, taking the example of Listerine® mouthwash.

  Is an antiseptic's inability to eliminate 100% of all germs due to its "chemistry", or is it due to physical factors?

In most of the cases, this is due to the physical factors. Clearly, your mouth is not a flat surface. It has many depressions and elevations. And these irregularities are the perfect hotels for all kinds of pathogens. Also, it is difficult for most chemicals to reach those spots and stay there for long enough so that they can act on the pathogens. Thus, most of these chemicals would be unable to kill 100% pathogens because of their inability to reach all of them. Also, in rare cases, it might also be due to chemical factors(!) Yes, I'm talking about antibiotic resistance. And in that case, it would be practically impossible to kill 100% pathogens, no matter whether they're hidden or exposed.

  Do antiseptics/mouthwashes/handwashes even kill 99.9% of all germs in the first place? Or is it (as I strongly suspect) an example of marketing fraud?

For that, lets first see what Listerine® contains. As given on its website, its main ingredients are (I'm simply copying what they write on their page, followed by checking whether its true):

Eucalyptol – with antibacterial properties, this eucalyptus-derived essential oil works as an anti-fungal agent within the mouth.
Methol – this natural oil as germ-killing abilities to help halt the growth of bacteria.
Thymol – this powerful oil is derived from the ajowan herb, and helps decrease the risk of gum disease.
Methyl Salicylate – for minty freshness from morning til night, the flavouring agent in this essential oil is, well… essential!

We just need to know whether these ingredients really work or not (why? We'll talk about this later on) and I'll skip methyl salicylate for this (they don't even claim that it is antimicrobial). Beginning with eucalyptol, it has been shown that oil of Eucalyptus globulus (of which eucalyptol is a component) has antimicrobial properties against Escherichia coli and Staphylococcus aureus (see Bachir et al, 2012). It has also been shown to possess antifungal properties (Safaei-Ghomi et al, 2010). Coming to methol, it has also been shown to have antibacterial properties against various Staphylococcus and Lactobacillus species (Freires et al, 2015). Finally, there have been lots of studies about the antimicrobial properties of thymol. You can check out the Wikipedia page for information.

So, where is the percentage? The point is, the exact percentage depends on a lot of factors. When an enterprise, such as Listerine®, claims that their product has been shown to be 99.9% (or any number) efficient against bacteria, they need to cite the particular study through which they claim this number. But they can not, in any case, be definite that their product will be 99.9% effective everytime. How effective a product is also depends on the conditions under which it is tested. Mostly, these tests are performed on a petri dish in a laboratory, something very different from your mouth. Thus, although they can claim that their product is scientifically proven to be 99.9% effective, they cannot claim it to be 99.9% effective when you use it. Again, they cannot claim 100% effectiveness because this makes them liable (saying our product has been shown to be 100% effective requires them to show that even a single microbe did not survive on the petri dish they used for experiment). Also, this gives them a way to escape in case anybody complaints about their product not being effective (since they caught infection even after using their product). In such situation, they can easily say that their product is not 100% efficient!


No, you cannot for certain ascribe it to competition, without further information. The mediation by a pathogen is similar to the effects on prey species that are indirectly caused by shared predators (e.g. Prey B increase -> Predator X increase -> more predation on Prey A). Such effects, which can be tricky to separate from direct competition, are usually called apparent competition (see e.g. the classic paper Holt. 1977. Predation, apparent competition, and the structure of prey communities. Theor Popul Biol 12).

However, to some extent, the terminology used may depend on what you view as "the environmental background". All species have lots of adaptations to certain aspects of their living environment, and these naturally differ between species. Some might be more resistant to a certain pathogen (of to drought or other abiotic factors), but this might trade-off against other traits. I that respect, you might view species B as outcompeting species A in a certain environment (e.g. in the presence of the pathogen). However, since you specifically know about the pathogen (which is the focal point of the question), and that species B will probably function as a host/source population of the pathogen, I think it is more useful and informative to label the effect as apparent competition. To partition the direct and indirect effects you will however need moe information.