Who was the first to talk about evolvability?

My literature searches have turned up dead ends, so this is less of a full answer and more of some groundwork, but Google ngrams suggests somewhere around 1931 for the first usage, with meaningful usages beginning in earnest int he early 70s.  Their book previews from that era are sadly lacking; I can't find the usage of the ones from the 40s and 50s they do list sadly, but there are definitely some misnomers that show up in programming.  There's a 1973 work and one from 1977 that at least appear to be the correct usage, with the one from 1973 using it as a "new" concept.


The phylogenetic definition of the clade Dinosauria

As of right now it is still the same, the evidence for sauropodomorpha being a outgroup is not statistically more reliable, this may change, however this will still not have much impact. There are several ways in which dinosauria is defined.

The most recent common ancestor of Megalosaurus and Iguanodon is also sometimes used since they were the original animals used to define the group.

The last common ancestor of Triceratops horridus, Passer domesticus, Diplodocus carnegii, and all of its descendants is also used just because of Baron's work.

Finally there are several unambiguous synapomorphies used to define the group, including such things as ankle structure. A full list can be found here.

In a group as well known as dinosaurs, a discovery like Baron's (if it holds up) is just going to lead to a change in the definition.


How does new species come into existence?

A paper from Müller et al. proposes a molecular marker called a CBC, differences in which can be used to call two different species, even when closely related: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1950759/

  In this study we are looking for a molecular classifier that might indicate that two organisms belong to different species. We are interested in an indicator hypothesis that is easy to work upon and additionally yields a certain probability that two organisms belong to distinct species. Compensatory base changes (CBCs) in the internal transcribed spacer 2 region (ITS2) of the nuclear rRNA cistron have been suggested as such a classifier.

Some mutation event that creates sufficiently different CBCs in a viable offspring capable of further reproduction, i.e., survives natural selection, would therefore lead to speciation, by this measure.


What is the importance of urea in mass spectrometry?

I think that the OP was asking about relevance of using urea with respect to the FASP method. In the FASP method, the primary denaturant is SDS . Protein are denatured with a ~4% SDS solution (buffered to pH 7.5 - 8.0). Then 8 M urea solution is used to replace the SDS. Urea serves two purposes here, first it keeps the protein denatured and in solutions as SDS is replaced/washed off. Second, because urea is a chaotropic agent, it reduces the size of SDS micelles which otherwise would block the pores of the membrane filter.

Read the original article here: http://www.nature.com/nmeth/journal/v6/n5/abs/nmeth.1322.html


Electricity generated by the body and its applications?

You'd think if such devices were used in humans, they wouldn't require a change of lifestyle.

They don't say the power always decreases over time:

  Katz’s snails, for example, produced up to 7.45 microwatts, but after
  45 minutes, that power had decreased by 80%. To draw continuous power,
  Katz’s team had to ramp down the power they extracted to 0.16
  microwatts.

This is really a chemistry question. The glucose has to be brought to the fuel cell some way. In this case, the glucose is oxydized directly in the hemolymph. As oxygen PP in the hemolymph is always greater than glucose concentration(1), your limiting rate (which is related to the power you can get from the device) is that of glucose intake at the fuel cell. Therefore, the more you oxidize glucose per unit time, the greater intake you need to keep the output from dropping.

The glucose intake at the fuel cell is a function of biological parameters such as quantity eaten, metabolic efficiency, metabolic speed, blood flow, but also diffusion. The kinetics of glucose intake at the fuel cell are such that you can't ask for too much power for too long.

I suggest you read the article to get a more detailed answer. Nature news is good, but there's nothing like reading the real paper.

1 http://pubs.acs.org/doi/full/10.1021/ja211714w


Long term storage of agarose-ethidium bromide gels that have already been cast

To increase storage life: after gel solidifies, dampen it with running buffer. Wrap the gel in polyvinyl chloride. Place in plastic container with a lid. Store in fridge in dark. It will last for a year as long as you re-dampen it with buffer each time you access it. Don't keep it submerged in buffer as the etbr will diffuse out. this is probably the cause of your problem. Notice when you order precast gels (either agarose or acrylamide) they are sealed and only a small vol of buffer is added to keep it hydrated. Additionally, the etbr and EDTA in the buffer helps prevent most mold growth although I have seen black mold grow a few times at around a year.

You can always spike the buffer with etbr adding it directly to the electrophoresis chamber before you run the gel (etbr doesn't even need to even be in the gel for it to work) although I find you get a little more sensitivity with the etbr in the gel. If you spike it be sure to mix and let it sit for about 20 min for the etbr to diffuse.

If you are trying to cut down on cost you are probably using a higher grade agarose than you really need for the application your doing so I would take a look at that

If you end up needing to store gels for rna work, add plain old Clorox bleach to a final concentration of 1% to your TAE gel just after microwaving. It sounds crazy but it works extremely well. You will completely inhibit RNAse and your rna bands will look nice!!!. The bleach also helps  with storage of the gel.


How come degraded eyesight still holds with a mirror?

It's been too long since physics to have a good answer, but I know that if you look at an object in a flat mirror, the light coming off the mirror would be identical to light coming a real object in the same position. The angles of the light rays are the same. Therefore, no matter how close the mirror is to your face, your eyes treat the image as if it's coming from 10 feet away, or however far the object in the mirror is away from the mirror. Bent mirrors will change this, that's why you get the "OBJECTS IN MIRROR ARE CLOSER THAN THEY APPEAR" warning.

I made a diagram to to try and explain it better.

The eye is looking at a mirror, the light from the arrow on the left of the mirror reflects off the mirror and toward the eye. The eye sees an image that appears as if it were behind the mirror, on the right.


Why we do not use RNAi to control ebola?

Delivering siRNA in vivo is a difficult prospect, but has been overcome in research environments and several commercial in vivo solutions are on the market see examples from Life Technologies here.

The bigger problems come from potential off-target effects. siRNA tend to be double stranded and both the 'guide' and 'passenger' strand can occasionally target multiple sequences that you did not intend. Additionally, siRNA tend to activate the body's immune system in ways that would inhibit therapy or cause excess inflammation and cell death. See the detailed review here.

In short, it is a good idea, and the current research in the field is working to overcome technical challenges, but we are not there yet.


Do the enzymes and compounds in saliva help with stain removal?

It would depend on the stain - and more specifically the material and staining agent. Saliva contains blood clotting agents so I doubt it would help with removing blood stains. The enzymes in saliva are unlikely to help with the stain removal.

The water in saliva would be more likely to help, dissolving the stain. So your probably better off with water.


Is there a binding affinity metric for interactions not in equilibria?

You should be looking at the interactions in terms of kinetics and not thermodynamics. k_on and k_off should do the trick.


When you read further you'll get it. Basically, when the antibody expressed on a B-cell recognizes an antigen, then the B-cell divides and expands its population to produce more antibodies (through plasma cells). This process is called clonal expansion.


Example of impossibility in the nested hierarchy?

Your view of evolution is wrong

  If an organism had characteristics that came laterally (?) across the nested hierarchy, as opposed to up or down through its ancestry, that would falsify the hierarchy

The expression "falsfying the hierarchy" does not mean much, so I won't comment on it.

Note two things

1) Convergent evolution
 - It is not so uncommon that different lineages evolve similar traits when facing similar selection pressures. This is called convergent evolution.

2) Horizontal transfer
 - It is not so uncommon that pieces of DNA find itself (via a number of different mechanism) in a different lineage. A gene can therefore jump from one lineage to another one. This causes the gene tree of a given gene to not match the species tree. Other processes can cause such mismatch though. This is called horizontal gene transfer.

So, in short, no your view of what you call "impossibility in the nested hierarchy" is wrong.

Intelligent design

Intelligent design is not a scientific hypothesis. It means that it does not make logical sense and it does not make clear predictions that can be tested. By contrast, the theory of evolution is a set of hypothesis all of which that have been formally tested have shown to be confirmed by evidence (that's why the theory of evolution is called a theory;
see here for the semantic).

It is therefore impossible to say whether intelligent design is correct or wrong because it does not say anything. One cannot compare the predictions of the theory of evolution with the ones of intelligent design as intelligent design does not make clear predictions. One can only argue why the theory of evolution
is a set of (confirmed) hypotheses while intelligent design is not a hypothesis (or set of hypotheses).


In Sanger sequencing, why do we resort to cloning? Why doesn't PCR suffice?

The error rate of PCR is still very high in comparison to natural bacteria DNA replication of its plasmids.

Natural bacteria DNA replication has an error rate of approximately 1 in 10 billion, and the best PCR polymerase commercially available (Q5 from NEB) has an error rate of approximately 1 in 1 million.

Therefore, cloning fragments into bacteria and sequencing the cloned plasmids ensures that you have the correct sequence for further downstream experiments, since the error rate of natural plasmid replication is far lower. With PCR, you are likely to have some errors introduced due to the higher error rates. This becomes more and more likely with increasing numbers of PCR cycles as well as increasing PCR amplicon lengths.

The fact that the PCR amplicon sequences correctly does not mean that DNA cloned from the PCR amplicon is correct. Therefore, if the PCR is intended for downstream experiments, it is best to sequence the cloned plasmid instead of the amplicon.

In addition, as WYSIWYG has pointed out in the comment, having the PCR amplicon cloned into a plasmid would also allow for the plasmid's regions flanking the cloning site to be used for sequencing. This allows standard sequencing primers on the plasmid to be used, instead of having to design new sequencing primers for each PCR amplicon.

Furthermore, since Sanger sequencing requires the primers to bind ~50-100bp upstream of the region to be sequenced, cloning the amplicon into a plasmid would also allow short amplicons to be sequenced in a single read, instead of requiring a forward and reverse read for sequencing a PCR amplicon.


Is life in the open ocean homogenously spread?

This is sort of a partial answer, but here is a map using chloryphyl density to map the global distribution of marine life. As you would expect, most is clustered around costal regions, but you can also see some pretty distinct zones in open ocean, with more primary production apparently in the northern and southern latitudes. Not sure how much this map projection distorts apparent distances, but it should help give you an idea.

Here's where I found this map.
And here's one of the links they references, which looks to have some more resources to explore.


Pedigree - Dealing With Unknown Parent Genotypes

Based on the information given in the pedigree, you can actually be certain that #2's mate has a genotype of CdCa because of the following:
Two of 5's siblings are albinos. Since albino is a recessive trait (lowest in hierarchy of dominance), both parents (4 and 4's mate) must have the Ca allele. Let's call 4's mate "8". Since 8 has the Ca allele, at least one of 8's parents must also have the Ca allele. Since you have already (correctly) determined that #2 is CCk, #2's mate must have the Ca allele, and must therefore have a genotype of CdCa.

Thus you can eliminate the extra (1/2) from your calculation, making the answer (1/2) * (1/2) * (1/4), or (1/16).


How fast is the blood flow in various vessels?

In the middle cerebral artery blood flow at rest is 73.7 cm/s. After a period of 3 minutes of hyperventilation, blood flow in the same artery decreases to 37.6 cm/s. This is published work.

Vena cava measures: Peak velocities during ventricular systole ranged from 30 to 45 cm/sec in the inferior, and from 10 to 35 cm/sec in the superior, vena cava, also published.


Why are sugars in whole fruits not digested the same way sugars in juice are?

Sugars in 100% natural fruit juices are chemically the same as in whole fruits. They mainly include glucose, fructose and sucrose:

Apple nutrition data (expand the carbohydrate section)
Apple juice nutrition data

Sugars in whole fruits are "incorporated" into the fruit, which means the digestive system first needs to physically decompose the fruit and then extract and absorb sugars, which takes some time. In fruit juices, sugars are "free," so they are absorbed quicker than from whole fruits, which results in higher blood glucose levels, which is a risk factor for diabetes type 2 (Defeatdiabetes, Diabetes.co.uk).

Also, fruit juices are liquid, so they pass through the stomach quicker than whole fruits, so they fill the stomach for a shorter time and may be therefore less satiating. This can make you drink more juice than you intended, which can result in unwanted weight gain.

If you eat foods high in fiber along with juice, the fiber will slow down the absorption of sugars from the juice (Nutrients). If you eat foods that contain mainly plain starch (white bread, cookies or rice, or potatoes) along with juice, the starch will be quickly digested and absorbed as glucose and will raise the blood glucose even quicker than the sugar from the juice.

The effect of nutrients from foods on blood glucose level after meals is expressed as glycemic index (GI): the higher the GI, the higher blood glucose (Harvard):

Glucose = 100
Cornflakes (mainly plain starch) = 81
Potato, boiled (mainly plain starch) = 78
White bread (mainly plain starch) = 75
White rice (mainly plain starch) = 73
Sucrose = 65
Honey = 61
Apple juice = 41
Apple: = 36
Kidney beans (high in fiber) = 24
Fructose = 15

In conclusion, natural sugars from whole fruits, fruit juices and artificially added sugars are all digested in the same way, but sugars from juices are absorbed quicker, which can result in higher blood glucose levels. Foods that contain mainly plain starch can raise the blood glucose levels much more than fruits and fruit juices.


What difference do trans and cis configurations of amide groups bring to the polypeptide chain?

Apparently the trans configuration is more stable, so more amino acids
  with a trans configuration can be found within a polypeptide chain.
  Does this pose any significant characteristic to a protein, and if so
  what is this characteristic?

As you said, the trans- form is energetically more favourable. However, in proline the cis- form is energetically similar to the trans- form. The cis- structure introduces a kink or bend in the peptide chain which is seen in case of proline (see this section of wikipedia page on proline).


What is the H+ gradient in mitochondria?

Lets start with a general definition: A gradient is the difference in the concentration of a substance (this can be a solutant in liquids, a gas or whatever) between two places. The image below shows the general definition. If nothing else happens what keeps the gradient stable, over time diffusion will cause an equilibrium between both places. The flow of substance always goes from the high concentration to the low (indicated by the arrows).

In biological systems the two parts of the gradient are usually divided by a membrane and are more stable. Gradients can be generated by active transport which requires the input of energy to work against the gradient. Examples would be the concentration gradient along a membrane like protons (positively charged hydrogen-ions), as this can be seen in the mitochondria. Here three complexes of the respiratory chain (I, III and IV) pump protons from the matrix in the intermembrane space, which requires energy. The fourth complex (V) pumps the protons back and uses the released energy from this process to make ATP. See the figure below which shows this process schematically (from here):


Link from VonBeche is good.
Proteins vary in amino acid content.  Humans can make some but we need 9 of them in our diets.

from https://www.ncbi.nlm.nih.gov/books/NBK234922/
    Nine amino acids—histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine—are not synthesized by mammals and are therefore dietarily essential or indispensable nutrients.

This guy http://michaelbluejay.com/veg/protein.html
is clearly a vegetable enthusiast but he makes a good point (and provides a nice table): just about any vegetable can provide enough amino acids if you eat enough of it.  Getting your entire caloric requirement from iceberg lettuce would a project, it is true.  But until I did the back reading for this answer I thought it would be impossible to take in the calories it would require to get all necessary amino acids from some of these plant foods.  Thanks michaelbluejay.

I here assert that animal foods have more amino acids per calorie than vegetable foods.  So, if you wanted to limit calories but meet your amino acid requirement it would be easier to do with animal proteins than with vegetable proteins.

But even all calories from potatoes can get you your amino acids.  The people who get into trouble are people who are not getting all the calories they need because they are starving, and the calories they do get are from low protein source foods like yams or bananas.  That is protein-calorie malnutrition.


In theory, would it be possible to create an injection of Vitamins, Minerals, sugars etc so that eating was no longer necessary?

The quantity of nutrients the body requires takes much more physical space than can be included in a simple pill or injection (used only a few times a day).  But nutrition can be provided by IV (intravenous administration), and it is used today for some medical conditions.  When the IV completely substitutes for normal digestion, it is called total parenteral nutrition (or TPN).  The procedure is simple and reliable enough that it can sometimes be used outside of a hospital setting and be self-administered by users at home.


The goal of the vaccine is to provoke an immune response, therefore some degree of inflammation is expected in order for the vaccine to work. As swbarnes2 says, vaccines contain adjuvants, pro-inflammatory molecules that produces local inflammation and recruits immune cells to the site of the inoculation.

Since you get the shot intramuscularily, intradermally or subcutaneously, it is local, and the inflammation does not spread. The reason why your whole arm seems to hurt (rather than the place where the vaccine was deposited) is, I think, that where you got your shot, you have not many pain receptors, and your brain is not able to determine the pain source very exactly.


Difference between Premature Atrial Contraction and Atrial Fibrillation

Atrial Fibrillation is a dysrhythmia while PAC is an early depolarization coming from the atria. An occasional PAC can be normal for some people. In that case their heart rhythm would be a sinus arrhythmia instead of a normal sinus rhythm.

In AF, the atrias don’t contract/pump at all, but they quiver/twitch due to the many simultaneous ectopic foci that are being discharged from random cells; similar concept to Ventricular Fibrillation. Due to the atrias not fully depolarizing, you won’t see any P waves on the EKG. If/when an electrical discharge reaches the AV node, it goes through the normal electrical condition system from there, forming a narrow QRS complex. AF is the only irregularly irregular rhythm, meaning that the QRS complexes have no regularity at all, and have no pattern to their irregularity.

Video example of AF.

Rhythm Strip

As for PACs, the atrias depolarize earlier than expected creating what looks like an early beat. The next beat though will be later than expected. The pacemaker cells “reset”, returning to their pattern after this early beat.

Both AF and PACs can be acute or chronic depending on the person.


The terms gray and white matter relate to their color in gross specimens (i.e., not microscopic specimens) that have been formalin fixed. Nissl granules describe a microscopic structure, the rough endoplasmic reticulum, and aren't directly related to the color of gross specimens. Here's an example of a frontal cross section from a University of Utah slide set:

You'll see it's generally a tannish-yellow (at least on my monitor, this image is a pretty good representation of what it looks like in person), but there are lighter "white" parts in the white matter areas, and darker "gray" parts in the cortex.

A live, or a recently deceased and not formalin fixed brain has different qualities, including color and consistency.

The color of the formalin fixed tissue is an artifact of the process of fixing, so it's not necessarily accurate to describe the gray color as something inherent to the cells in the gray matter, but generally yes, the whiter color in the white matter of formalin fixed brain is because of the high lipid concentration. The grayer color of the gray matter is because of the lower lipid concentration. This lovely old JBC article from 1929 discusses some of these issues, mostly regarding white matter in response to staining after fixation, but also gray and white matter before staining.


For recombinant Taq polymerase, industrial-scale production produces liters of highly concentrated enzyme in a single run.  It comes in such small, dilute quantities when sold that only a few preps a year would be necessary to satisfy research lab demand.

I don't know the Thermus aquaticus protocol, but considering the achievements in yield for E. coli, and the minimal price difference between the two enzymes, I'd imagine that yields are similar there.  That would say to me that nobody's farming hot springs for T. aquaticus.


Does human digestive system benefit from eating same kind of food consistently?

I think it would depend on the benefits you are looking for.

If you ate the same thing everyday, it's possible your intestinal flora, and the rest of your GI tract would optimize themselves for maximal nutritional extraction. It is known that the flora in you GI do affect nutrition. I recall reading about obese patients who had gut-bacteria which made more nutrients available.

However, if you were in an environment where your diet could change unexpectedly, this optimization could actually be detrimental, since you wouldn't be ready to switch foods when necessary.


What is the difference between Founder effect and Bottleneck effect?

Genetic drift is an EVOLUTIONARY PROCESS

Source: Wikipedia > Genetic Drift

  Genetic drift (also known as allelic drift or the Sewall Wright effect2 after biologist Sewall Wright) is the change in the frequency of a gene variant (allele) in a population due to random sampling of organisms.

I think that these terms are used without a perfect semantic. An obvious case

A population bottleneck is a DEMOGRAPHIC EVENT

Source: Wikipedia > Population Bottleneck

  A population bottleneck [..] is a sharp reduction in the size of a population due to environmental events (such as earthquakes, floods, fires, disease, or droughts) or human activities (such as genocide)

A founder effect is an EVOLUTIONARY PROCESS THAT RESULTS FROM A FOUNDING EVENT

Source: Provine 2004

  The “founder” principle, as introduced by Mayr in 1942, was an auxiliary mechanism (less important than random drift) for producing reduced variability in an isolated population started by a few individuals or even by a single fertilized female. Mayr saw a distinction between the “founder” effect and random drift. The founders were not a random sampling of the main population, but, once isolated as a small population, would undergo random drift

In other words, a founder effect does NOT refer to the ppulation bottleneck causing by a founding event. A founder effect refers to the increase in genetic drift (loss of genetic diversity is expected) caused by a founding event. A founding event is the event by which few individuals (eventually only one) quit a large population to settle down a new small populations. As such, a founder event is a type of population bottleneck. I think that one could further extrapolate the term "founder effect" to any increase in genetic drift caused by a population bottleneck.

Do all authors use the same definitions?

I have not done a good literature review to answer this question but I would not be surprised if different authors, use slightly different definitions.

For example, some authors (e.g. Peery at al 2012, Raymond and O'Brien 1993, Duarte et al. 1992) have used the term "genetic bottleneck" instead of "population bottleneck". Wikipedia indicates that these two terms are synonyms. However I could not find any paper that formally define the term genetic bottleneck but all the papers using this term seem to be specifically interested into the genetic signature of population bottleneck. As such, the semantic relationship between population bottleneck and genetic bottleneck could be the same as between founding event and founder effect. Genetic bottleneck could be defined as the increase of genetic drift that is caused by population bottleneck.


Pseudomonas aeruginosa biofilms grows stronger after 95 % ethanol treatment

@Chris is right. ~70% ethanol is the way to go.

From a discussion here :

  The effectivity of ethanol as e.g. desinfectant or antiseptic agent depends on the concentration of ethanol-water-mixture: An ethanol percentage of 50-80% destroys the cell wall/membrane of bacteria by denaturing their proteins and dissolving their lipids (effective against most bacteria, fungi and some viruses; ineffective against bacterial spores). Therefore, the ethanol has to pass the bacterial membrane/wall to get into the bacteria - if you use 100% ethanol instead, the bacteria get 'sealed' and they will survive... An other mechanism is the high osmotic pressure of ethanol/water-mixtures; and the 70% has the highest one.

By using a high ethanol concentration, you're effectively creating a layer of coagulated protein on the surface of the biofilm, "sealing" the bacteria in below that top layer.

As to why water seemed more effective than alcohol, I would venture a guess that some of the bacteria from the biofilm was flushed off. Maybe check the water for bacterial count to verify? :)


Which factors besides the thermodynamic stability are important for the hairpin in intrinsic transcription termination?

The RNA hairpin transcription terminator in prokaryotes is terminated by the GC rich hairpin followed by 4+ uracil bases as you describe it.

The original reference describing the hairpin, described the sequence requirements as being for the thermodynamic stability of the hairpin, but the protein nusA has also been found to stimulate termination.

You might think that there would be some protein that would precisely bind this motif and mediate the termination, but at least as far as I can find, it appears that the hairpin clogs up the polymerase itself, causing termination.  This review linked here has some nice pictures of the RNAP bindig pocket model.


What is the reaction mechanism of dopamine hydroxylase converting dopamine to norepinephrine?

There are various studies on the mechanism of action of dopamine beta-hydroxylase (DBH).

This review (sorry, non-free article) by Kaufman and Friedman was written less than 10 years after the discovery of the reaction of conversion of tyrosine into [nor]adrenaline in the adrenal gland:

DOPAMINE BETA-HYDROXYLASE - Kaufman S., Friedman S. - Pharmacol Rev. 1965 Jun;17:71-100.

It makes for an interesting read, as they start detailing the history of our knowledge on adrenaline synthesis (well, at least at that point in time!), the various hypotheses and models that were thought of, experiments with radioactive labeled precursors and so on.

They then procede to talk about the mechanism of the enzyme. Without going too much in detail, they report experiments showing that oxygen, ATP and Mg++ stimulate dopamine beta-hydroxylase enzymatic activity, with the following note on Mg++:

  [...] Mg++ is required for the uptake of catecholamines by the adrenal vesicles. EDTA inhibits the uptake of the precursor, hydroxytyramine, but does not inhibit the enzymatic conversion to norepinephrine if the vesicles are intact.

They also list the requirement for two cofactors: ascorbate and copper

  The first indication that Dopamine-beta-hydroxylase is a mixed-function oxidase was the demonstration of a requirement for ascorbate. It was found that this reducing agent
  could stimulate the hydroxylation reaction even in adrenal particles, and the requirement for ascorbate became more pronounced as the enzyme was purified.

Bringing to the reaction:

  Dopamine + ascorbate + O2 → L-norepinephrine + dehydroascorbate + H2O

For the Cu:

  Only recently, however, was the enzyme obtained in a pure state and the metal characterized by direct analysis. The metal is copper and it is present in a concentration of 0.65 to 1.0 ug per mg enzyme (4 to 7 moles of copper per mole of protein). It can be removed by treatment with concentrated potassium cyanide. This copper-free enzyme is inactive but can be reactivated by addition of Cu.

They then proceed to detail some basic mechanism of action, which I will not report here for briefness.

A few years later, researchers from the same group authored a book chapter for the American Chemical Society entitled:

The Mechanism of Action of Dopamine β-Hydroxylase - Kaufman S., Bridgers W.F., Baron J - in Oxidation of Organic Compounds, Chapter 73, pp 172–176, 1968 - Chapter DOI: 10.1021/ba-1968-0077.ch073

From the abstract (I do not have access to the full text of this):

  Dopamine β-hydroxylase catalyzes the side-chain hydroxylation of dopamine and other phenylethylamine derivatives. Ascorbic acid serves as a specific electron-donating cofactor. The enzyme from bovine adrenal glands contains Cu2+ and a smaller amount of Cu+. When the enzyme oxidizes ascorbate to dehydroascorbate, most of the Cu2+ is reduced to Cu+. Added substrate is hydroxylated, and Cu+ is reoxidized to Cu2+.

To get to some more recent years...

In this review

New insights into copper monooxygenases and peptide amidation: structure, mechanism and function. - Prigge ST, Mains RE, Eipper BA, Amzel LM. - Cell Mol Life Sci. 2000 Aug;57(8-9):1236-59.

A mechanism for Peptidylglycine alpha-hydroxylating monooxygenase (PHM; EC 1.14.17.3) is proposed, and

  Since PHM is homologous in sequence and mechanism to dopamine beta-monooxygenase (DBM; EC 1.14.17.1), the enzyme that converts dopamine to norepinephrine during catecholamine biosynthesis, these structural and mechanistic insights are extended to DBM.

A structure of PHM along with a modeling of DBH is shown in Fig 14. You can see the two catalytic copper atoms and the possible binding of dopamine to the site.

They also show a mechanism of action for PHM. Essentially, through the oxydation of ascorbate the Cu++ becomes Cu+ and can then bind an oxygen molecule that will be used to hydroxylate the product:

Finally, a detailed computational model of the enzyme, and its active site is shown in this paper:

Structural Insight of Dopamine β-Hydroxylase, a Drug Target for Complex Traits, and Functional Significance of Exonic Single Nucleotide Polymorphisms - Kapoor A, Shandilya M, Kundu S - PLoS One. 2011;6(10):e26509. Epub 2011 Oct 20.

The active site is shown in Fig. 7, where you can clearly see the two copper atoms in purple and green, the most important aminoacids at the active site and two water molecules in red:

Active site of DBH http://www.plosone.org/article/fetchObject.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0026509.g007&representation=PNG_M

Figure 10C shows the interaction of dopamine with the aa of the active site (Fig 10A and B show superposition between rat and human enzymes and Fig 10D shows the interaction of a drug with the enzyme):

Residues important for catalysis http://www.plosone.org/article/fetchObject.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0026509.g010&representation=PNG_M

Finally, a remark on your question. You say:

  Evolutionarily speaking - the enzyme has evolved to add OH to the beta-carbon rather than somewhere else.

As I said somewhere else: not everything has an evolutionary explication, and evolution is not finalistic. This specific enzyme structure appeared at some point and it was evidently working fairly well, and at the time the rest of the pathway may or may not have been like it is at present, but the important thing is that the enzymatic network managed to work together. It could had well evolved to hydroxylate another position, but probably in that case we would have different enzymes downstream. The important thing to remember is that the enzyme did NOT evolve with the finality of oxydating the beta carbon.


Why do the major and minor groove exist in DNA?

Pitch is not a great word for this, as its meaning is ambiguous. It's hard to find a universal nomenclature for DNA geometry, but see the "Base pair geometry" section of this wikipedia page. The relevant property is what they call "opening".

From the biochemistry textbook by Berg:

To explain in words, if the glycosidic bonds (which attach the nucleic base to the sugar in the backbone) stuck straight out at 90 angles on both sides, then the grooves in double-stranded DNA would be symmetrical. Because the glycosidic bonds are at an angle (relative to the interface between the AT or GC pairs), one of the "faces" of the base pair is larger than the other.

Words and flat pictures, however, will never really give you a good intuitive sense of what's going on with the 3D structure of the grooves. A good modeling kit will be of great help to you.


You are almost on the right path.

This schematics from Wikipedia is quite clear in my opinion.

Slightly more chemical explanation (which you do not necessarily need to do bioinformatics, however I think it is always better to know exactly what you are dealing with outside of the computer!)

The idea is that you have four basic nucleotides: cytosine and thymine are called pyrymidines and adenine (A) and guanine (G) which are called purines. Pyrymidines are characterised by a 6 carbon azo-ring which is called a pyridine, while purines have a larger double ring, formed by a pyridine ring + an imidazole ring.

A transition is defined as the passage purine -> purine or pyrimidine -> pyrimidine.
A transversion is the passage purine -> pyrimidine, or viceversa.

These mutations can be caused for instance by certain chemicals, such as alkylating agents, or by ionizing radiations.

In your specific example, given the sequences

 ACGATG
 TCAGTG

You have 3 mutations:

A -> T
G -> A
A -> G

So you have 1 transversion (from the purine A to the pyrimidine T) and two transitions (between the purines A and G).


Are Na+/K+ active pumps and K+/Na+ "Leak" channels same as given in the figure?

Below is the structure of a Na+/K+ ATPase, i.e., the sodium/potassium pump shown on the left in your figure:

(image from here)

Compare to the structure of a potassium leak channel (the type of channel depicted on the right in your question):

(see this publication; image from here)

It's clear they are quite different beasts, without much similarity at all besides both being membrane proteins with several transmembrane domains, which is a characteristic they share with countless other proteins with an incredibly wide range of functions.

The only similarity the pictures from your textbook are meant to convey is that they are both membrane-bound proteins and that they accommodate Na+ and K+; besides that, they are completely different. The figure clearly shows a different mechanism of transport, and the remaining similarity is just from the very abstract way that they are represented.


What bacteria results in a Gram +ve cocci and catalase +ve? What test comes next?

At this point you have staph, you can use this flow chart (from here) to figure out what staph exactly.

If the test comes back as coagulase positive be very careful as Staph aureus is pathogenic.


Can coronavirus contaminate public water systems?

Viruses can survive a few days in water, i.e. SARS can survive 22 days in lab grade reagent water and 7 days in pasteurized sewage. That is the time the virus takes to be at 99% of it's original concentration. (from "survival of surrogate coronavirus in water").

Viruses can also spread via swimming pools, i.e. hepatitus A and norovirus have been associated with swimming pools. (from "a review of waterborne viral deseases associated with swimming pools").

Boiling water will kill viruses. Children have very little reaction to the virus when they carry it, so it's likely that they act as a transmitter more than water does. I'm not worried about it at all by the way, just do what the doctors advise.


Is the empty GI tract a hollow tube with air inside, or is it generally collapsed until food is eaten?

Under normal circumstances the stomach and GI tract have very little "gas" in them - whether it be flatus, air, CO2, or anything else - and so are essentially collapsed with the walls against each other. However, gas is continually being produced by the microorganisms that inhabit our gut, and can also come from swallowing small amounts of air, fizzy drinks, etc., so the environment is never 100% gas-free. A typical person produces on the order of 500-1500 ml (0.5-1.5 liters) of gas per day.

If you're interested, the Wikipedia article on flatulence is a good introduction.


What kind of fish is this white blue-stained fish?

I don't know whether this helps, but that looks like a parrot fish.  I had a look online and also didn't find anything with that distinctive pattern. The closest I could find was Scarus ghobban (common names include blue-barred and blue-trim parrotfish), which is highly variable but the blue edges on the fins seem constant.

According to the sources linked above this fish can be seen in areas with sandy bottoms, so that seems consistent with your photograph.

Reference pictures:


The immortal jellyfish can revert back to its immature polyp stage after reaching maturity, then mature again, over and over. You can read more on the wikipedia page, but this ability means it can potentially avoid senescence altogether.


Speed of electric signal vs chemical diffusion

Membrane potential is a directed force, while diffusion is a random walk

Your confusion is entirely justified, as you're correct that both diffusion and depolarization rely on the speed of ion travel. Where they differ is that depolarization is a directed force, occuring only in one direction along the membrane, whereas diffusion is subject to the stochastic walk of ions in water.

When membranes depolarize, the whole membrane begins with a certain amount of "pressure" built up behind it. As the signal propagates, a small area of this pressure is released at a time and triggers the next section to trip. That next section is essentially identical to the previous one, with the same amount of pressure behind it initially. In this way, you can imagine membranes "conserving" the initial concentration, so that the signal strength isn't dependent on the distance from the signal itself.

Diffusion, on the other hand, is stronger initially and decays over distance because of its stochastic nature. It's a probabilistic force, and so depends in general on something like the square root of the distance. If you imagine a thousand ions taking a step forward in one moment, in the next it's equally likely that five hundred take a step backward even as an equal amount moves forward. So the signal degrades over time and distance from the source.

If that was confusing, the following metaphor may help. Depolarization acts like a line of dominos, while diffusion acts like a complex dance. Check out this video of the largest human mattress dominos: the speed they're falling over is pretty constant when they're not turning. Compare that to two dancing humans who are equally likely to move forward and backward, and hopefully you can see that the mattress dominos is the faster way to go, even though each one is theoretically limited by how fast a human could move.


Understanding entropy and the second law of thermodynamics as involved in metabolic processes

2nd law of thermodynamics states that the overall entropy of the universe cannot decrease at any time. This can also be stated as the fact that the universe naturally falls towards the lowest energy state, or equilibrium. This becomes important in metabolic reactions. Reactions which seem to increase the state of energy, or perhaps the 'order' of the universe, have done so at the expense of another part of the universe, usually through the conversion of energy from molecules such as ATP or NADPH.

Think of the ATP Synthase on the cell membrane. It is creating ATP (Adenine tri-phosphate) molecules from ADP (adenine di-phosphate) and a phosphate group. This too seems like a system changing molecules from a low energy state to a high energy state. It is, but it can only do so by the natural flow of H+ ions which have accumulated on one side of the cell membrane and naturally flow from their high concentration to their low concentration on the other side. So while the ATP synthase molecule is making higher energy molecules (decreasing entropy) it is doing so as H+ naturally flows towards equilibrium, which increases the overall entropy in the universe.

In essence: things are always going towards a low energy state, i.e. equilibrium, i.e. maximum entropy. If any system goes against this, it does so via an outside energy source which has increased the entropy of the universe somewhere else.


Receptors for red and far-red light in plants: Shade avoidance

As far as I know there are 5 receptors for far-red and red light which are the phytochroms(phyA-phyE) Its all about the ratio between red and far-red light.

Each phytochrom has an inactive(PR) and an active(PFr) conformation. phyA is the only phytochrom which is activated by far-red light, so its active state is PR. (Only if the ratio between red and far-red light is low.) The other phytochroms, are activated by red light (high ratio between red and far-red).

An active phytochrom blocks the COP1/SPA complex. This complex is a E3 ubiquitin ligase which ubiquinates transcription factors for the light answer like HY5 or HFR1.

Example:
Under normal light conditions, phyB-phyE is active. They block the COP1/SPA complex so the transcription factors for the light answer are not getting ubiquinated. The plant can get a light phenotyp.
In the case that a plant grows under another plant, it gets less red light because the higher growing plant uses it for its photosynthesis. phyB-phyE become inactive. COP1/SPA can ubiquinate the transcriptions factors. The plant gets an low light phenotyp by trying to grow out of the shadow.

The function of phyA is to produce a light phenotyp if there is a lot of far-red light but almost no red light. Than it is getting activated and blocks the COP1/SPA complex. Under red light phyA is not only inactivated it also gets degraded.

I just found a paper for further reading: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2828699/


There is no perfect cut-off. It always depends on what you're doing. The e-value is basically a measure of how many such alignments you would expect to find in a database this size by chance. Therefore, e-values greater than 1 mean that you'd expect at least one alignment similar to what you've found by chance alone.

As others have stated, the e-value is not a rigorous measure of significance. It depends on

The length of your alignment.
The alignment's bit-score score (this takes into account amino acid substitution scores based on the matrix being used, BLOSUM65 by default).
The size of the database you are searching in.

I have at different times and for different projects used e-values ranging from 10 to 1e-100 or less. You always need to take into account what you are looking for. For example, to run a tBLASTn looking for distant homologs, you'd use a relatively high e-value, say 1e-10 or even 1 or greater depending on the details. For example, the default e-value for ncbi-tBLASTn is 10.

To find extremely similar sequences in closely related species, you'd use a much smaller one. Say 1e-20 or 1e-50. Normally, you tweak these settings after seeing your results.

After running a few hundred blasts, you get the hang of it and you can have a pretty good estimate of the e-value cutoff you want to use. Until you get that experience, you will have to use trial and error. Just remember that the conclusions you can draw from your data will be heavily influenced by that e-value. Don't try to publish something claiming you've found a homolog if the supporting BLAST hit has an e-value of 45 for example.

Personally, when looking at BLAST out files, I check the e-value, the alignment's length (as a percentage of the query), the alignment's %id score and the bit score itself. Of these, the most reliable is the bit-score but, again, that too changes depending on what question you are attempting to answer.


How do viroids propagate to other hosts?

Viroids are commonly thought of as remnants from the "RNA world" since they are composed of only RNA and have ribozyme activity.
Viroids can be considered as plant parasites of the transcriptional machinery of the organelles (nucleus or chloroplast), since they are non-coding and they replicate by RNA–RNA transcription (in a rolling cycle mode).

Viroids infect the epidermis of their hosts after mechanical damage of the plant cell wall. After entry to the first cell layers, viroids initiate replication in the nucleus or in the chloroplast and then are transported to neighbouring cells, reaching the vascular tissues and virtually all plant tissues.

The transmission of viroids is both "natural" and human-driven. Viroids are mostly transmitted via mechanical methods by contaminated machinery and tools, pruning, and other mechanic argricultural techniques. Transmission also occurs through infected seed and pollen, they don't have important natural vectors from the animal kingdom. Also contact between adjacent plants can be another (inefficient) way to transmit viriods.

I have found a reference here for further informations. It isn't open access but it is possible to watch an abundant Google preview.


EEGs are often analyzed in the frequency domain, where signals are subjected
to spectral analysis, typically by Fast Fourier Transformation, or FFT.

What an FFT basically does is decomposing a signal in the time domain into one in the frequency domain. It does this by decomposing the input signal (any signal, including EEG) into a series of sinusoids. These sinusoids are not present in the original signal; it is a mathematical trick. If you would add all the sinusoids back together, the approximate original signal is restored.

Typically not a single frequency is analyzed, but a band of frequencies, because the frequencies within these bands are associated with similar brain states. The frequency bands that are typically reported on are shown in Table 1, including the brain state they associate with as well as sample EEGs:

Table 1. Typical analyzed EEG frequency bands. Source: Conorrus Somanno

Reference
- Nelson Garcia et al. Device and method for cognitive enhancement of a user (2014). Patent EP 2681729 A1


The largest database of curated ChIP-seq data is currently Encode and it supports an API.  You can use JSON to get at all tracks.

That page will have a link to Getting Started that should get you going. You can visualize raw data, normalized data, and processed data tracks in genome browsers that load in ENCODE data.  My favorite genome browser is:

WashU Epigenome browser


Unlike humans, why do plants not have something blood-like to transport $O_2$ throughout their body?

In plant cells, O2 enters through stomata or lenticels. Then, the O2 molecules are transported to the cells through the process of diffusion. Stomata and lenticels are found all over the surface of plant body, i.e., leaves, stem and root. Because of this, plants don't need blood like connective tissue to transport O2 and CO2.


If silver nanoparticles kill bacteria by penetrating the cell membrane, why don't they also kill human cells on contact?

The nanoparticles from your sock will most certainly not reach to your foots cell membrane (Walls are for plants/fungi)  because of the thick layer of dead skin, oils, than about 30 cell thick cornified layer (stratum corneum) build up from practically dead cells (with no nuclei or organelles) but lots of filamentous keratine. This is the most outer shell of your epidermis followed by layers and layers of 4 other tissue types , then comes the "actual" skin dermis and the hypodermis beneath.

If some of the silver-sock -nanoparticles would actually make it through there to basal tissue and reach the cells plasmamembrane, they enter via endocytosis, and start to release Ag+ they break all kinds of things, because Ag+ is cytotoxic it induces ROS, damages you Mitochondira, disturb some pathways... you get the point.

However this was proven to happen within human in vitro celllines.

a few in vivo studies showed that Ag-NPs cause adverse effects on reproduction, malformations, and morphological deformities indifferent non-mammalian animal model.

Says "Review: A systematic review on silver nanoparticles-induced cytotoxicity: Physicochemical properties and perspectives
https://doi.org/10.1016/j.jare.2017.10.008


Why does the pulmonary artery have higher glucose concentration than the pulmonary vein?

Gas exchange doesn't but the cells of the tissue it occurs in do consume glucose, even the cells in the walls of the artery will consume some.  The cells in the lungs still need to be fed and only one of those two vessels has flow going into the tissue so it is the one that has to carry that glucose into the tissue.


What are chemical candidates for replicator molecule?

There is no accurate answer  , as you say we talk about candidates . there is lots of strong theories about the origin of self replicators . RNA world was a strong candidate since latest experiments that suggest there is a good chance that some molecules that have simpler structure than RNA , could have a chance to do self replications .
    there is also strong theories such as :

1.Prions that delivered by space objectives and Meteorites .

2.Life's origins may result from low-energy electron reactions in space:

http://phys.org/news/2016-06-life-result-low-energy-electron-reactions.html

first self-replicator recreated in lab:

RNA, or something very like it, has long been a strong candidate as the first self-replicating molecule in the origin of life. This is because it can both catalyse chemical reactions and carry genetic information.
But chemists first needed to explain how a large, complex molecule like RNA could form spontaneously to begin the process. They had done so for some, but not all, components of the RNA molecule.

https://www.newscientist.com/article/2088006-building-blocks-of-lifes-first-self-replicator-recreated-in-lab/

The origin of replicators and reproducers:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1664675/

you can also check the topic :The RNA World and the Origins of Life
from the book :

Molecular biology of the cell by Alberts B, Johnson A, Lewis J, et al.

after all this article was so innovative for me . I think it's a good explanation for self replication of molecules simpler than RNA.

http://www.nanowerk.com/nanotechnology-news/newsid=40896.php

"Maslov and Tkachenko's model imagines some kind of regular cycle in which conditions change in a predictable fashion—say, the transition between night and day. Imagine a world in which complex polymers break apart during the day, then repair themselves at night. The presence of a template strand means that the polymer reassembles itself precisely as it was the night before. That self-replication process means the polymer can transmit information about itself from one generation to the next. That ability to pass information along is a fundamental property of life"


Can you measure ECG from a single location?

I am afraid you cannot build the classic ECG using only 1 hand.

Probably, you can measure HR - heart rate accordingly to pressure detection and similar sensors and from that you can simulate ECG by picture. Simulate I mean you cannot build any reliably ECG curve on the monitor, but can show some waves after every heart beat.


Both natural selection and artificial selection require genetic variation in the underlying population to work.  The exact source of this genetic variation is not particularly important theoretically.  In reality this genetic variation originally comes from mutations of various sorts (not just point mutations, but also duplications, recombinations, etc.).  If you had no genetic variation then artificial selection would not be effective.

You might be interested in Stephen Jay Gould's essay "A Dog's Life in Galton's Polyhedron" (found in the collection "Eight Little Piggies"), where he explains that domestic dogs have very little variation in skull length (relative to body size), but large variation in skull width.  It seems that it is very difficult to artificially select for dogs whose skull and body don't have the correct ratio, even though you can wildly change the sizes of dogs, the width of their skulls, the length of their legs, etc.


Do cold blooded animals generate any heat?

They do generate heat. They just do not SPEND energy specifically on heating their bodies by raising their metabolisms. This is a form of energy conservation. The metabolic rate they need to live is not nearly enough to heat their bodies.

An example of spending energy to heat the body is seen in humans  shivering. Here muscle is activated not for its usual purpose, but to function as a furnace. "Warm-blooded" and "cold-blooded" is somewhat a misnomer. The correct way to think of it is...

Endotherm or ectotherm. Does the heat primarily come from within (endo) or from the surroundings (ecto). Endothermic animals include mammals. Most of their body heat is generated by their own metabolisms. Ectothermic animals include reptiles and insects. They absorb most of their body heat from the surroundings. This is not the same as saying they let their body temperature fluctuate with their surroundings, some avoid this by moving around to accomodate themselves.

Homeotherm or poikilotherm. Homeotherms want to maintain homeostasis for their body temperatures. They don't want it to change. Poikilotherms do not exhibit this behaviour, instead their body temperatures vary greatly with the environment.

We can have endotherm poikilotherms, such as squirrels, who let their body temperature drop while hibernating. Endotherm homeotherms, such as humans, where temperature is constant by means of complex thermoregulation. Ectotherm homeotherms, such as snakes (moving into shadow or into the sun to regulate temperature), and ectotherm poikilotherms, such as maggots.


Currently, the big thing in Neuroscience is imaging in vivo Calcium release which correlates with neuron action potentials, seen here. Each white speck is a neuron, the black lines and circles are blood vessels. Using this method you can visualize distribution and activity of neurons in real time.


How to correctly and accurately identify a few species of trees from their leaves?

A good first step is to pay attention to common differences between tree structure:

1. Alternate vs. Opposite structure

MADHORSE = your common eastern US opposite-leaved trees are Maple, Ash, Dogwood, and Horsechestnut (AKA buckeye).

2. Simple vs. compound leaves

3. Toothed ("entire") vs. untoothed leaves

4. Lobed vs. unlobed leaves

5. Differences in texture, hairiness, & color of leaves

both b/w species and b/w top/bottom of leaves of the same species

Generally when you come across a new tree in Eastern N. America I'd recommend going through these steps:

Is it alternate or opposite?
Is it simple or compound?
Is it toothed, doubly-toothed, or smooth along the edge?

If you can answer yes to (any or all of) those questions you typically SIGNIFICANTLY reduce your options.

You also want to make sure you're aware of large variations in some species (especially oaks and hickories). One good example is the difference in shape, texture, and color of sun leaves vs. shade leaves of many species.

Importantly, paying attention to WHERE the tree is located (and what else is growing around it) as this can really help narrow your choices. You'll also start recognizing common cohabitants of certain regions.

Finally, don't be afraid to use your many senses (smelling, feeling and even tasting) -- though get to know poison ivy well before you start licking plants!!

Ok, now for some useful hints:

Red Oak = stereotypical oak shape, smooth on both side of leaf, lobes are not deep. You'll find 'spikes' at the end of each lobe. Bark looks like it has vertical shiny stripes.
White Oak = rounded SMOOTH lobes. Bark light grey/white with flaking appearance when mature
Red Maple = OPPOSITE. Leaves serrated (toothed). Smooth grey bark (with few low-hanging branches)
Sugar Maple = OPPOSITE. Leaves NOT serrated. Smooth whiter grey bark.
Striped Maple = OPPOSITE. Maple-like shape, but with rounded/butt-shaped (cordate) base. Bark = very striped in appearance.
Tulip Poplar = Leaf-shape looks like a tulip flower. Tree tall and straight.
Black Cherry = Oval/round leaves with fine single-toothing along edge. Tuft of brown/white fur along mid-rib on underside of leaf. Bark = horizontal striping due to lenticels; gets flaky when mature. Bark/twigs have strong bad smell when scratched (cyanide).
White Pine = 5 relatively long wispy needles per cluster.
Virginia Pine = 3 Short, dense needles per cluster.  Bark has cornflake appearance.
Dogwood = OPPOSITE. round leaf with deep ribbing veins and drip tip. Leaves often look to be growing in pairs. If you pull a leaf apart carefully, you'll find some thin tissues dangling between the halves. The bark is cobblestone (mosaic bumpy) and the shape of the tree is typically flat-umbrella-esque.
Hickory Species = VERY DIFFICULT TO TELL SPECIES APART (though I can give you a bunch of hints to help). Fairly easy to tell apart from other species, though. Is ALTERNATE + COMPOUND with generally 5-9 leaflets per leaf. (unlike ash = opposite/compound or walnut = compound with MANY leaflets). Leaves often carry some odor and large seeds can be found nearby
Sourwood = Long, oval, tiny-toothed leaves that have strong sunken midrib and thin leaf texture. Tastes very sour. Bark is dark and ridged, and trunks very rarely grow straight (so look for crooked or leaning trees!).
Cucumber Magnolia = Look for LARGE, strongly veined leaves that are often drooping. Look for circular ring (stipule scar) beneath leaf petiole base.


There are two different ways to detect PCR product in real-time PCR: dyes which bind to DNA in general, such as SYBR Green I, or probes specific to your PCR product. There's a summary of the benefits of each here, with the following table:

You can buy either online; they'll be fairly expensive but I can't think of an obvious way to get them cheaper if you're interested in high-confidence validation.

[edit] forgot to mention that you will also need to normalise the reporter signal against a reference dye such as ROX (https://www.thermofisher.com/order/catalog/product/12223012).


Why are Birds and Reptiles with abundant yolk sac polyspermic?

My professor says that

  The yolk sac is not connected to the mechanism of polyspermy or
  monospermy. [Amount of yolk inside the oocyte is then again.]  The
  oocytes of reptiles and birds are yolk rich  - polylecithal  for instance.

where
lecithal = yolk containing and some pieces of information about here.


Is there a specific word for bacterial death?

Death is appropriate. Using this word to describe both unicellular and multicellular organisms places them in the same hierarchy. This hierarchy is the domain of life.

Both prokaryotes and eukaryotes have unicellular and multicellular species.

If you choose another word for death I would suggest not using it exclusively for bacteria. If a reader finds the idea of bacterial death esoteric, they may be inspired to dig deeper into the subject. Encouraging an informed reader would seem to be an effective device in a paper for communicating scientific information.

You could qualify the word 'death' to be more precise. Senescence is the natural process of deterioration of life with age.

Google has a great tool for tracking word popularity. Here's a Google graph for 'senescence'.


There are a bunch of possible answers;

On my own property I have such a line.  Turned out it was an old fence line.  One side was farmed intensely for 90 years, the other side left in bush.  The farmed soil is enough different that it doesn't grow good trees.  Even the grass is different.
Another place I have an abrupt line of willows.  That one turns out to be water level from the local creek.
A third one has an abrubt chaange in types of grass.  That one is caused by a clay seam coming to the surface.  Uphill the surface soil is sandy.  Water hits the clay, and moves downhill, coming out at the grass line.
I've seen another one, in the mountains, that I think is due to cold air drainage.  The valley floor and 20 feet up the sides are bush.  I think the cold air settles and kills young trees.


What are the most efficient heat exchange sites on the human body?

From personal experience, the best places to put a cooler (at maximum metabolic load) are across the back and over the neck and head.

Good candidate areas for a heat sink or exchanger:

Any region where large volume per unit time of blood travels close to the skin. Some dinosaurs are thought to have cycled blood through spiny fins on their back to cool down (obviously this works for non-dinosaurs too, and even better if the blood vessels in the fin are pressurized (see Are there any known examples of animals with air-conditioner type cooling? ).

Regions where a lot of metabolic activity takes place, including muscles in active use and "brown fat" (see https://www.webmd.com/diet/features/the-truth-about-fat)


Can plant fruit and seeds be albino like animals?

When thinking of albinism in fruits, the only thing I could think of is strawberries. Yes, there can be albinism in strawberries! They are nearly always assocoated with excess nitrogen and are usually tasteless. According to a research by Lieten et al, their mineral composition also differes. Albino strawberries contain higher N:Ca and K:Ca ratio than normal fruits. Another study by Sharma et al shows that albino strawberries show less lipoxygenase activity. Also, Hwang et al and team found that presence of more than normal silicon also causes, among many other things, albinism.

You can get more information here, here, here and here. Obviously, there could be numerous other examples, but albino strawberries is all I could remember.

PS the exact genetic cause and mechanism of albinism in strawberries is not known yet. When searching online, I only found a study by Plante et al which suggests presence of mixoploid cells over a critical number which might have an effect on it.


How does heat generated by metabolism differ compared with heat generated through exercise?

First, you have to convert your numbers to the same units for any comparison to make sense. Consider that the average human body has a surface area of about 1.8m$^2$ and a volume of about 66L = 0.066m$^3$. Then your numbers are equivalent to 2230W metabolic heat and 1050W exercise heat for an average person.

The value 2230W for basal metabolic rate (from Table 1 of the Bagum et al paper) is nowhere near what's measured in practise. Basal metabolic rate ("metabolic equivalent", 1 MET) would be 105W for an average person according to the wikipedia page you cited, which equals 2150 kcal / day. That's about the recommended daily calorie intake, so it makes sense. I don't know where their value of 33,800 W/m$^3$ for "metabolic heat generation" comes from, perhaps it's meant represent something else (can't say I understand the article) but it's not the metabolic rate for an average human tissue.


Do Japanese have a different pelvis position than Europeans?

According to this study there are significant pelvic position differences between Caucasian and Asian populations. However the biggest difference is lumbar lordosis (the curve at the small of the back) where Caucasians have almost 10 degrees more curve. The study doesn't explicitly say it but that would suggest Caucasians butts are higher.


Is vermiform appendix no more a vestigial organ?

Short Answer: No, the appendix is still considered a vestigial organ.

Long Answer: The idea that that vermiform appendix is vestigial originated when Kumar et al (1989) removed it from the body, but failed to find any side-effects. From then on, it got widely established that vermiform appendix is a vestigial organ and has lost all its functions during the course of evolution. The reason behind appendix becoming vestigial was given by Darwin himself in The Descent of Man, and Selection in Relation to Sex where he stated that appendix was used by early primates to digest leaves, and slowly became vestigial as ancient humans shifted towards foods like cereals and meat. This theory was also supported by presence of very long cecum in herbivores like koala and horse.

The only problem with this idea was that the role of appendix in only digestion was being considered. As appendix was connected to large intestine, so early scientists (kinda) presumed that it should be related to only digestion.

This theory got its first challenge when Parker et al (2007) suggested the appendix to be a safe-house of healthy bacteria when illness (such as diarrhea) flushes them out of the GI tract. It was based on the understanding, which came in 2000s by Sonnenburg et al (2004) and Everett et al (2004), about how the immune system supports the growth of beneficial intestinal bacteria. This was experimentally established when Dunn et al found that individuals without an appendix were four times more likely to have a recurrence of Clostridium difficile colitis.

After this, more functions of appendix were discovered, especially those related to immune system. It is because of the efforts of Zahid et al (2004) (the one you cite) and Rankin et al (2016) that appendix is now identified to be more related to immune system than digestive system in humans.

Also, research by Laurin et al (2011) and Smith et al (2013) concluded that during the evolutionary course, appendix has evolved about 38 times and lost as many as 6 times, suggesting that the cecal appendix has a selective advantage in many situations and argues strongly against its vestigial nature.

Conclusion:

Vermiform appendix is identified as Gut Associated Lymphoid Tissue (GALT) and important component in mammalian mucosal immune function, B-cell mediated immune response and extrathymically derived T-cells.
This structure helps in the proper movement and removal of waste matter in the digestive system, contains lymphatic vessels that regulate pathogens, and lastly, might even produce early defences that prevent deadly diseases.
It is thought that appendix may provide more immune defences from invading pathogens and getting the lymphatic system's B and T cells to fight the viruses and bacteria that infect that portion of the bowel and training them, so that immune responses are targeted and more able to reliably and less dangerously fight off pathogens.

Discussion: The problem is in the definition itself of vestigial organs. The point is that being vestigial is not equal to being useless. See this definition by Wikipedia (emphasis mine):

  In the context of human evolution, human vestigiality involves those traits (such as organs or behaviors) occurring in humans that have lost all or most of their original function through evolution. Although structures called vestigial often appear functionless, a vestigial structure may retain lesser functions or develop minor new ones. In some cases, structures once identified as vestigial simply had an unrecognized function.

Now, since vermiform appendix does not perform its (suggested) original function of digesting cellulose and other indigestible materials, and performs much less of its (possible) function in immune system, it is still officially considered as vestigial organ.

References:
 • Vermiform Appendix - Wikipedia
 • Human Vestigiality - Wikipedia
 • Kumar, Vinay; Robbins, Stanley L.; Cotran, Ramzi S. (1989). Robbins' pathologic basis of disease (4th ed.)
 • Darwin, Charles (1871) "Jim's Jesus". The Descent of Man, and Selection in Relation to Sex
 • Bollinger, R.R.; Barbas, A.S.; Bush, E.L.; Lin, S.S.; Parker, W. (21 December 2007). "Biofilms in the large bowel suggest an apparent function of the human vermiform appendix"
 • Sonnenburg J.L.; Angenent L.T.; Gordon J.I. (June 2004). "Getting a grip on things: how do communities of bacterial symbionts become established in our intestine?"
 • Everett M.L.; Palestrant D.; Miller S.E.; Bollinger R.R.; Parker W. (2004). "Immune exclusion and immune inclusion: a new model of host-bacterial interactions in the gut"
 • Dunn, Rob. "Your Appendix Could Save Your Life"
 • Zahid, Aliya (2004-04-01). "The vermiform appendix: not a useless organ"
 • Rankin, Lucille C.; Girard-Madoux, Mathilde J. H.; Seillet, Cyril; Mielke, Lisa A.; Kerdiles, Yann; Fenis, Aurore; Wieduwild, Elisabeth; Putoczki, Tracy; Mondot, Stanislas (2016-02-01). "Complementarity and redundancy of IL-22-producing innate lymphoid cells"
 • Laurin M.; Everett, M.L.; Parker W. (2011). "The cecal appendix: one more immune component with a function disturbed by post-industrial culture"
 • Smith H. F.; Parker W.; Kotzé, S. H.; Laurin, M. (2013). "Multiple independent appearances of the cecal appendix in mammalian evolution and an investigation of related ecological and anatomical factors"


How does regurgitated food go to the 3rd stomach chamber instead of going to the 1st?

Your question supposes a very linear version of the flow of stomach contents of:

1->2->mouth->3->4

In reality, it is not so linear. Firstly some background: The rumen and reticulum form the first two parts of the four, and are in fact a single chamber/organ (collectively known as the reticulorumen). They have different wall structures, and perform initial digestion of different particles (mostly heavier particles in the rumen such as grain and more digested hay). This reticulorumen chamber is where the initial microbial fermentation of the feed occurs. Matter passes from rumen to reticulum and back regularly by means of two distinct muscle contractions.

To aid in the breakdown of the feed, the cud is regularly regurgitated, chewed and then re-ingested. The re-ingested cud returns to the reticulorumen. From there, in order to advance down into the later stages of the digestive tract, it must pass through the reticulorumen orifice into the third compartment - the omasum. The orifice allows particles up to 4mm in size in cattle.

The omasum chamber removes water and some nutrients. The contractions of the omasum remove water and move solids through the system, and the contractions are speculated to filter out any larger particles and return them to the reticulorumen. Matter that has been processed by the omasum is passed along to the fourth chamber, the abomasum.

So to answer your question in brief, after mastication the cud returns to chambers one and two, potentially going round this loop several times until it is sufficiently broken down by chewing, saliva and bacterial action, and then it can proceed from there to the third chamber.

The "digesta circulation and reticulo rumen motility in the ruminent" paper (C. Poncet, C.H. Malbert, R. Baumont) has this to say:

  The outflow of digesta, allowed by the opening of the ROO [reticulorumen orifice] during the second phase of the reticular contraction, is highly selective. The effluent does not contain particles greater than 2mm in sheep and 4mm in cattle. This is due to the buoyancy of the large particles in the reticulum, to the self filtration of the digesta during the passage through the ROO and perhaps to backflows from the omasum to the reticulum.

You may find it useful to get a copy of this collection of papers (quote from p.366): http://books.google.co.uk/books?id=Bcsa8Z4u-E4C&printsec=frontcover#v=onepage&q&f=false


How are presynaptic burst firing signals transmitted post-synaptically?

Short answer
It depends.

Background
It all depends on the neuronal circuit and neurotransmitter system under investigation. For example, raphe neurons release 5-HT in a burst-like fashion onto cortical dendrites. However, the postsynaptic effect is inhibitory, so no action potentials there (Gartside, 2000).

Intracortical recordings in the rat have shown that each action potential in a burst resulted in neurotransmitter (glutamate) release and subsequent excitatory postsynaptic currents (EPSCs) and potentials (EPSPs) (Williams & Stuart, 1999). So that would positively answer your question, at least in this specific neuronal circuit.

Reference
- Gartside, Neurosci (2000); 98(2): 295-300
- Williams & Stuart, J Physiol (1999); 521(2): 467–82


What is the functional significance of the difference in cardiolipin/cholesterol ratio in different membranes?

According to wikipedia, cardiolipin is found in two places, the inner mitochondrial membrane, and bacterial membranes. Given the endosymbiotic origin of mitochondria, it makes sense that they would retain some remnant of their bacterial ancestry. But more importantly, cardiolipin plays a role in the enzymatic functions of mitchondrial membranes. Cardiolipin forms a bicyclic resonance structure that allows it to trap a proton, which helps oxidative phosphorylation.

Because this structure also responds to pH and divalent cations, it can change it's conformation and aggregation behavior as cellular conditions change.
Cardiolipin also plays a role in holding enzyme complex quaternary structures together. Mitochondrial Complex III requires 1 cardiolipin, Complex IV requires 2 cardiolipin, and Complex V binds 4 cardiolipins.
Cardiolipin also plays a role in apoptosis, where it is oxidized and undergoes conformational changes that cause it to move from inner to outer mitochondrial membranes and generate pores that cytochrome C can escape through and trigger apoptosis.
Cholesterol can be easily oxidized into oxysterols, which are thought to perform a variety of functions, but are not fully understood. If cholesterol levels in the mitochondria were high, I think it would be oxidized and cause trouble.
http://en.wikipedia.org/wiki/Oxysterol


A timeline of the odds for survival for fertilized eggs and fetuses

here I found an answer. Not sure how accurate is is, though.

Data seems to be from the US

Here is a rewrite of parts of that article:

266 days before birth, all we have is a fertilized egg.  (~33% chance of living birth).
The odds are calculated using data from in-vitro fertilization, and the next stage is 66%.
In in-vitro, some 50% of the eggs cannot fix to the uterine wall
262 days before birth, the egg has implanted (~66% chance of living birth)
After implantation, there is still a decent chance that the embryo will be aborted (and maybe the woman will not even know that she was pregnant).
Half of the embryos that die from here on will die because of chromosome abnormalities.
241 days before birth (~88%)
178 days before birth, entering the second trimester (~97%)
At this stage, problems are more likely to stem from the mother, not the fetus' genome. Problems with the cervix, the uterus or the placenta are (some ?) likely causes of death.
89 days before birth, entering the third trimester (~99%)
At this stage, doctors will consider the fetus a patient, and treat it if needed.


What is this droplet of liquid that comes out of a mosquito?

Short answer
Excretion of blood and urine may prevent overheating by reducing body temperature through evaporative coolong (akin to perspiration). Excretion of blood and urine also concentrates the ingested blood.

Background
Female Anopheles mosquitoes seek blood for nutrients necessary to egg production. The cold-blooded insects may excrete some freshly ingested blood as a way to avoid overheating when consuming blood as warm as 104 degrees Fahrenheit (40°C). It is thought that excretion of a droplet of fluid aids in evaporative cooling, similar to perspiration in humans, to reduce the animal's temperature. The excretion of urine may serve a similar purpose, namely avoiding overheating during blood ingestion. By keeping the urine or blood droplet attached to the abdomen, excessive heat can be eliminated (Lahonde & Lazarri, 2012).

In the malaria mosquito (Anopheles stephens) the excretion of fluids has been investigated in detail. Females ingest blood meals that are equivalent to more than twice their unfed body mass. Engorged animals can fly only with great difficulty, making them more prone to predation. The blood meal serves primarily as a source of protein for egg development, but it also contains considerable amounts of unwanted salts and water that threaten haemolymph homeostasis. To counter this, a rapid natriuresis and diuresis commences even before the blood meal is completed, and ∼40% of the imbibed plasma volume and salt are voided within 1–2 h of feeding (Coast et al., 2005).

References
- Coast et al. Exp Biol (2005); 208: 3281-91
- Lahonde & Lazarri, Curr Biol (2012); 22: 40–5

Further readings
- Do mosquitoes urinate on you when they bite you?


Why does high blood pressure not damage the body during exercise?

Actually it can. See https://clinicalhypertension.biomedcentral.com/articles/10.1186/s40885-016-0052-y for instance:

Deleterious effects of HRE [hypertensive response to exercise] on structure and function of left ventricle (LV) has been reported consistently. Theoretically, individuals with HRE would be exposed to abnormally high pressure loads to left ventricle (LV), which may result in global subendocardial ischemia due to mismatch between demand and supply from excessive rate-pressure stress. Indeed, a previous study demonstrated a greater likelihood of new or worsening abnormalities of wall motions from echocardiography in individuals with HRE, even in the absence of angiographically significant coronary artery stenosis.

The issue is that you're confusing somewhat high blood pressure with abnormally high blood pressure during/after exercise, i.e.


How does sugar enter neurons if they don't use insulin?

Insulin is not directly involved in sugar uptake. It accelerates sugar uptake by upregulating glucose transporters and activating glycogenesis.

Neurons have many glucose transporters including GLUT1 and GLUT3 which are responsible for glucose uptake.

Moreover, insulin being an endocrine molecule has effects throughout the body including neurons. So neurons need not secrete insulin.


What is the percentage of people living in England in 1500 AD whose lineage is still alive?

Here is a partial answer that also expands upon a previous comment:

Between 1900 and 2013, 20,000 English surnames had gone extinct according to the Daily Mail's summary of research on surnames. This is a partial answer because it only tells us how many names are gone and is from the wrong time period.

To completely answer your question, I suspect you need to conduct primary research. I would suggest the following broad steps:

Gain access to the data needed to answer your question. British Census records only appear to available from 1841 to 1911 so you most likely need to sample old names (e.g., graveyard based studies).
Use the data to parameterize a statistical model such as a Galton-Watson branching process models.

I doubt the answer to your question can quickly be found unless somebody has already done it. Although, if done well, it could probably be a masters' thesis. However, before embarking on such a project, I would suggest doing a good literature search to make sure it has not been done before.

Note: If anybody finds the answer, please feel free to take content from my answer and include it yours.


How are neural networks encoded in the DNA?

Here's at least one paper describing some of what is known about development of neural network in Caenorhabditis elegans

http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1001044

It mentions at least one relevant gene

" There is evidence showing that several guidance molecules like Netrin and Nerfin-1 are expressed in the early stages of development. Netrin is a protein involved in axonal guidance in vertebrates as well as in invertebrates [21], [22], [23] and is specifically known to influence early path-finding events [23], [24], [25]. Nerfin-1 belonging to a highly conserved family of Zn-finger proteins, is found transiently expressed in neuron precursors and plays a role in early path finding. Studies involving pioneering neurons in the central nervous system of Drosophila melanogaster have shown that Nerfin-1, whose expression is spatially and temporally regulated [25], is essential in early axonal guidance. "

You can also have a lot at the Wikipedia article called  "Development_of_the_nervous_system_in_humans"

One interesting fact is that C. elegans has 20 000 genes, 302 neurons and about 5000 chemical synapses, 2000 neuromuscular junctions and some 500 gap junctions. In humans there are an estimated 20 000-25 000 genes in humans, about 85 billion neurons and 100 trillion synapses.

This excerpt from http://www.tandfonline.com/doi/full/10.3109/0954898X.2011.638968 explains this seeming paradox though

"studies in a range of species suggest that fundamental similarities, in spatial and topological features as well as in developmental mechanisms for network formation, are retained across evolution. ‘Small-world’ topology and highly connected regions (hubs) are prevalent across the evolutionary scale, ensuring efficient processing and resilience to internal (e.g. lesions) and external (e.g. environment) changes. Furthermore, in most species, even the establishment of hubs, long-range connections linking distant components, and a modular organization, relies on similar mechanisms."


Is there a known minimal stretch of DNA that can distinguish any two people in the world?

Here is what the data says. UK government must have had some scientific evidence when it settled on a 10 variable-length sections of genome for their database, SGM+. In one such variable sections, some people have 10 repeats of CTTT, others have 11, others have 12 etc. The largest of those fragments, at its maximum length, are about 350 base pairs. The US government uses 13 such variable-length sequences for its CIA database, called CODIS. On both sides of the Atlantic, roughly 3-4 thousand base pairs were judged to be enough, with some safety margin, by the most advanced geneticists in the world, working on public money.

The catch is that these variable length sequences are disjoint, so you end up requiring far more than 4,000 bp. If you need these markers on the same DNA strand (chromosome), you should space them by 50 centimorgans, at which distance they recombine independently. But according to http://www.sciencemag.org/site/feature/data/genomes/265-5181-2094.pdf , the longest chromosome only has 350-400 centimorgan. It means you cannot get 10 independent DNA sequences on a human chromosome, be it the longest.

I predict there is no such continuous DNA stretch, that would tell apart any two non-twins. Since it is much better to use multiple chromosomes in DNA fingerprinting, I doubt you will find more relevant experimental data.


Which is more susceptible to dehydration — extracellular and intracellular fluid?

You should understand that the body is an open system which is held at a steady state. Water can diffuse in and out of the cell such that the osmolarity is balanced on both sides of the membranes. If the water potential changes in either of these compartments (intra- and extra- cellular) because of addition or removal of water molecules, both the compartments would be affected such that finally the osmolarity is same in both the compartments. It may, however, take some time to achieve the steady state.

If you refer to sweating when you say "activity" then you should note that it is a complex process with extensive neurological control. The water that is secreted by the eccrine sweat gland primarily comes from the blood. However, profuse sweating will lead to water loss from both the intra- and extra- cellular compartments.

  Prolonged exposure to hyperthermic conditions and/or prolonged
  exercise in the heat can induce water deficits due to profuse
  sweating, resulting in hypohydration. This water deficit lowers both
  intracellular and extracellular volumes and results in plasma
  hyperosmolality and hypovolemia; both of which impair sweating.

  Shibasaki, Manabu, and Craig G. Crandall. "Mechanisms and controllers of eccrine sweating in humans." Frontiers in bioscience (Scholar edition) 2 (2010): 685-696.

So, for your experiment it is better to measure the osmolarity of the extracellular fluid or the blood plasma because:

It is easier to measure
It would not be sensitive to local and temporary effects


Is there any convincing evidence for the existence of nanobacteria?

There are two convincing papers (1,2) arguing that the observed "nanobacteria" are in fact mineral/protein complexes and not any living organisms.

In (1) Martel and Young created very similar looking particles from calcium carbonate in vitro. The calcium carbonate precipitations can even look similar to dividing cells:

  After 5 days of serum incubation, a white precipitate formed and
  adhered on the bottom of each flask. When examined by scanning
  electron microscopy (SEM) and transmission electron microscopy (TEM),
  the precipitate was seen to consist of particles with a size ≈500 nm
  (Fig. 1 A, B, and E), an observation consistent with normal bacterial
  morphology, which peaks at one particular size specific to the strain
  on hand. Some forms resembled cells undergoing division (Fig. 1 D,
  arrow).

One strong argument against those nanobacteria being living organisms is that they don't seem to contain any nucleic acids. Of course non-DNA based organisms are theoretically feasible, but that would be an absolutely extraordinary discovery.

The autors of (1) also observed these particles after filtration through a 0.1um filter. They argue that this size could not be sufficient to contain all the cellular machinery bacteria need:

  Because an earlier workshop commissioned by the NAS had suggested that
  the minimal cellular size of life on Earth must exceed 200 nm in
  diameter to harbor the cellular machinery based on DNA replication
  (19), it is unlikely that nanobacteria represent living entities
  unless they contain some other type of replicating mechanism.

(1) Martel J and Young JD, Purported nanobacteria in human blood as calcium carbonate nanoparticles. PNAS 2008, 105(14):5549-54

(2) Raoult D. et al., Nanobacteria Are Mineralo Fetuin Complexes, PLoS Pathog. 2008, 4(2): e41.


Which factors may affect a choice of an oviposition place in nocturnal moths?

The winter moth's preferred host plants are mainly deciduous trees, oak being the main food plant and also many fruit trees, birch and hazel. Females generally deposit eggs in bark crevices, under bark scales, bark snags and under lichen along tree trunks of host species. Eggs are initially small and green but gradually change colour to orange and then red before hatching (reference 1 and reference 2).

Though the oak is preferred,

  There does not seem to be much discrimination in selection of host
  plant or oviposition site by the female (Wint 1983), as the choice of
  larval food plant depends on the female's pupation site and the
  direction she takes on emerging, as she just climbs up the nearest
  tree. So it might be fair to say that the larvae contribute more to
  host plant choice than the adults, as the larvae can balloon if the
  host plant is unsuitable. However there is the possibility that year
  after year each generation of females will climb up the same tree as
  their mother, and oaks (one of the most common host plants) can be
  hundreds of years old, so there could have been hundreds of
  generations of winter moth on the same tree (reference).

So that in effect means, that the thickness of branches or being indistinguishable should not be a factor. Regarding abiotic and biotic condition, the main abiotic conditions are precipitation, temperature and photoperiod.

An increase in temperature leads to more activity and a faster metabolism (reference) Since leaf buds open faster, there is a chance for eggs to be laid faster according because the larva needs to burrow into the buds before the leaf opens (bud-burst) Hatching is temperature dependant but I do not think that it effects the number of eggs much. Biotic factors like the presence of parasitic predators reduce population but does not seem to reduce the number of eggs.. (reference)


Are there any organisms that perform photosynthesis-like processes with thermal energy alone?

Thermophiles are organisms that are capable of surviving high temperatures. It doesn't mean they use or harvest the thermal energy in any way. Normally proteins start to unfold and degrade at temperatures above about 41 °C and all other organisms have a hard time coping with the effects.
Usually biology uses chemical energy. Photosynthesis is the one exception of a biological system converting the energy of photons directly into chemical energy stored in complex biomolecules for all others to use as nutrition.
Organisms that do not rely on those complex biomolecules but can support themselves are called autotroph. So photosynthetic organisms are  photoautotroph and micro organisms that use chemical energy from inorganic compounds are chemoautotroph. The inorganic compounds used can be as simple as decomposed water by radioactive decay.


Can you please identify these yellow dot parasites which grow on non-living surface?

This looks like the work of an insect, perhaps a fly.
You can check by experimentation.
Try covering part of one surface with a fly-proof covering.
Take photos at weekly intervals of exactly the same area, compare images.
black-and-white images below from
Forensic Science International 137 (2003) 152–159
"Distinction of bloodstain patterns from fly artifacts"
Mark Beneckea, Larry Barksdale
DOI: 10.1016/j.forsciint.2003.07.012
Bar on images is 1cm


What biological constraints are there on how large a spider can grow?

The standard view on this is that the size of terrestrial arthropods like insects and spiders  is limited by the atmospheric concentration of oxygen. This is because they rely upon diffusuion of oxygen into the 'blood' or haemolymph via a system of tubes called trachea that open on to the body surface at the spiracles. As the body grows larger the proportion that has to be taken up by the trachea gets larger. Consistent with this is the presence of fossil giant dragonflies, Meganeura dating from the Carboniferous era when oxygen levels were at an all time high. However you will find that if you go to the Wikipedia page for Meganeura that this idea has been disputed, so the answer may be that no-one really knows.

In relation to alternative explanations; a recent paper by Clapham & Karr (2012) compares fossil insect wing lengths and oxygen concentrations to study the historical drivers of evolution of body size. They conclude that oxygen seems to be the main driver until the end of the Jurassic, but after that biotic interactions (such as bird predation) could be more important.


Can chitosan affect the absorption of unsaturated fatty acid?

It seems that there is no difference in the effects of chitosan on the uptake of saturated and unsaturated fatty acids. The study cited below (which has been done on guinea pigs) fed the animals a diet which contained different digestion-resistant fibers (maltodextrin, cellulose and chitosan) and also fats. Then the fatty acid content of the feces was measured afterwards.

Only for the group which got additional feeding of chitosan showed a significant increase in the excreted fatty acids. This was true for the saturated (lauric, myristic and palmitic acid) but also for the unsaturated fatty acids (Oleic, linoleic and α-linolenic acid). This effect is specific for fatty acids, The uptake of neutral sterols and bile acids was not affected in any of the experimental groups.

The second paper suggests that chitosan forms an emulsion with fatty acids under the acidic conditions of the stomach. This emulsion is stable and later excreted with the feces.

References:

Selective in vivo effect of chitosan on fatty acid, neutral sterol
and bile acid excretion: a longitudinal study.
Interaction between chitosan and oil under stomach and duodenal
digestive chemical conditions.


Do transcription factors bind to both strands of DNA?

The short summary is that typical TFs bind and read both strands together, as a basepair sequence. Some proteins instead recognise a site on the helix by its shape and flexibility. ssDNA-binding proteins obviously bind one strand but they do this in a non-specific manner.
RNA-binding proteins recognise the sequence on a single strand by inserting intercalating planar residues between bases! All of this binding is non-covalent.
Transcription factors recognise sites in dsDNA, with DNA-binding domains. The rest of the protein might surround (partially, to varying degree) the negative outer surface of the dsDNA double helix with positively-charged surface, in order to hold it on to DNA as it scans (perhaps) along its length.
DNA-binding domains: major groove

The following domains are found in many transcription factors, and they all recognise both strands. More correctly, they recognise basepairs and their orientation. The first 5 pages of this lecture slideshow demonstrate that the chemical groups on the side of basepairs, accessible in the major groove, allow proteins to distinguish A:T, T:A, C:G & G:C by the order of hydrogen-bond donors, acceptors, and a methyl group.
Hence, TFs recognise a sequence of basepairs - oriented such that one strand is (e.g.) pTpCpApG, and the complementary strand is pCpTpGpA; and the bulk of the protein may 'sit' on one strand or the other - or a nearby gene may locally define one strand or the other as the coding strand but this does not mean that this one strand is read.

Zinc fingers probe the major groove with reading helices.
Helix-turn-helix motifs do much the same.
Leucine zippers also do much the same.

These are common domains that all recognise basepairs in the major groove by interactions with residues on a probing aplha-helix.
TATA-binding protein: minor groove
TATA-binding protein (TBP) is a different, interesting case. It binds the 'TATA-box' via the minor groove, where the exposed chemical groups only distinguish [A/T] from [C/G], but not their orientation. This means that the sequences on each strand cannot be easily read from the minor groove. TBP instead recognises the shape and flexibility of the double-helix at the TATA-box, 'grips' it by the minor groove and bends the DNA, which aids the melting of the strands to the transcription 'bubble'.

The TATA-box sequence is usually pTpApTpApApA on the coding strand upstream of the transcriptional start. This is the convention when giving the sequence of a TF-binding site, but you couldn't say that TBP actually reads TATAAA - it doesn't!
Here is another, similar set of lecture slides.
Even better, here is the same material covered in a popular textbook.


So that looks to me like the Ophioninae family of wasps, genus Ophion. I'll query the list of known species to try to find a more direct match.

Some evidence exists which notes Ophion may sting when threatened, but at the same time (and I don't have the reference ready) it's believed that the sting contains no toxin.

As for a positive identification, it's difficult without examining the the features of the wasp extremely close up. Identification keys exist here.