The RNA world hypothesis states that self-replicating RNA (that is, an autocatalytic RNA polymerase) was the first form or precursor of life. So, in that context, your question is basically asking how life originated. The obvious answer is that we don't know (currently anyways), but I'm going to take this opportunity to describe a few really neat experiments which might give you some insight over a possibly contributing mechanism of how self-replicating molecules may have developed. I won't go over the Miller-Urey or Oró experiments, but let's assume that the early Earth contained organic molecules (especially nucleotides for our purposes). It's also important to keep in mind the immense time scales over which these processes occurred (the Earth is ~4.5 billion years old).
Anyways, let's talk about in vitro evolution, also known as systematic evolution of ligands by exponential enrichment (SELEX). SELEX is a procedure whereby an initial library of random RNA sequences (flanked by known sequences to be used as primer sites) undergoes a selective process followed by amplification and mutation of the selected molecules. This is repeated several times. As an example, this process can be used to create aptamers, which are small RNA molecules which bind a specific ligand. A pool of random RNA is passed over a column containing the immobilized ligand. By chance, some RNA will have some amount of affinity to the ligand. Poorly bound RNA is washed off non-stringently and then slightly better bound RNA is eluted. This RNA is reverse transcribed and amplified by PCR. The PCR primers contain the T7 RNAP promoter which allows transcription of the cDNA to produce a new  RNA pool. Somewhere in this regeneration process, mutations are introduced so that the new pool contains randomly modified copies of the RNA which had some affinity. Through repeated steps of increasing stringency, an aptamer with high affinity can be developed.

(Ellington, 1994); Outline of the SELEX process.

So how does this apply to the origin of the first RNA polymerase? It just so happens that Bartel and Szostak (1993) used in vitro selection to produce a ribozyme (a catalytic RNA molecule). This ribozyme was a ligase, that is it catalyzed the formation of a phosphodiester bond between two RNA molecules that are aligned on a template.

(Bartel and Szostak, 1993); Methodology of the selection used to generate a ribozyme ligase.

While the ribozyme created was not autocatalytic, the experiment had implications on the origin of self-replicating RNA and life in general, which were discussed in the paper:

The ribozymes that we have isolated from a pool of random sequences catalyze a chemical transformation similar to that catalyzed by polymerases. Their abundance in the random-sequence pool is therefore relevant to the hypothesis that life began with an RNA replicase that originated from prebiotically synthesized random-sequence RNA. We detected about 65 sequences (Fig. 8, pools 3 and 4) capable of carrying out a particular ligation reaction in a pool of more than $10^{15}$ initial sequences, or a frequency of occurrence of one in about $2*10^{13}$ sequences.
[...]
Presumably, sequences capable of acting as efficient template-directed RNA polymerases are more rare than this, and sequences capable of acting as an RNA replicase are even more rare. Evidently, catalysts of moderate activity could arise spontaneously from relatively small quantities of RNA (and perhaps related polynucleotides); however, a catalyst with the activity, accuracy, and dual functionality (enzyme and template) of an RNA replicase would be so rare that it could only arise spontaneously and in a single step from a truly enormous amount of RNA. The problem is compounded because two such sequences would be required for autocatalytic replication to begin, one to act as the polymerase and a second to act as the template. Therefore, an RNA replicase could only have arisen from primordial sequence pools that were not truly random. Joyce and Orgel anticipate this difficulty and propose that nonenzymatic, template-copying reactions may have had a dual role in generating primordial sequence pools that are more likely to give rise to a replicase (21). The initial pool may have been biased in favor of local secondary structure by a mechanism involving intermittent use of intramolecular sequence as the template. In addition, some sort of nonenzymatic catalysis was probably necessary for the initial copying of the replicase sequence to generate a molecule that could be used as a template, the copying of which by the replicase would generate more replicase molecules, thus initiating the autocatalytic explosion of life.
[...]
The ribozymes that we have selected provide a new starting point for the evolution or design of RNAs with RNA polymerase and replicase activity. A series of issues including sequence-independent primer-template binding, the use of mononucleotide triphosphates as substrates, fidelity, and product-template dissociation now need to be addressed before an RNA replicase activity, an activity that has probably been extinct for over 3 billion years, can be fully resuscitated.

Johnston et al. (2001) took this experiment even further: starting with a pool of slightly mutated ribozyme ligases developed in a previous SELEX experiment, they were able to generate a ribozyme polymerase. This polymerase was able to catalyze the addition of nucleotides to a growing oligonucleotide chain up to 14 bases long and based off of an RNA template. The polymerase was also quite accurate.

(Johnston et al., 2001); Excerpts from the in vitro evolution of a ribozyme polymerase.

However, the authors are skeptical of this being the sole mechanism behind the rise of an autocatalytic ribozyme:

How could general polymerase activity have arisen on early Earth? If emergence of the first RNA replicase ribozyme coincided with the origin of life, it would have had to arise in a single step from prebiotically synthesized RNA, without the benefit of Darwinian evolution. Our shortest construct retaining activity was 165 nt, with about 90 nt involved in important Watson-Crick pairing and at least another 30 critical nucleotides (23). Ribozymes with the efficiency, accuracy, and other attributes of an RNA replicase might have to be even larger than this. However, current understanding of prebiotic chemistry argues against the emergence of meaningful amounts of RNA molecules even a tenth this length (1). This difficulty is anticipated by those who propose that life, and Darwinian evolution, began before RNA. Some speculate that in this "pre-RNA world," life was based on an RNA-like polymer, yet to be identified, that possessed the catalytic and templating features of RNA but also a more plausible prebiotic synthesis (1). The pre-RNA life forms presumably later developed the ability to synthesize RNA, facilitating the emergence of an RNA replicase ribozyme, which in turn enabled the transition to the RNA world.

There are other, similar experiments where people have made self-replicating ligases (Paul and Joyce, 2002) or a system of two, cross replicating ribozymes (Lincoln and Joyce, 2009). While the question still remains unanswered, perhaps from all of this you can get a sense of the plausibility.
References:

Bartel DP, Szostak JW. 1993. Isolation of New Ribozymes from a Large Pool of Random Sequences. Science. 261(5127):1411-1418.
Ellington AD. 1994. Aptamers achieve the desired recognition. Curr Biol. 4(5):427-429.
Johnston WK, Unrau PJ, Lawrence MS, Glasner MR, Bartel DP. 2001. RNA-Catalyzed RNA Polymerization: Accurate and General RNA-Templated Primer Extension. Science. 292(5520):1319-1325.
Lincoln TA, Joyce GF. 2009. Self-Sustained Replication of an RNA Enzyme. Science. 323(5918):1229-1232.
Paul N, Joyce GF. 2002. A self-replicating ligase ribozyme. P Natl Acad Sci USA. 99(20):12733-12740


Are aquatic filter feeders effective at cleaning water to a safe level?

My answer from the top of my head is that they will not be very effective at cleaning the water. One reason is that if the substances and organisms are harmful to the filter feeder as well, they will avoid eating them or they will die from them or have their health reduced. In either case they will be filtering less.

Another reason is that if you use the tap and replenish the water with new contaminated water regularly, the filter feeders will probably not filter all water in the tank, and the outflow from the tap will still contain the contaminant. This is certainly the case if the tank is also the culture vessel for your filter feeders. In this case, the tank has come close to being a continuous culture. There are decades of science (including R* theory) which show that resource levels in such systems settle at a positive level (and you propose that the harmful micro-organisms are used as resource or at least eaten in proportion to the resource if the filter feeder cannot be selective). This positive level will then thus also be present in the effluent from the tank (your tap water).

An alternative is to grow the filter feeders in a dedicated tank, and than add them later in high concentrations to your drinking water. This would not be efficient because you need to feed your filter feeders with something.

Finally, the harmful substances may be absorbed by the filter feeders, but also be excreted, in which case the will end up in your drinking water anyway.

For getting rid of the harmful micro-organisms, it is probably more efficient to boil your water!


If a gene altered causes cancer and creates a protein for cancer can the new protein be isolated in some way?

From how I read your question, you're wondering if there is some technology to somehow isolate oncogenic proteins inside the cell so they don't do harm, is that correct?

The answer is somewhat complicated, as it depends on the protein. First, though, you need to understand that cancer is a very complex disease, and cancer is not caused by a single mutation alone. The "multiple-hit" or Knudson hypothesis essentially states that a cell progresses from a normal cell to a cancerous one, accumulating multiple mutations along the way. In pretty much all cases, at least two specific mutations are needed - the constitutive activation of a proto-oncogene, a group of proteins responsible for cell growth and proliferation, and the deletion or inactivation of one or more tumor suppressor genes, which are used to keep growth and proliferation under control. This way, you have a tumor driver (often this is a single protein, like a growth factor receptor) "driving" the oncogenic process, with no "brake" or regulation.

As I said, mutations in tumor suppressor genes generally result in loss-of-function changes, or complete deletion/inactivation of the gene altogether, so "isolating" these proteins in the cell wouldn't do much good. The focus of many tumor therapies is to down-regulate, inhibit, destroy, or otherwise remove the function of the protein that is driving the uncontrolled growth and proliferation of cells, forming tumors and metastases. If we're lucky, the tumor driver is an extracellular domain-containing protein (like a cell-surface receptor) that can be identified and targeted from outside the cell. Once this has occurred, scientists and doctors can use specially-derived monoclonal antibodies to target and kill the cells containing these proteins:

Monoclonal antibodies for cancer. ADEPT, antibody directed enzyme prodrug therapy; ADCC, antibody dependent cell-mediated cytotoxicity; CDC, complement dependent cytotoxicity; MAb, monoclonal antibody; scFv, single-chain variable fragment.

From WikiMedia Commons, released into the public domain.

There are a number of ways the cancer cells can be killed, from delivery of radiation or other cytotoxic compounds, to attracting killer cells from the immune system, to activating the complement system. However, all of these depend on the surface presence of biomarkers for the cancerous cells, so as to avoid non-specific killing or off-target effects.

The reason so much focus is put on killing the cancerous cells instead of trying to isolate the "bad guys" inside the cells is that by the time the cell has become cancerous, it already has accumulated so many mutations that a) the cell isn't really worth saving, and b) it would take an extraordinary amount of effort to corral all the mutated proteins together, and leave whatever unaffected or "wild-type" proteins were left to do their jobs.

You may recall that each gene we have (except for some on the X and Y chromosomes) is present in duplicate, one copy from our mother and one from our father. The initial mutations that begin the progression to the fully cancerous state may at first only affect one of those two copies of the gene, leaving a working version around for a while. However, as oncogenesis progresses, and more and more regulatory proteins are inactivated, chromosomal damage grows, and frequently the surviving "normal" copy is either mutated itself or completely destroyed. Once this occurs, even if you could isolate the misbehaving proteins, there would be no good proteins left to do the jobs of the cell. Therefore, killing is really the only option.

I hope I've covered what you were interested in. Please let me know if you don't understand any of it, or you can always ask a new question.


Why can only small molecules pass through the phospholipid bilayer of the cell membrane?

The plasma membrane consists of a phospholipid bilayer which separates the internal environment of the cell from the external environment. It regulates the movement of substances in and out of the cell and helps keep a constantly regulated internal environment of the cell.

The plasma membrane consists of a phospholipid bilayer, which, as the name suggests, is made up of phospholipids(lipids that have a phosphate group attached to them.).
The phospholipid has two regions a hydrophilic (water-loving / has an affinity for polar molecules) and hydrophobic (water-hating / has an affinity for nonpolar molecules).

So what happens is these molecules come together and arrange themselves in such a way that it faces the least amount of repulsions. Hence, the fatty acid tails (Hydrophobic part) face inside and the polar part(Hydrophilic part) face the outside, to look something like this.

Now, what happens is that when a molecule has to enter the cell it first has to interact with the polar part of the lipid membrane and then with the inner non-polar part of the membrane to pass through, hence if it is a polar molecule it will face repulsions and will not be able to pass through without the assistance of transmembrane proteins (it doesn't matter whether it is small or large, it simply won't), but, in the case of non-polar molecules, there is no repulsion from the fatty acid part of the phospholipids and hence it can pass through the membrane. When the non-polar molecules are too big some other mechanisms may be utilized (like receptor-mediated endocytosis).

With regard to your doubt regarding the "mechanism" with which a molecule passes through the membrane, in the simplest case, it will simply slip in between the phospholipids and through the bilayer. But, this is, as I said the simplest case, there may be transmembrane proteins which create channels for diffusion (aquaporin is a good example), or as I mentioned earlier they may be taken into the cell by endocytosis, through pumps like the Na-K pump etc.

And also cholesterol acts like a buffer to ensure that the spacing between the individual phospholipids is maintained so that it stays fluid (i.e. to maintain optimum rigidity of the membrane).

This is what an actual membrane looks like in an actual cell:

Hope you got a general idea.

You can refer to Chapter 11 of Molecular Biology of the Cell (by Bruce Alberts et al) if you want a  more rigorous explanation.


Adventitious roots into epiphyte mats aren't all that uncommon, and aren't restricted to the tropics. They can occur in old growth forests in the pacific northwest (my neck of the woods). A well-developed bryophyte mat in a single upper canopy tree can store up to six metric tons of water, plus all the mineral nutrients from atmospheric deposition. For the tree, it's a huge advantage to be able to tap into that epiphyte mat rather than rely on bringing up water from their subterranean roots. As far as visualizing it goes, yes, you would have to remove the mat to see them, but they look very similar to subterranean roots. Not sure if this is helpful, but I like to think of it like this: when a new meristem is formed, it's basically undifferentiated, and if there's sufficient water and mineral nutrition it can develop into a root (or a shoot if it's getting sunlight). The tree doesn't care if that's below ground or in the canopy.


Algae or Lichen identification. Coastal BC, Canada

I want to propose you expand your search to a broader taxonomic scope. Specifically, I think you might be looking at a species of "red" green algae (family: Trentepohliaceae).

From Nelson et al. (2011):

All Trentepohliaceae have filamentous growth forms and often contain large amounts of carotenoid pigments (ß-carotene and hematochrome), causing the algae to appear yellow orange in color (Thompson and Wujek 1997, Lo´pez-Bautista et al. 2002).

The Trentepohliaceae contains five genera: (Trentepohlia, Printzina, Phycopeltis, Cephaleuros and Stomatochroon) and 70+ species worldwide.

For example, the following algae (picture from England) looks fairly similar to your specimen:
Trentepohlia aurea

 Source: David Fenwick
If your specimen is a species in this family of algae, it is most likely in the Trentepohlia genus (or possibly Printzina genus).
Trentepohlia is a genus of filamentous chlorophyte green algae in the family Trentepohliaceae.

Typically orange or yellow in color.
Live on tree trunks and wet rocks or symbiotically in lichens.

Here's a picture of a free-living Trentepohlia species from coastal Oregon, USA:

 Source: Richard C. Hoyer (2015)

The source notes that the specimen was simply ID'd as "Trentepohlia sp." by Tim Rodenkirk (Botanist with the Coos Bay BLM in North Bend, Oregon).


Obtaining protein atomic co-ordinates from dihedral angles

As I indicated in my comment:

You need the amino acid sequence and values for bond lengths before you could determine the atomic co-ordinates from the dihedral angles.
Originally the dihedral angles are calculated from the experimentally atomic co-ordinates (with the help of the sequence), so that what you propose is in its nature an academic exercise.

There is, however, a situation in which I have — in effect — done that, in exploring the structures that would be produced if the dihedral angles were varied. Rather than a command-line tool, there is a graphical tool that allows you to vary the angles interactively and see the results. This is the excellent Ramachandran Plot Explorer (Rama) by Bosco Ho. And yes, it can also generate the co-ordinates — you can save the results in PDB format to reopen or to visualize with other protein graphic software, such as JSmol.

The only problem is that the last version of this software was released in 2006, and is not 64-bit, so it will not run on the next version of Mac OS X (no idea about Windows). Bosco’s blog is still active, so perhaps he could be persuaded…


Where do migratory birds go when it rains?

Obviously, as you point out, some birds, such as waterbirds (ducks, puffins, auks, sandpipers) are perfectly fine in the rain, as they spend much of their time in the water anyhow and have oil glands that waterproof their feathers.

For other birds, rain can increase heat loss. For instance, rain increases metabolism by up to 22% in eagles (Stalmaster & Gessaman, 1984), although the actual impact on average daily metabolism was 'negligible'. However, eagles were able to feed their offspring only half as much, and therefore had only half as many eaglets, when it rained (Elliott et al., 2005). (On the other hand, the authors point out that in the Tropics, eagles actually do better when it rains because there is more food available).

Migrating birds stop migrating, hide where they can, and wait until it dries up before they continue (Erdi et al, 2002); those that don't, often end up far away from where they should be and, eventually, dead. In short, some birds don't mind the rain (e.g. seabirds), others sit it out in misery (e.g. nesting eagles) and others hunker down wherever they can find shelter (e.g. migrating birds).


Do thymine and uracil ever appear in the same strand of RNA?

tRNA molecules contain a T in the T arm. I believe that this results from post-transcriptional modification of a U by uridine methylase.


Short answer
Birds emit infrared.

Background
Objects with a temperature higher than the background emit detectable infrared (IR). Endothermic (warmblooded) animals keep their body temperatures at around 37oC and given the relatively cool temperatures at the earth's surface, endotherms generally emit more IR than the background. Endothermic animals include the mammals and birds, but also some fish.

Infrared image of a hummingbird. Source: Nature Conservancy.

Note that dinosaurs were probably not ectothermic (coldblooded), but they are believed to have been mesotheroms, that is somewhere in-between ecto- and endothermic (Grady et al., 2014).

Also note your IR recordings will benefit from lower temperatures and reduced light-pollution from the sun, hence your recordings will be better at night than during daytime.

Reference
- Grady et al., Science (2014); 344(6189): 1268-72


Meaning of Phred score - probability of base calling error

Phred score is a measure of the probability that a base call is wrong/right.

Your understanding of this probability as "if Phred assigns a quality score of 10 to a base, the chances that this base is called incorrectly are 1 in 10", is not entirely accurate.

Quality scores calculation and base calling are specific to the machine. The way an Illumina HiSeq calls a base is different from how PacBio does it.

For example, Illumina uses high precision cameras to record the colors generated during sequencing (each color represents a base). Moreover, it does not sequence a single molecule of DNA but a cluster. Now, the machine's base calling software will calculate the reliability of the light signal being interpreted as a base (let's say A). Several parameters are considered in this calculation.

  For each base call, a number of quality predictor values are computed.
  Quality predictor values are observable properties of clusters from
  which base calls are extracted. These include properties, such as
  intensity profiles and signal-to-noise ratios, measure various aspects
  of base call reliability. They have been empirically determined to
  correlate with the quality of the base call.

   Illumina Technical notes: Understanding Illumina Quality Scores

Likewise, different machines have different techniques for reading a base signal and computational models to calculate the accuracy of the signal.

  How is it possible to have 10 possiblities when you can only have 4
  bases (ACGT) ?

Why not? You are just calculating what is the probability that a base is not adenine. The minimum probability should be more than 1/4, at or below which the base call wouldn't probably even assign the base as adenine.

Imagine it like this: if adenine is represented by blue light and you see that in the spot there is not a pure blue signal but some interference of other colors (noise) which represent 10% of the signal. There can be other parameters too that make the calculated blue signal to deviate from the "ideal signal". The percentage of non-overlap with the perfect signal would be the error.


The electrons for shuttling are mainly generated in the cytosol from glycolysis. NADH can easily pass the outer membrane, but must be shuttled over the inner membrane. It is important to consider that the electrons must be fed to oxidative phosphorylation from the matrix of the mitochondrion, and not the intermembrane space.


Difference between facilitated diffusion and secondary active transport in cells

Short answer
Facilitated diffusion is a passive process in which membrane channels mediate the transport of polar, or big molecules that are not solvable in the cell membrane. Co-transport, on the other hand, is active transport, as it depends on the electrochemical gradient of ions across the cell's membrane, particularly Na+. Because ATP or other energetic compounds are not directly involved in co-transport, it is referred to as secondary active transport. The electrochemical ion gradient is mainly established by the Na+,K+-ATPase.

Background
As commented upon by others, your question is not entirely clear and the best way to approach this question is by defining the various terminologies and physiological mechanisms used in your question:

Active transport needs an energy source such as ATP. For example, the Na+,K+-ATPase is an enzyme that pumps Na+ and K+ ions against their concentration gradients into the cytosol (K+) or out of the cell (Na+). Note that both Na+ and K+ are transported against their chemical gradients (and Na+ also against its electrical gradient as the cell is negative). Therefore your statement that [...] in the active process, substance x is transported against the gradient, and substance y down its electrochemical gradient is untrue, and likely the cause of your confusion.
Passive transport is mediated by diffusion, which typically occurs through a concentration gradient. Only small, relatively hydrophobic molecules are able to diffuse across a phospholipid bilayer at significant rates. Examples are gases (such as O2 and CO2) in the lungs, and small polar but uncharged molecules (such as H2O and ethanol) (Cooper, 2000).
Facilitated diffusion is an example of passive diffusion, but aided by membrane-spanning channel proteins that span the lipid bilayer. Therefore the particles (molecules or ions) do not have to dissolve in the cell membrane's hydrophobic lipid bilayer, allowing hydrophylic and larger molecules (carbohydrates, ions) to be transported into the cell. No external source of energy is needed and  travel across the membrane in the direction determined by their concentration gradients and, in the case of charged molecules, by the electric potential across the membrane (Cooper, 2000).
Co-transport is active transport, where the energetically unfavorable transport of a particle against its electrochemical gradient is facilitated by the co-transport of a favorable one down its gradient. In other words, multiple particles are transported so as to neutralize the sum of the transport. For example, sodium-dependent glucose tranporters transport glucose into the cell against the concentration gradient (unfavorable) and Na+ is transported along with it into the cell which is a favorable transport (Haraki & Inagaki, 2012). This is an example of a symporter. An example of an antiporter is the Na+/Ca2+ antiporter found in the heart to transport Ca2+ out of the cell against a steep concentration gradient and electrical gradient, while 3 Na+ is imported into the cell to balance the unfavorable Ca2+ transport. Note that all these mentioned co-transporters and many others are dependent on the Na,K-ATPase that ultimately generates the Na+ and K+ gradients by pumping Na+ out of the cell and K+ into the cell using ATP (Freeman, 2000). This generated membrane potential works like a battery being charged, and co-transporters discharge it by using the energy stored by importing Na+. Hence, it is referred to as secondary active transport, as no direct energy input from ATP is needed, but instead it utilizes the electrochemical gradient created by the Na+,K+-ATPase.

These considerations should clarify your issues and answer your question on what co-transport exactly is. Specifically, the glucose transporter mentioned, GLUT1 as you refer to, is a symporter that mediates secondary active transport.

References
- Cooper, The Cell, 2000
- Haraki & Inagaki, J Diabetes Invest 2012; 3: 352-3
- Molecular Cell Biology, 2000


What is the difference between muscle fascicle and muscle bundle?

Short answer
Muscle fascicles are the building blocks of skeletal muscle.

Background
Skeletal muscle, or striated muscle is composed of many units called muscle fascicles. The fascicles are bound together by a type of connective tissue called fascia.

Fascicles in skeletal muscle are composed of muscle cells, called mycocytes. These cells are referred to as muscle fibers in skeletal muscle. Myocytes contain small strands called myofibrils, which are the contractile elements in the muscle cells. The myofibrils move as skeletal muscle contracts.

Putting it all back together, myofibrils are the contractile elements in muscle cells (muscle fibers); muscle fibers make-up muscle fascicles; and muscle fascicles are bound together by fascia to compose the skeletal muscle.

Hence the part labeled 'muscle bundle' is a muscle, made out of a bundle of fascicles.

Source: Penn Medicine


Why is Homo sapiens not categorized as an invasive species?

Ignoring for the moment the question of politics, let's consider the various definitions of the term "invasive species" that are in use. Colautti and MacIsaac write in their discussion of invasive species terminology (1):

  The greatest confusion [among the discussed ecological terms]
  surrounds the common term ‘invasive’ and its various derivatives
  (Richardson et al., 2000a). Explicit or implicit definitions for
  ‘invasive’ include: (1) a synonym for ‘nonindigenous’ (e.g. Goodwin et
  al., 1999; Radford &Cousens, 2000); (2) an adjective for native or
  nonindigenous species (NIS) that have colonized natural areas (e.g.
  Burke & Grime, 1996); (3) discrimination of NIS established in
  cultivated habitats (as ‘noninvasive’) from those established in
  natural habitats (e.g. Reichard & Hamilton, 1997); (4) NIS that are
  widespread (e.g. van Clef & Stiles, 2001); or (5) widespread NIS that
  have adverse effects on the invaded habitat (e.g. Davis & Thompson,
  2000; Mack et al., 2000).

Note that except for #2, all the definitions require that the species is a nonindigenous (non-native) species in the area under consideration. Therefore, while humans may be considered to have been an invasive species for much of our species history, under most definitions of the term we no longer qualify because except in a few places (mainly the arctic, antarctic and marine environments, where human presence is minimal) we are now a native species.

See also http://www.smithsonianmag.com/science-nature/are-humans-an-invasive-species-42999965/?no-ist


Insect identification request - Is this a bed bug?

I got curious and after some image search I got two candidates:

Plagiognathus repetitus

Mullein Bug


Is it possible to obtain single strands of DNA in solution?

There is usually a denaturation step in a typical PCR protocol, see e.g. here, which serves exactly this purpose: the strands are thermally divided (typically at 95 °C for a few seconds). As you can see, this is a very common process, but the strands only remain denatured if kept at high temperatures.

Room-temperature strand separation in regular buffer solutions will be very hard, because annealing (the opposite process, where two complementary strands pair up) is thermodynamically favourable.
More permanent separation might be obtained by dissolving DNA in particular solutions, as described here, where DMSO seems particularly effective.
This results in separated strands at room temperature, but both strands will clearly still be present. One might think about separating the two with various methods (e.g. HPLC), but I doubt these solutions are compatible with regular HPLC columns.


Can an organism obtaining a part of its genome via horizontal gene transfer be called a "hybrid"?

As you point out, there isn't a singularly accepted biological defnition of 'hybrid.' The most basic would be a single organism that exhibits traits of two individual organisms, but that will find perfectly acceptable disagreement depending on who you talk to. You, for instance, are human - but a hybrid of your parents' genomes.

So I would personally say that horizontal gene transfer is equivalent to gene inheritance, and that as long as the organism exhibited traits of both 'parent' individuals - then yes, it is a hybrid. Some might include that even if it didn't exhibit traits and merely contained the genes in any inherited genomic data that the hybrid label would be appropriate.


Where do the 2 electrons and H⁺ go when NADPH is turned into NADP⁺ during the Calvin Cycle?

A reasonable source of information about the Calvin Cycle is Berg et al., but for this reaction the full structures are not shown. I therefore show them below in a diagram of my own:

I have coloured the hydrogen atoms to show where they go in reducing the phosphoglycerate (acid) to an aldehyde. You can think of the two electrons being used to form the additional covalent bond.

(The hydrogen phosphate is actually in equilibrium with other phosphate species, but this is not relevant to your question and so is not shown.)


Insect identification request. Long anteni. Grasshopper legs

That is a camel cricket, Rhaphidophoridae. https://www.pestworld.org/pest-guide/occasional-invaders/camel-crickets/
Likely some species of Ceuthophilus


If during exercise the affinity of oxygen for haemoglobin is decreased, what are the general consequences for tissues?

It may help to consider the diagram below which shows the percentage saturation of haemoglobin with oxygen (and hence how much it takes up or releases) at the different partial pressures in different tissues. (The actual pattern — and values — depends, of course, on the blood flow to different tissues.)

In general, the curves show that at the high oxygen pressure of the lungs haemoglobin is near saturated with oxygen — Hb takes O2 up —, whereas at the lower oxygen pressure in the peripheral tissues the saturation is less — Hb releases some O2. So in normal circumstances oxygen will be gradually released to tissues as it circulates through the body. The oxygen pressure in the tissues is acting as the control valve for release.

In cases where there is a vastly increased demand for oxygen, this normal control is insufficient. The hydrogen ions in the acids produced by respiration (carbon dioxide and perhaps lactate) act as an additional control as they cause the oxygen dissociation curve of haemoglobin to change e.g. from 1 to 2 in the diagram. (The molecular mechanism of this is understood, but that is not the question.) Hence at the same oxygen pressure, more oxygen is released (cf. the percentage saturation at 1 and 2).

Does this harm tissues other than the ones producing the acid? They obviously have lower priority, but you can see there is still oxygen left at 2, and physiological mechanisms (faster heart beat etc.) will increase the blood flow in general. So it is wrong to think of this as ‘all or nothing’, but as part as a general response which alters the balance towards the tissues in greatest need.


Weasels don't hibernate.  See http://icwdm.org/handbook/carnivor/Weasels.asp

Both will die when the temperature falls below a certain level.  The difference between snakes (ectotherms) and weasels (endotherms) is that the snake's body temperature will fluctuate more, depending on the surrounding temperature.


Spermatogenesis in humans - timing of phases and chromatin modifications

Spermatogenesis (Beginning to end):

64 +- 8 days (range 42 to 76)

There is considerable individual variation. This includes time in epididymis.

Amann 2008 argue for 74 days based on early study by Clermont 1972.
Also argue that biopsies are still needed on top of radiolabelling.

Substages:

Calculated from Amann 2008, Figure 1 using percent time in 16 day cycles.

Leptotene:

26.5 days (~70 days total - 26.5 days = ~ 43.5 days pre-ejaculation/conception)

Zygotene:

31.2 days (~70 days total - 31.2 days = ~ 38.8 days pre-ejaculation/conception)

Pachytene:

32 days (~70 days total - 32.0 days = ~ 38 days pre-ejaculation/conception)

Histone-Protamine transfer:

68.8 days (~70 days total - 68.8 = ~2 days pre-ejaculation).

The resolution of the data doesn’t really let us get at Epididymis vs. histone-protamine transfer, though.

Time in the Epidymis:

10-14 days.

References:

  Misell LM, Holochwost D, Boban D, Santi N, Shefi S, Hellerstein MK,
  Turek PJ. 2006. A Stable Isotope-Mass Spectrometric Method for
  Measuring Human Spermatogenesis Kinetics In Vivo. The Journal of
  Urology 175:242–246.

  Amann RP. 2008. The Cycle of the Seminiferous Epithelium in Humans: A
  Need to Revisit? Journal of Andrology 29:469–487.

  Durairajanayagam D, Rengan AK, Sharma RK, Agarwal A. 2015. Sperm
  Biology from Production to Ejaculation. In: Schattman GL, Esteves SC,
  Agarwal A, editors. Unexplained Infertility. New York, NY: Springer
  New York. p. 29–42. Available from:
  http://link.springer.com/10.1007/978-1-4939-2140-9_5


In cancer, why do cells duplicate themselves?

This article covers some of the key issues of cancer in layman's terms.
Essential, cancer is caused by multiple mutations in key regulatory genes which function in maintaining the cell cycle. This provokes uncontrollably rapid cell division, with only furthers the problem with genetic mutation. Here are some quotes from the article to strengthen your understanding in cancer cell mutations.

Image source

The cells become progressively more abnormal as more genes become damaged. Often, the genes that are in control of DNA repair become damaged themselves, rendering the cells even more susceptible to ever-increasing levels of genetic mayhem.
[...] Most cancers are thought to arise from a single mutant precursor cell. As that cell divides, the resulting 'daughter' cells may acquire different mutations and different behaviors over a period of time. Those cells that gain an advantage in division or resistance to cell death will tend to take over the population. In this way, the tumor cells are able to gain a wide range of capabilities that are not normally seen in the healthy version of the cell type represented.
[...] Mutations in key regulatory genes (tumor suppressors and proto-oncogenes) alter the behavior of cells and can potentially lead to the unregulated growth seen in cancer.


For 95% of the work I do with protein, I find this chart very helpful, showing common post-translational modifications, for each amino acid, with molecular weights, associated codons, pKa values, 1- and 3-letter amino acid codes, chemical structure and chemical properties (polar, non-polar, aromatic, acidic, basic).


Why is flash light harmful to what aquatic life forms?

I am sure the main reason is that flash lights, certainly in a dark aquarium, are very frightening and might cause temporary blindness for the animals. If someone flashes in your eyes, you can't see for a few seconds as well. That will cause distress for the animals and distressed animals live considerably shorter.

The total amount of light is indeed much to small to cause algal growth and real blindness is not likely from camera flashes.

EDIT:
I've found this article that will certainly be of interest to your question.


What is the definition of "Natural Selection"?

Official definition

  Is there an official definition of natural selection that is adopted by biologists nowadays? and what is that definition exactly?

I don't think there is such a concept as an "official definition" of any concept in science. There are common definitions though.

The definitions you cite

Let's go through your three definitions

  Natural selection is the differential survival and reproduction of individuals due to differences in phenotype.

This definition lacks the idea that this fitness differential must be caused, in part at least, by genetic variation.

  Natural selection, a process that results in the adaptation of an organism to its environment by means of selectively reproducing changes in its genotype or genetic constitution.

Part of the phrasing is about the consequence of the process rather than the process itself. The part that describes the process itself is "selectively reproducing changes in its genotype, or genetic constitution", which is a rather unusual phrasing and I would argue is slightly vague.

Note that while most authors refer to natural selection as the fitness differential, it is not impossible to refer to natural selection as the resulting change in allele frequency. I have never seen cases where this semantic difference matters though.

  Natural selection, then, can be defined as the differential reproduction of alternative hereditary variants, determined by the fact that some variants increase the likelihood that the organisms having them will survive and reproduce more successfully than will organisms carrying alternative variants.

I have never encountered the expression "alternative hereditary variants". I think the author made it up. It sounds like the author tried to avoid the term "allele" by replacing it with "alternative hereditary variants". The author also seems to have tried to avoid the term "fitness" by replacing it with "likelihood that the organisms having them will survive and reproduce more successfully".

But overall the definition sounds correct to me. There is an important difference between the first and the third definition is that in the first definition, it emphasizes the fact that the genetic elements that explain fitness variance are doing so via its effect on the phenotype. The third definition just ignores phenotype. As such, I would consider the first definition more complete (and more compact).

  Natural Selection is a mechanism of evolution that leads to non-random spread of genes due to the effect that genes have on reproductive success

Here, the definition is again very much based on the consequence of the process rather than the process itself. Only "due to the effect that genes have on reproductive success" refers to the actual process of natural selection.

I don't really like the term "random" here as the concept of randomness is somewhat unpleasant to define outside of a well-defined model. I don't really like the term "genes" either because selection doesn't only act on genes (but can act at any locus) and because the term "allele" would be more appropriate even if the phrasing would still remain unclear.

So in short, shame on us, the StackExchange definition is pretty bad!

  The preservation of favourable variations and the rejection of injurious variations

I shall not talk here about how different is Darwin's theory of evolution from today's theory of evolution (which is called the "modern evolutionary synthesis"). I shall not talk either whether this single short sentence is a good summary of Darwin's representation of natural selection (see @Luaan comments for more information).

This definition is short and a bit vague. One would want to think of this definition as applying to a genetic variant, without regard to the phenotype, however, Darwin did not know anything about DNA.

My favourite definitions

Lewontin's recipe

A very simple way to think of natural selection is to consider Lewontin recipe. The Lewontin recipe says that natural selection occurs whenever:

Individuals in a population vary in terms of a given trait
This trait has a non-zero (additive) heritability. See this post for a definition of heritability.
The fitness varies (not necessarily linearly) as the trait varies

Single sentence definitions

If you prefer a shorter and simpler version I would personally suggest

  Selection is the fitness differential among genotypes in the population.

This definition lacks the concept of phenotype but talking about the fact that an individual fitness is dependent on its phenotype (among other things) is, IMO, not required to mention in the definition of what natural selection is. Not that I also removed the term "natural". I don't quite like it because it leads people to think that natural and artificial selection could be fundamentally different. Same applies to sexual selection, IMO, but I shall not go down this slope now!

In a very similar post, I wrote the definition

  Selection is a fitness differential associated to a genetic variance among individuals in a population.

I also like this definition because it highlights that selection acts on populations (and not on individuals or on species).

Mathematical modelling

You might want also to consider as a definition the mathematical modelling of the process. In absence of genetic drift (assuming infinite population size), assuming a bi-allelic locus with alleles a and A, one can model (haploid) selection as

$$p_{t+1} = \frac{p_t W_a}{p_t W_a + (1-p_t) W_A}$$

, where $p_t$ is the frequency of the allele a at time $t$. $W_a$ and $W_A$ are the fitness of the genotype with alleles a and A, respectively. Of course, you can extend this model to any kind of ploidy and any number of alleles. You can also extend this model to include genetic drift (typically done via the use of diffusion equations or via branching patterns).

For more information about these mathematical modelling, please have a look at an intro book in evolutionary genetics (see here for book recommendation).


I'm trying to unserstand Yamanaka's iPS cells paper

Suppose you want to insert a cassette in a gene.  How will you know it is there?  What if only a small percentage of cells are successfully transfected?  What if your reagents were bad.  You do not want to waste time on cels that did not take up your cassette.

Those resistance genes are for detection of the presence of the cassette in a cell (or colony derived from a single cell).  You can have other things ride along with your cassette that will let you detect its presence.  Neomycin resistance: if you grow the cells that you have engineered in the presence of neomycin, only the ones that successfully got your cassette will live because the cassette gave them resistance.  All the ones that did not take up the cassette, or took it up wrong will die.

An active beta-galactosidase gene can work on a substrate to make a blue color.

  An active enzyme may be detected using X-gal, which forms an intense
  blue product after cleavage by β-galactosidase, and is easy to
  identify and quantify.

Again this lets you detect cells (or colonies of cells) which have successfully taken up your cassette.


How are Stem Cells Produced for Stem Cell Based Therapies?

I didn't get your question exactly. If you wanna ask how to maintain the potential of stem cells, yes, there are several compound that could keep stem cells, such as Leukemia Inhibitory Factor (LIF). As far I know, the using of pluripotent stem cell, such as ES, iPS, still has the problem of formatting teratoma in vivo studying. It means totally differentiating pluripotent stem cell still need to be work out.


Why doesn't ovulation occur in both ovaries simultaneously?

Each ovary has hundreds of thousands of follicles. And, of course, each one of those follicles is exposed to the same blood supply.
Therefore, your question...

Why isn't ovulation seen in both ovaries together?

... is the same of:

Why isn't ovulation seen in two follicles (regardless the ovary)?

All follicles are stimulated by FSH and they indeed start to mature at the same time. However, in a given cycle, normally only one follicle fully grows1. What we have here is a competition among follicles.
Guyton is not my favourite book on physiology, but it suggests an explanation for this:

Only One Follicle Fully Matures Each Month, and the Remainder Undergo Atresia:
After a week or more of growth — but before ovulation occurs — one of the follicles begins to outgrow all the others; the remaining [...] developing follicles involute (a process called atresia), and these follicles are said to become atretic. The cause of the atresia is unknown, but it has been postulated to be the following: The large amounts of estrogen from the most rapidly growing follicle act on the hypothalamus to depress further enhancement of FSH secretion by the anterior pituitary gland, in this way blocking further growth of the less well developed follicles. Therefore, the largest follicle continues to grow because of its intrinsic positive feedback effects, while all the other follicles stop growing and actually involute.
This process of atresia is important, because it normally allows only one of the follicles to grow large enough each month to ovulate; this usually prevents more than one child from developing with each pregnancy. The single follicle reaches a diameter of 1 to 1.5 centimeters at the time of ovulation and is called the mature follicle.

Therefore, the reason why we don't see both ovaries ovulating at the same time is the same reason why we don't see one ovary ovulating twice at the same time: the fastest growing follicle inhibits the growth of the other follicles (in the same ovary or in the contralateral ovary, it doesn't matter).
Besides that, it also explains the pattern of ovulation: in a given cycle, the left and the right ovary have equal chances to ovulate. Thus, the ovaries don't take turns like this (L is left and R is right):
L → R → L → R → L → R → L → R → L → R → L → R → L → R → L → R → L → R etc...
The real pattern is probably random:
L → L → R → R → L → R → R → R → L → R → L → R → L → L → R → L → L → L ETC...
According to Ecochard (2000):

It is concluded that in normally fertile women, the cycle length and the hormonal profile are independent of the, most probably random, site of ovulation. (emphasis mine)

Sources:

Hall, J. and Guyton, A. (2011). Textbook of medical physiology. Philadelphia, Pa.: Saunders.
Ecochard, R. (2000). Side of ovulation and cycle characteristics in normally fertile women. Human Reproduction, 15(4), pp.752-755.

1Note that, for answering this question, we will (wrongly) assume that there is no polyovulation in humans. However, as polyovulation does occur in humans, ovulation can sometimes be seen in both ovaries.


How can a virus be determined to cause a disease?

A modified form of Koch's postulates is used to guide experiments that establish that a particular virus causes disease.

As a specific example of such a study, the SARS-CoV virus was determined to cause the SARS disease by fulfilling these criteria:

SARS virus is found in people suffering from SARS, and not found in those who are healthy.
The virus can be isolated from infected people and grown in cell cultures (here, Vero cells).
Viruses grown in culture can be reisolated and compared with (and found identical to) the suspected pathogenic virus.
This isolated virus can re-infect people (or infect model organisms; in this case, a species of macaques).
Virus in reinfected organisms can be isolated, grown in culture, and found identical to the original pathogen.
The immune system is observed to respond in similar ways to the infection (pneumonia and lung tissue lesions).


This is a classic application of dynamic programming in bioinformatics, and is one of the first dynamic programs that I was exposed to in university! Let's begin..

Overview of algorithm

Step 1. Conceive of a scoring system.
 Step 2. Create a table using the two character sequences.
 Step 3. Iteratively fill in each cell, row by row, left to right. This is achieved by selecting the maximum (most positive) value coming from either:

(1) the cell that's located diagonally (top-left) to the current cell, plus the "cost" to align the two characters in consideration (cost value is obtained from scoring system).

(2) the cell to left of the current cell, plus the gap penalty (score issued for insertion/deletion mutation); looking at your example, the gap penalty is -1.

(3) the cell just above the current cell, plus the gap penalty.

Again, the greatest (most positive) of these three [sum] values will be placed in the current cell.

..

If you want the recurrence relation for this, then, if $T$ is the table being filling in, and $T(i, \ j) \equiv T(row, \ column)$, then

$$T(i, \ j) \ = maximum \begin{pmatrix}
T (i-1, \ j-1) + [alignment \ cost],\\
T (i, \ j-1) \ + [gap \ penalty],\\
T (i-1, \ j) + [gap \ penalty]
\end{pmatrix}$$

Scoring system

For simplicity sake, and to remain true to your example, I'll define and use the following:

Character match score: 0
Character mismatch score: -1
Gap penalty: -1

The character scores are potential alignment costs, and which to use is determined by if the two characters in consideration (row vs. column) are the same or not.

Now, to fill in table $T$..

Let sequence 1 run along the rows of $T$, and sequence 2 run along the columns, as you already have. If $T$ is initialized with a value of zero at location (0, 0), then, in order to fill in the first row [going from cell (0, 1) to (0, 9)], since there are no diagonal cells that exist yet, nor is there yet a row above the current row, for all cells in the first row we will use the second option that was mentioned above to obtain each cell value. So then, with the gap penalty being defined as -1, the first row will range from 0 to -9.

Make sure to keep track of which adjacent cell was used to obtain the value for each cell. This descriptive will later be used to trace $T$ once it's completely filled out, in order to obtain the optimal solution. If you're writing this on paper, people usually just draw arrows (from current to adjacent cell), however, if it's on a computer, an adjacency matrix is created & filled in.

In cases where more than one adjacent cell yields the greatest value, draw an arrow to each one. This is to say that there can be more than one optimal solution.

Next, we start with the first cell of the second row. Since a left & diagonal cell doesn't exist, that omits options 1 & 2, and leaves only option 3, which yields a value of -1 (only gap penalty). And, as you maybe have noticed by now, this behavior will always be true for the first row, and for the first column, and so, this is why you're able to so immediately fill out the table as you already have.

Continuing, to compute cell (1, 1), we now have to compare all three potential values and choose the maximum. For options 2 & 3, they both yield a value of $-1 + (-1) = -2$, however, option 1 yields $0 + [alignment \ cost]$, and, since both characters are the same (V and V), cell (1, 1) will have a value of $0 + (0) = 0$.

If we're to then fast forward a little and calculate cell (2, 1) ...

Considering option 1, we have $-1 + (-1) = -2$, since the characters being compared are I and V (and are a mismatch). Option 2 yields a value of $-2 + (-1) = -3$, and option 3 gives $0 + (-1) = -1$, hence, cell (2, 1) = -1.

Continue doing this for all cells until $T$ is filled.

Obtaining an optimal solution..

As mentioned, multiple optimal solutions may exist. In order to obtain an optimal solution, you must trace $T$, using the arrows you've been drawing (or the adjacency matrix), as a guide.

To obtain the path for best alignment, simply begin with the bottom-right most cell of $T$, i.e. the most recent/last computed cell, and trace your arrows to create a path back to the first cell (the top-left most).

To then construct the alignment, you will traverse this alignment path, beginning with the top-left most cell, and going to the bottom-right most cell, and, when considering the orientation of each arrow when going from cell to cell (diagonal, horizontal, vertical), you will do one of the following:

Diagonal arrow

For the first alignment sequence (top), simply add the character that's in the column of the cell you just moved to; for the second alignment sequence (bottom), use the character that's in that row. So then, when considering your example, and for both sequences, the first characters of an optimal solution when going from cell (0, 0) = 0 to cell (1, 1) would be:

V

V

Vertical arrow

When this happens, it means that there is a gap in the [initial] sequence that runs along the columns, since there are two rows for one column. Because of this, for the first alignment sequence, you will use a - to denote a gap. For alignment sequence two, use the character that's in the row.

Within the context of your sequences, for the optimal solution, a gap isn't encountered until the 7th character, at which point, the partial optimal solution will look like:

V I V A D A -

V I V A L A S

Horizontal arrow

This is the same concept as the vertical arrow rule, except it implies there is a gap in the row-oriented sequence, and so, a - will be placed in the second alignment sequence; the first alignment sequence will use the character in that column.

After all is said and done, your optimal solution is:

V I V A D A - V I - - S

V I V A L A S V E G A S

An interactive version of this algorithm can be found here.


What is the progressive evolutionary advantage that leads to flying?

The honest answer to this and many other similar evolutionary questions is that we don't know the answer. We can sample information from many different points along an organism's developmental timeline using the fossil record, genetics, etc. and reconstruct various states of said organism's development. The overwhelming evidence is that evolution is the process that connects these various states, but reconstructing the detailed trajectory that leads from one developmental state (e.g. flightless) to another (e.g. flying) is often formally impossible due to the low time resolution of the information that we have.

That being said, plenty of people have speculated as to the origins of flight, and there's an excellent wikipedia article on the subject. From the article:

  Powered flight has evolved only 4 times (birds, bats, pterosaurs, and insects)... Insects were the first to evolve flight, approximately 350 million years ago. The developmental origin of the insect wing remains in dispute, as does the purpose prior to true flight.  One suggestion is that wings initially were used to catch the wind for small insects that live on the surface of the water, while another is that they functioned in parachuting, then gliding, then flight for originally arboreal insects.


This dates back to the 1980's when these M13 primers were first cloned.

Heidecker G, Messing J, Gronenborn B. 1980. A versatile primer for DNA sequencing in the M13mp2 cloning system. Gene 10(1):69-73.

In this paper, they discuss the construction of a primer for sequencing of the M13mp2 phage vector. An EcoRI/AluI digest releases a 92 bp fragment from a portion of the lac operon. This fragment contains what are now called the M13 forward -21 and -40 primers. I do not know who first named these primers but, counting from the centre of the EcoRI palindrome, I think it's clear where these names came from:


Why did we evolve to be able to see this specific set of wavelengths only?

Well humans actually have a reduced spectrum compared to non-mammals. Reptiles and birds have 4 color sensitive cell types (cones), mammals lost two of these as modern mammals are descended from early mammals who were nocturnal. Primates evolved a third cone, (a mutant variant of one of the two they had before) Primates did this because many a frugivores and color is excellent for determining when fruit is ripe.


Do all prokaryotes have ATP synthases and an electron transport chain?

This is an interesting question (I really mean this — see below), for which a straight answer is remarkably difficult to find on the web. When I googled for it I got pages with statements that obligate anaerobic bacteria still had the electron transport chain (ETC) and ATP synthase as there were different electron acceptors other than oxygen. Yes, we know that things are different in thermal vents and hot springs, but what about gas gangrene? I am not a microbiologist, but I did play with the metabolism of some bacteria for a biochemical bioinformatics lab some years ago, so I can give two instances where anaerobic bacteria appear to lack either the ETC or both the ETC and ATP synthase.

Clostridium perfringens

This is the anaerobic fermenting bacterium that leads to gas gangrene in infected wounds and was a major cause of limb loss and mortality in the First World War. The DNA sequence of Clostridium perfringens has been determined. I quote at length from the paper as it describes the fermentation, but italicise the key statement for those who wish to skip this:

  We could not find any genes coding for tricarboxylic acid (TCA) cycle- or respiratory-chain-related proteins, in contrast to C. acetobutylicum, which has incomplete TCA cycle enzymes. Similar to C. acetobutylicum, we could construct a pathway map for anaerobic fermentation resulting in the production of lactate, alcohol, acetate, and butyrate, all of which have been commonly detected in C. perfringens cultures. In the fermentation pathway, pyruvate is converted into acetyl-CoA by pyruvate-ferredoxin oxidoreductase (CPE2061), producing CO2 gas and reduced ferredoxin. Electrons from the reduced ferredoxin are transferred to protons by hydrogenase (CPE2346), resulting in the formation of hydrogen molecules (H2) that are released from the cell together with CO2.

The related bacterium, Clostridium acetobutylicum, mentioned in the extract, is also an obligate anaerobe. (It ferments a variety of plant mono- and poly-saccharides to acetone, butanol and ethanol — used to produce explosives in the First World War.) Although it has some enzymes of the TCA-cycle, it is unable to use the cycle oxidatively, and, like Clostridium perifringens, lacks the enzymes of the electron transport chain and an ATP synthase.

Ureaplasma urealyticum (Ureaplasma parvum)

This micro-organism is a micoplasma (Mollicute) rather than a bacterium — i.e. it lacks a cell wall. It infects the human urogenital tract. It lacks the components of an electron transport chain but does possess a functional ATP synthase. It generates a hydrogen ion gradient, not by increasing the hydrogen ion concentration within the inter-membrane space by the oxidation of NADH in the ETC, but by reducing the intracellular hydrogen ion concentration by generating ammonia from urea (plentiful in its habitat) in a reaction catalysed by the urease it encodes. The sequence of the organism and references to previous work on its urease activity can be found here.

Evolutionary considerations

The reason I find this question interesting is that anaerobic organisms preceded aerobic organisms, so the question arises whether there are any contemporary anaerobic bacteria that have evolved from these primaeval anaerobes and have never possessed an electron transport system — or are all contemporary anaerobic organisms lacking an ETC derived from organisms with an ETC (aerobic or using some other electron acceptor) and have just lost these functions through non-use (as is most likely in the examples above)? This question must surely have been considered by those in the field.


How can cancer preventing genes from animals be transferred to humans?

While this research is interesting and might help curing cancer at some point, it's not a ground breaking revelation.

The gene in question here is TP53, coding for the very-well known tumor supressor protein p53. Humans do have this gene, but apparently elephants hav acquired multiple copies of it (~20) during evolution and that might explain why they don't get cancer so easily.

The problem of testing this is not a technical one. Using modern genetic engineering methods it should be fairly easy to multiply the gene in human or mice embryos, or introduce the additional variants from the elephants. Someone might already be planning to do that in mice.

For use on humans however, this is highly unethical. Without proof that these gene copies actually prevent cancer (and one observational study is not a proof), you can't just use a new medical treatment. Secondly this treatment would require genetic modification of an embryo (because its actually cancer prevention, not acute treatment) and that is illegal almost everywhere on earth (even genetic modification of somatic tissue for cancer treatment is just now becoming an experimental therapy).


How can an animal live without a head / brain?

In general, and this is somehow speculative, the animals that you mention have more autonomy in their extremities and less control from a head, muscles have evolved autonomous responses perhaps as an evolutionary advantage, ( i.e. having a brain be in charge of reactions can add precious milliseconds ), there also seems to be a relationship in between brain size ( specific motor control areas) and this autonomy, which introduces a metabolic cost (i.e. our big heads need a lot of energy)  Further, there are other biological considerations for providing extremities with their own resources and thus to a degree be more independent, perhaps another evolutionary strategy. At the other end of this control-autonomy relationship, the head takes control of the extremities most of the time and their interdependance is greater, so if you cut it no movement will happen, although we still possess a few hard coded reflexes that work for a while provided they have enough energy left or a blood source.

To give you an example: a cat ( somewhere in the middle ) can still walk when you cut the connections from the brain /head  to the legs due to reflex actions ( the cat has to be on a treadmill though).


Can the same target gene be regulated differently by the same transcription factor under different conditions?

Short answer - yes but probably somewhat rarely.

Transcription factors aren't necessarily limited to being either repressors or activators. In practice they mostly do one a lot more than the other - e.g. if they have an 'activation' domain then they will mostly activate, but they can still do the opposite, directly or indirectly.

A single TF will often regulate different genes in different directions. This can be due to indirect effects - our activator activates a repressor which then switches off a gene. It can however also happen through direct means - for instance a factor might bind a repressing or activating domain at different locations, or displace different factors.

Most of this variation is probably specific to the target gene, so factors are probably more specific in their effect on a given gene. However, since our factors action depends on other genes,and different genes will be active in different conditions, there's no reason a factor couldn't do different things under different conditions while at the same location - perhaps one condition activates a repressor that binds with it, or a stronger activator that it competes with.

It's a matter of ongoing research, but I would expect this kind of thing to be the exception rather than the rule. In general complex interactions between TFs at a given location seem to be rarer than more or less additive effects.


Are tongues red because they contain blood?

Mammalian tongues are red because of haemoglobin. Blue/black colouration is due to the additional presence of melanin.

  At the boundary between the epidermis and dermis are melanophores, cells that contain melanin. This brown pigment absorbs ultraviolet radiation from the sun that might otherwise damage the underlying dermal tissue. Melanin in the dark tongues of giraffes (Giraffa camelopardalis) protects the tissue from sunburn as the animals lift their heads into the top branches of trees to forage for leaves. In humans, synthesis of melanin increases upon exposure to sunlight and produces tanning. Extensions of melanophores reach into the epidermis where they inject their pigments into developing hair cells. In a few cases, such as the bright ischial callosities of baboons, pigmented patches of skin are used as visual signals. The blue and red coloration on the scrotum and perineal region of male vervets (Chlorocebus aethiops) is used in dominance displays.

From: Mammalogy: Adaptation, Diversity, Ecology by George A. Feldhamer, Lee C. Drickamer, Stephen H. Vessey and Joseph F. Merritt (2007) p 97 The Johns Hopkins University Press; 3rd edition edition


Why are organs not harvested from deceased cancer patients?

There are different reasons why cancer patients are mostly excluded from donating organs.

Although the probability of transmitting cancer is small, it is not zero. Also tumors tend to form metastases over time, which spread throughout the body. It is possible that a cancer has formed metastases in other, distant organs, which are too small to detect. Since recipients of organs have to take strong immune suppressing medication to prevent the rejection of the transplant, the immune system might not be able to fight the cancer cells anymore. Because of this medication, transplant patients already have a higher chance of getting cancer, because their immune system does not capture cells when they go rogue. See reference 1 for a more general description and 2 for the detailed report, reference 3 for the higher cancer risk of transplant patients.
Tumors can go dormant when they are treated with chemotherapeutics to evade destruction, but these dormant cells can re-wake. If this happens after the transplantation of an organ, this is obviously bad for the recipient. See reference 4 for details on mechanisms.
Cancer patients who died from the disease have often been treated with agressive drugs like chemotherapeutics. While these attack mostly the fast dividing cells of the tumor, they also have more or less strong side effects on the body. A lot of organs are simply not in the state (or have a strong chance of being in this state) anymore to be transplanted. Nobody wants to transplant a dysfunctional organ. See reference 5 for details.

References:

Cancer Spreads from Organ Donor to 4 People in 'Extraordinary' Case
Transmission of breast cancer by a single multiorgan donor to 4
transplant recipients
Cancer in the Transplant Recipient
Tumor dormancy as an alternative step in the development of
chemoresistance and metastasis - clinical implications
Long-Term Side Effects of Cancer Treatment


Server for protein structure prediction for multiple sequences

Unfortunately it is impossible to predict the tertiary structure of proteins using raw amino acid sequence. The information required to be computed in the construction of the dynamic protein shape is too large for any computer at the moment.

There are actually a list of research facilities that are looking for people to donate their computer's idle CPU time to help sequence proteins.

Here is a list: (http://www.hyper.net/dc-howto.html).


Can molecular genetics make a boolean variable from a continuous variable?

Positive feedbacks can be one alternative. Positive feedbacks exhibit bistability and can therefore adopt one of the two stable states depending on the initial condition. A famous example of a positive feedback switch would be that between cI and Cro in λ-phage, which repress each other. Positive feedbacks also display hysteresis: if the state of the system is dependent on an inducing ligand X such that system attains state S2 at high levels of the ligand, then to switch from S2 to S1 the concentration of X would have to be reduced below the level that was required for the S1 to S2 switch; and vice-versa. In other words, the system tries to remain in its current state.

If the transcription factors that constitute the genetic positive feedback have a co-operative behaviour then you can expect a steep switching curve.

For details see this review.


Can anyone identify this locust / grasshopper in Florida, USA?

It appears to be Romalea microptera, or the eastern lubber grasshoper, which is commonly found in the southeastern United States, including Florida.

https://en.wikipedia.org/wiki/Romalea_microptera
http://eol.org/pages/965190/overview

Photo by Steve Smith.


How is bad garlic breath eliminated by swalllowing a bit of raw garlic?

Searching the net for "how to avoid garlic breath" some references come up.

Enter Ohio State University to help. Researchers there have evidence suggesting that we can neutralize bad breath naturally before it offends those around us. According to science, here are three ways to do it.

Recommended: raw apples, lemon juice, green tea.

Green tea is very high in antioxidants called polyphenols. As with the enzymes in the apple, polyphenols cover up the odor-causing chemicals in garlic.
Sheryl Barringer, one of the study's lead researchers, said that it’s best to use the bad breath cures at the same time you’re eating garlic. So we’d recommend adding some apples to that salad with garlicky dressing or using some lemon juice in your next garlic dip. Unless you want to squeeze the citrus straight into your mouth, that is.

And in a link found there, the chemical explanation is:

According to the researchers, foods deodorize garlic breath through two mechanisms. First, enzymes in the raw foods help to destroy the odors, and then, phenolic compounds in both the raw and cooked foods destroy the volatiles. This is why raw foods were generally more effective because they contain both the enzymes and the phenolic compounds.

It must be that raw garlic taken just before eating garlicky stuff works the same way. No magic. Maybe the researchers will see this and do a proper experiment :).


Why aren't introns found on the ends of pre-RNA?

RNA splicing refers to a certain kind of RNA processing mechanism which leads to the excision and exclusion of some regions of the primary transcript. You should note that this is not the only method by which such a thing can happen; Endo-ribonucleases can clip the ends of the transcript and this happens in the case of tRNA-processing. But as "splicing" happens it is essential that the excised region be in the interior of the transcript. See the figure.


Examples of species whose extinct common ancestor is well documented?

Not with fossils.
Very very few organisms ever fossilize and most of the organisms tissues are not represented in fossils. Less than 0.01% of all animal SPECIES have left a single fossil and most of those have not been found yet.
Because of how incomplete the fossil record is we can never say a species is definitively part of a lineage. in fact the basic assumption in paleontology is that you never have a direct ancestor (individual or lineage) and extraordinary evidence would be needed to demonstrate otherwise.
Only direct observations or high genetic sampling would allow something to be considered definitively a common ancestor at the species level. Now we do have this for some species. We also have fossil localities with really high resolution making common ancestors highly likely, but never definitive.
Part of the issue is also defining species, the definition for species used in paleontology is very different than the one used in say population genetic. Species are nota real things but a human category stuck onto what is basically a continuous spectrum, it only works because most of the spectrum is dead. There is no concrete point at which two groups are definitively separate species. Its a bit like trying to define the exact cut off between two colors. Some groups of biologists favor definitions which increase the number of species others ones that decrease it, and both work because for the actual practice of biology whether two closely related populations are or are not separate species really does not matter.


What type of animation software is used to create these molecular motor motions?

Most any reasonable animation/modeling software can handle this sort of animation. I have developed an educational iOS app with interactive biological macromolecules, including several animations. Here is how I would approach this, I suspect something similar was done here.

The models are likely built up from PDB files, or equivalent. These files allow viewing and manipulating large molecules in 3D with special viewers.  Many 3D modeling/animation apps can also view and convert these molecules into polygonal models that can be used as components and then animated within the app. I use Cinema 4D, not cheap. There is a free, downloadable program called Blender. I'm sure Blender can handle the animation but not certain whether it can read and convert the PDB file. If not, there may be other options for this.

This is not a challenge to be taken lightly. The person doing the animation you reference also knew how to assemble the parts as well as how the movement is effected. There is also a steep learning curve to using this type of software.


c4 cycle in photosynthesis occurs in monocots or dicots

monocots don't lack bundle sheath cells.  In fact, they are much more likely use c4 respiration than dicots.  There are actually about 10 times more c4 monocot species than c4 dicot species.  the c4 cycle is really primarily a monocot adaptation.  I think that the confusion often comes from the fact that dicots appear to be "more sophisticated" than monocots when you look at them, with their pretty, well organized vascular bundles and branching veins, which makes it intuitive to assume that they would be the ones using the "higher tech" c4 system.


What do the letters 'p' and 'c' mean in mutation descriptions?

According to the HGVS guidelines, a letter prefix should be used to indicate the reference sequence used. Accepted prefixes are:

“g.” for a genomic reference sequence
“m.” for a mitochondrial reference sequence
“c.” for a coding DNA reference sequence
“n.” for a non-coding DNA reference sequence
“r.” for an RNA reference sequence (transcript)
“p.” for a protein reference sequence


Where do the H+ ions come from in light reactions?

The photolysis of water is coupled to the reduction of plastaquinone (Q) in photosystem II (PSII) as summarized in this diagram, adapted from Berg et al.:

The overall reaction (which balances) is:

2 H2O + 2 Q + 4 H+ = O2 + 2 QH2 + 4 H+

But the 4 H+ on both sides of the equation are not the same. The generation of the hydrogen ions in the thylakoid lumen is coupled to the uptake of hydrogen ions from the stroma as the plastoquinone is reduced. This is made possible because of the membrane disposition of the components of photosystem II. Hence an electochemical gradient is established that can be used for generating the ATP needed for photosynthesis.


Sometimes!

The causes of epilepsy are legion.  There's a massive Wikipedia page listing various causes, and, wow, I get tired just reading the table of contents.  None of those are genetic causes, but it should perhaps therefore be not surprising to learn that the genetic causes of epilepsy, although the minority of cases, are also quite varied.  Apparently most of the causative genes involve ion channels (whether voltage- or ligand-gated), but there are a truly large number of genes that can be related to epilepsy.

This 2011 paper has quite a lot of information.  Some facts it presents on the genetics of epilepsy:

Something like 1-2% of all mutations in mice present with epilepsy symptoms.
Concordance is around 50-60% for monozygotic twins, and 15% for dizygotic

The majority of twin concordance is likely from the same (genetic) cause

Monogenic causes (versus complex causes of epilepsy) account for around 1-2% of human cases.

In direct answer to your question, there is this paragraph (emphasis added) explaining the rough breakdwn:

  Monogenic inheritance is suggested by the familial aggregation of cases that share a similar phenotype and are distributed in the pedigree according to a Mendelian mode of transmission: autosomal or sex-linked, dominant, or recessive. Autosomal recessive epilepsies are often associated with structural or metabolic abnormalities of the brain and with neurologic comorbidities, so most of them are not in the category of idiopathic epilepsies. Examples of these are pyridoxine-dependent epilepsy (PDE), several progressive myoclonic epilepsies (PMEs), and some malformations of cortical development (MCDs). Most of the monogenic idiopathic epilepsies follow the pattern of autosomal dominant inheritance, implying the presence of multiple cases in successive generations and male-to-male transmission.

In short:

If it's genetic, it's likely to be complicated and controlled by many genes
If it's controlled by one gene, it's likely to be dominant

The paper also presents the following table which may be of interest, listing monogenic causes of epilepsy:


Does pheomelanin have a useful biological function?

I don't think that the role of pheomelanin is known yet. To produce larger amounts of it, you need mainly two conditions: A weak (or absent) MC1R signalling and the availibility of the amino acid cysteine. If MC1R signalling is strong, the preferred way goes into the direction of eumelanin. Its known for quite a while that pheomelanin produces reactive oxygen species which either directly cause DNA damage or do it indirectly by using up the cells storage of antioxidants. You can find more details in this review as well as links to a number of original papers.


What are the ESSs among hawks, doves, retaliators, bully and prober retaliators?

I think Dawkins answers this in the book as well.

The point was that most strategies are not stable because the "random" introduction/mutation/evolution of some alternate strategies will disrupt a population of the first strategy.

The example was a group of doves being invaded by a single hawk (the conspiracy of doves). Because the hawk does relatively better (by winning every conflict against a dove), than even after generations of entirely doves, the random addition of a hawk (say by mutation) will take hold because the hawk always wins against a dove. Whatever feature/gene that created a hawk in the pool of doves will be passed to some offspring.

If I remember correctly, the only stable case was prober-retaliator, since all others get invaded by someone else.


This appears to be the larva of a drain fly (aka moth fly; family Psychodidae).

 Top left is larva; Source: YourWildlife.org; Credit: Matt Bertone
You can use a dichotimous key to help you ID to family. For example, from Bouchard et al. (2004)+:

Body cyclindrical; non-leathery integument...
Head capsule fully visible and completely separated from thorax
Prolegs absent
Thoracic segments not fused or swollen
Abdomen non ending in long respiratory tube
Body segments with 2-3 secondary divisions (annuli); body grey or brown

You can use Arthur Frost's comment to help ID to lower taxonomic levels.
How it got there:
From Orkin:

These pests are particularly likely to be found in bathrooms and kitchens, typically getting into homes through:

Basements
Drains
Windows

 +  Bouchard, R.W., Ferrington, L.C. and Karius, M.L., 2004. Guide to aquatic invertebrates of the Upper Midwest. (Chapoter 13: "Diptera")


Which modern methods of antibiotic production are there?

For Penicillin production try from page 165 of:
Industrial Microbiology: An Introduction
by
Michael J. Waites
Neil L. Morgan
John S. Rockey
Gary Higton
There is also a table in that chapter listing the other antibiotics and which organisms are used to produce the basic form.
I found it very readable.


If DNA methylation inactivates genes, does DNA demethylation activate them?

Here is a series of articles explaining DNA Demethylation from Sience Direct.

In the most broadest of senses, DNA methylation adds methyl groups to DNA preventing the transcription complex from forming and transcribing the gene into mRNA. By demethylating the DNA, it allows the transcription complex to form and mRNA to be transcribed for translation.

When it comes to cancer, Most of the tumor suppressor genes are down regulated to allow for genes like stat3 to be upregulated. Ideally, by removing the suppression of these genes, they can reduce the levels of oncogenes and slow the growth of the cancer.

Think of it like this A -| B. Cancer decreases A so B can increase in expression A↓ -| B↑. By demethylating A, we  A↑ -| B↓.


Why does the right bundle branch not have any terminal filaments in the IVS of the human heart?

Why is a philosophical question, but you can see, below, the most common anatomic variation, with the ventricular septum receiving terminal branches from the septal fascicle off of the left bundle branch though it can come off the common bundle. The left ventricle is larger, and as might be expected, has a greater portion of the conducting system than the right ventricle.


Before I move my arm the brain sends signals - what causes the brain to send signals?

Action potential - I haven't read through the entire Wikipedia article so I can't vouch for its accuracy (not that my neurophysiology is good enough to critique it), but it's probably a good start.
Broadly speaking: the brain contains different regions that are each responsible for fairly specific tasks. In the case of picking up a glass of water we can, at a high level, describe the mechanism behind thirst. Your blood contains electrolytes in water; you can consider the electrolytes as being like cordial (reduce the water and you have a higher concentration of cordial / electrolytes). A sensing mechanism (beyond the scope of this answer) will trigger action potentials between the relevant areas of the brain (motor, memory, etc.) to result in the final movement.


Help me identify this animal from Bangladesh

Looks like the Large Indian civet. Notice the size and the fur coloration pattern on the neck.

From wikipedia:

  The large Indian civet ranges from Nepal, northeast India, Bhutan,
  Bangladesh to Myanmar, Thailand, the Malay peninsula and Singapore to
  Cambodia, Laos, Vietnam and China.[1]

Looks like it is found in eastern parts of Bangladesh including Noakhali district – the place where the picture was taken.


Which shades/hues of color are easiest to distinguish for humans?

I've read somewhere that humans are most capable of distinguishing shades of green, that is a human can differentiate more shades of green than any other color. Is it true?

I'd say it's plausible, depending on your definition of "Green." While your eyes do, indeed, have RGB receptors (cones) and Rods for grayscale - they don't perceive the Visible Spectrum equally. Here are a few graphs I found from Photo.net regarding the human eye and the sensitivity of the Cones (first and second) and Rods (third):

What you should be noticing above is not necessarily the Y axis, but the X axis - which represents the Wavelength, and amount of Wavelength our eyes are sensitive to each color. While our eyes perceives the most Red wavelengths and the least Blue wavelengths, Green comes in just under Red's range for Wavelength coverage. However...

When combined with our Rod sensitivity, though, Green wavelengths produce nearly double the sensitivity the Red Wavelengths - and nearly quadruple the Blue wavelengths. What that means is that in low-light situations when the Cones are unable to produce a precise color image, your Rods will be able to pick out Green things (with a slightly loose definition of 'Green') more than other colors - which is perhaps the reason why night-vision goggles often use Green since they increase the Intensity of the light, which presumably stimulates the Rods more (although not knowing precisely how the image is produced - if the green coloring is enhancing that particular bit of the spectrum of falsely colored - take this with a grain of salt).

Does that explicitly prove you can see more Green shades than others? No. Your brain does a lot of processing - the entire color Yellow is a construction of your brain, and Tetrachromats (people with 4 types of Cones) are real.

However, like I said above, I'd say it's plausible.


Our ability to maintain sleep or wakefulness is because of "mutual inhibition" between the wake-promoting neurons and the sleep-promoting neurons. The areas in brain which regulate wakefulness by activating the cortex also inhibit neurons present in ventrolateral preoptic nucleus (a cluster of neurons situated in the anterior hypothalamus). And when VLPO neurons are activated, they induce sleep, and this also inhibit activity in the arousal centers like neurons in tuberomammillary nucleus (TMN).

Transitions between these states of wakefulness and sleep is very rapid, usually in seconds. Various researchers have reported this neurological mechanism for "flip-flop switch" in form of electrical circuit.

The mechanism  for mutual inhibition is regulated by sleep drive or the circadian signal. When one of this body signal is sufficiently strong, it transits to the opposite state from wakefulness to sleep or vice versa. This mechanism is analogous to mechanism involved in  transition between rapid eye movement (REM) sleep and non-rapid eye movement (NREM) sleep.

Humans require some time to relax and then fall asleep, and deep sleep needs 20 or more minutes after sleep onset. Sleep onset and associated loss of consciousness is related to one another and occurs instantly.

Many intrinsic and extrinsic factors  regulate sleep cycle. Adenosine is one of the chemical which accumulates during wakefulness and later induces sleep by inhibiting wake-promoting neurons. And caffeine inhibits adenosine activity and helps in wakefulness.

The time needed for transitions between sleep and wakefulness  is  maintained by biological clock located in the suprachiasmatic nucleus. This is small structure consisting of about 50,000 brain cell. And it receives light signals from eye  via  optic nerve. Light controls the day-night cycle and which in turn regulates various biological functions including temperature, hormone release,  sleep and wakefulness. The SCN stimulates wakefulness by producing a  alert signal which inhibits sleep. The SCN also helps in inducing sleep by turning off alert signal.

(Via:  http://healthysleep.med.harvard.edu/healthy/science/how/neurophysiology)


Iris is a thin, circular structure in the eye, responsible for
controlling the diameter and size of the pupil and thus the amount of
light reaching the retina. The color of the iris gives the eye its
color. In optical terms, the pupil is the eye's aperture and the iris
is the diaphragm that serves as the aperture stop.

Color and structure of iris is greatly depended upon genetic links, but the patterns are not. Iris is developed by the prenatal(before birth) growth through a process of tight forming and folding of the tissue membrane.

The human iris begins to form during the third month of gestation. The structures creating its distinctive pattern are complete by the eighth month of gestation, but pigmentation continues into the first years after birth. The layers of the iris have both ectodermal and mesodermal embryological origin, consisting of (from back to front): a darkly pigmented epithelium; pupillary dilator and sphincter muscles; heavily vascularized stroma (connective tissue of interlacing ligaments containing melanocytes); and an anterior layer of chromataphores and melanocytes with a genetically determined density of melanin pigment granules. The combined effect is a visible pattern displaying various distinctive features such as arching ligaments, crypts, furrows, ridges, and a zigzag collarette. Iris colour is determined mainly by the density of the stroma and its melanin content, with blue irises resulting from an absence of pigment: longer wavelengths differentially penetrate while shorter wavelengths are reflected and scattered, a phenomenon resembling that which makes the sky blue. The heritability and ethnographic diversity of iris colour have long been studied, but until the present research, little attention had been paid to the achromatic pattern complexity and textural variability of the iris among individuals.
Reference

Iris Recognition vs. Retina Scanning
Iris and retinal scanning are ocular based biometric identifiers. Iris recognition uses a camera to capture image of the iris. Iris is the only internal organ visible from outside the body. Iris scanners can acquire an image of the eye from a distance of 3 to 10 inches.
In retinal scanning, the device send a beam of light deep inside the eye to capture the image of retina, which is located on the back of the eye. retinal scanning is not widely used due to the intrusive methods used to capture the image.
Factors which enhance the iris scanning system,

reference


Minimum size for a peptide/protein to be immunogenic in human?

There's a few limiting factors including how proteins are presented that constrains the actual size needed to get peptide presentation. These depend largely on the MHC molecules (HLA in humans). The binding groove in MHC-I actually limits the size of peptides it can load to 8-10 amino acids, 9 being the most common. This is because "pockets" at either end of the binding groove are said to actually grasp the peptide, and it doesn't allow for much longer sequences. MHC-II lacks these grasping pockets, and so it can bind much longer sequences (Figure 1). MHC-II typically binds sequences of 13-25 amino acids.

Figure 1. Difference between the MHC-I and II binding groove.

There are also a given number of requisite anchor residues that complement the binding pocket of the MHC binding groove that mostly display a particular character at the given position (normally polar at a given position, etc.) (Figure 2).

Figure 2. Just a sampling of possibilities across HLA isoforms.

All information and figures courtesy of Parham "The Immune System," 4th ED.

If the presented peptide has met the prerequisities and has been identified by a leukocyte, in theory it should produce an immune response. I think these are some good considerations to make when you're thinking about how small can a peptide be. I'm assuming here that MHC-II would be handling your injected protein through an extracellular pathway (I can't know for sure), and so the smallest literature MHC-II peptide range I've ever seen is 11 amino acids on the low side. There are a number of computational studies out there that attempt to predict MHC affinity, but it's problematic due to the range of sizes MHC-II may bind and there is variability among the binding cores that contain the anchor amino acids.


How would constantly growing nails have aided early human?

I can't say anything for sure (and, with questions like this, it's rare that anyone can), but my guess would be that human nails grow constantly for the same reason as the (analogous) claws of most mammals do: to keep them from accumulating damage.

Your bones, if they suffer mild to moderate damage, are capable of healing through the concerted action of several specialized cell types in your body.  This healing process, however, is only possible because the bones are inside the body, surrounded and permeated by living tissue.

Your nails, however, are simple sheets of keratin, and contain no living cells that could heal them, nor any blood vessels that could keep such cells alive.  Being exposed to the outside of the body, outside the skin barrier, they cannot really support living tissue that could heal them.

Instead, the way human nails (and animal claws, more generally) "heal" is by growing.  Since the nail itself cannot contain cells that would rebuild it, those cells are instead located in the nail matrix, which is located under the nail and from which the exposed part of the nail continually grows out of.

(Indeed, the same is true of most of the exposed parts of your body: your hair and even the surface of your skin itself are also composed of non-living keratin constantly growing from an underlying matrix.  This is necessary to maintain the skin barrier between the interior and the exterior of the body.)

The reason human nails must keep growing all the time is that they do continually wear down and suffer damage from various causes (and would surely have worn down much faster yet for our primitive ancestors, who had to sustain themselves through hard manual labor with few or no tools).  If your nails just stopped growing after you reached adulthood, they'd be in horrible shape even just a few years down the road, not to mention decades later.

While the rate at which human nails do grow is pretty slow — it takes several months for a damaged fingernail to fully regrow, and up to a year for a toenail (a fact I can confirm from personal experience, having broken my toenail last summer) — it's still enough to ensure that your nails will only bear less than a year's cumulative damage at any moment, rather than every nick and scratch and cut they've suffered during your entire lifetime so far.

In a relatively sheltered modern lifestyle, it's quite likely that even this moderate growth rate may exceed normal wear on your nails, requiring them to be clipped regularly.  Still, the fact that you can clip your nails (or, in a pre-modern society, just bite or scrape or cut them down) reduces the selection pressure against excessive nail growth.  On the other hand, not having your nails grow back as fast as you wear them down through hard manual work could be quite bad for your fingers, and could easily reduce your working ability or even lead to harmful infections.  Thus, it makes sense that evolution has optimized out nails to grow at a rate that, on average, tends to somewhat exceed the typical rate of wear.