The situation is definitely an extremely complex one, and you should probably forget about having an exact equation to define it.

When talking about the effects of a substance on the organism there are several factors to take into account. These are generally put together under the term pharmacodynamics.

Some of the factor to take into account are:

The dose of the substance
The route of administration
The metabolism of the substance
The target organ

The problem is, not all ethanol you drink will go to the brain, and it will not necessarily go there immediately, or all at the same time. All of this will change the effects on the brain. Also, there are several confounding factors, some of which I have tried to list.

I have summarized here a few information about ethanol metabolism, taken mostly from Principles of Forensic Toxicology - Chapter 10 by Barry Levine and Yale H. Caplan

Ethanol is normally taken through drinking, which means that it will have to pass through the gastrointestinal (GI) tract (i.e. stomach and intestine) before getting into the bloodstream. This route permits practically 100% of absorption of ethanol in the body, with the major site of absorption being the small intestine, absorbing ~75% of a dose of ethanol. The rest will be absorbed in the stomach and in the other parts of the intestine.

The absorption in the GI tract is dependent on the type of beverage: for instance carbonated alcoholic beverages are absorbed faster than "plain" ones.
The alcohol content also is important: a very diluted drink is absorbed slower than one with 10-30% of ethanol, as the latter will generate a bigger concentration gradient between the GI tract and the circulation, so it will diffuse faster. However, >30% ethanol will enhance mucus formation, which will slow down absorption. Furthermore, absorption depends on the status of the GI tract: preexisting conditions (e.g. inflammation) can modify the rate at which the alcohol enters the bloodstream.

But, we are still far away from the brain! After being absorbed, ethanol goes into the vena cava, and passes through the liver, where it can be metabolized (destroyed) by an enzyme called alcohol dehydrogenase (ADH), which converts ethanol into acetaldheyde, effectively reducing the ethanol concentration in the blood.
This is a well-known phenomenon for many drugs, and it is called first pass effect
Importantly, the human stomach also expresses ADH, so this first pass effect can start even before reaching the liver! The effects of ADH in the stomach obviously depends on how long the ethanol stays in there. So, it will be lower for an empty stomach then after a big meal.

Food, in fact, is also a well known factor that reduces the amount of ethanol in the blood.

For instance, these graphs show blood ethanol content in four healthy subjects after a 10 hour fast (filled circles) or after breakfast (empty circles), after drinking the same dose of 0.80 g ethanol/kg body weight, in 30 minutes.

From: Food-Induced Lowering of Blood-Ethanol Profiles and Increased Rate of Elimination Immediately After a Meal - Jones AW and Jönsson KA - J Forensic Sci., 1994.

As you can see, eating strongly decrease the ethanol blood content. Also see how there is quite a bit of variation between the different subjects (if you open the paper you will also see the graphs from other 6 subjects).

Also, you can look for instance at this paper (just got a random study, there seems to be a ton of them around):
First pass metabolism of ethanol. - Lieber CS et al. - Alcohol Alcohol Suppl., 1994

Coming out of the liver, ethanol goes into the right side of the hearth, and from there to the lungs. This poses no particular issue for most drugs, but ethanol is volatile! So, part of the ethanol is released through respiration (in fact the "classic" way of saying if someone has drunk alcohol is to smell his breath). However, this only accounts for a minor decrease in blood ethanol levels.

Finally, ethanol can start going around the body. Being a water-soluble molecule it will tend to diffuse into water-containing parts of our body (i.e. you will not find much ethanol in fat), which include the brain.

In the meantime, however, the process of elimination has started: ethanol can be excreted in urine, sweat and breath, although the major route of elimination is epathic metabolism by ADH, accounting for >90% of ethanol elimination.

There is a neat formula to express all of this, called the Widmark equation:

$A=\frac{Wr(C_t+\beta*t)}{0.8z}$

where

$A$ = number of drinks consumed
$W$ = body weight (important because of the content of water in the body)
$r$ = Widmark constant (depends on sex, age, etc.)
$C_t$ = blood ethanol concentration at time t
$\beta$ = acohol elimination rate
$t$ = time since the first drink
$z$ = volume of alcohol per drink

You can find examples of this formula in this PDF about Widmark equations

And now to the brain: ethanol does indeed have various effects on neurons. Short term effect essentially involve depression of neuronal activity, ethanol being able to modulate GABA signalling in the brain. Long term effect range from reduced neurogenesis (i.e. birth of new neurons) to reduced volume of certain brain areas, probably due to loss of neurons, to inflammation in the brain.

Again, the situation is very complex and it depends on the frequency of drinking, the amount of each drink and many other factors. A single dose of ethanol will probably have irrelevant effects on your neurons... as the amount needed (in one shot) for serious neurotoxicity will probably send you into ethilic coma. The exact mechanisms for these effects are only partially known and very likely to be derived by the interaction of numerous diverse effects.

This article explains some of the mechanisms for loss of neurons in the cerebellum.

Mechanisms of ethanol-induced degeneration in the developing, mature, and aging cerebellum. - Jaatinen and Rintala - Cerebellum, 2008

  These mechanisms include: (i) excitotoxicity; (ii) dietary factors, especially thiamine depletion; (iii) glial abnormalities; (iv) changes in growth factors; (v) apoptotic mechanisms; (vi) oxidative stress; and (vii) compromised energy production.

I will not go into the details of all of this, but it should be clear by now that all the things I mentioned so far (and many other factors I did not talk about) make it extremely difficult to give an exact quantification of the number of cells killed by ethanol. Surely the relationship is not linear, in fact, for instance, positive effects of small doses of alcohol have been reported numerous times.

A few more references on effects of alcohol on the brain:

Reduced neurogenesis

Long-lasting reduction in hippocampal neurogenesis by alcohol consumption in adolescent nonhuman primates. - Taffe et al. - PNAS, 2010

Adolescent binge alcohol exposure alters hippocampal progenitor cell proliferation in rats: effects on cell cycle kinetics. - McClain et al. - J Comp Neurol., 2011

Brain volume decrease

Decreased volume of the brain reward system in alcoholism. - Makris et al. - Biol Psychiatry, 2008

Amygdala volume associated with alcohol abuse relapse and craving. - Wrase et al. - Am J Psychiatry., 2008

Hyperhomocysteinemia as a new risk factor for brain shrinkage in patients with alcoholism. - Bleich et al. - Neurosci Lett., 2003


The estimate is probably going to depend on the source, but it's generally at least an order of magnitude more than that.

Back in 2002, John Moore, an anthropologist at the University of Florida, calculated that a starship could leave Earth with 150 passengers on a 2000-year pilgrimage to another solar system, and upon arrival, the descendants of the original crew could colonize a new world there—as long as everyone was careful not to inbreed along the way. [...]
A starting population of 40,000 people maintains 100 percent of its variation, while the 10,000-person scenario stays relatively stable too. So, Smith concludes that a number between 10,000 and 40,000 is a pretty safe bet when it comes to preserving genetic variation.

For the general concept see minimum viable population.


Purifying a linear plasmid after restriction digest?

Can't exactly say what problem you are facing but you can follow these steps for efficient restriction digestion and elution.

Never set up a digestion reaction with more than 1µg DNA per 20µl; if you require more digested DNA, then set up multiple 20µl reactions with maximum of 1µg DNA in each (500-700ng is ideal).
10µl enzyme for a 230µl reaction: bad idea. Set up 10×20µl reactions with not more than 0.5µl enzyme per reaction tube.
Avoid overnight incubations; 4 hours should be sufficient (NEB PmeI is 10 units/µl and 1 unit is the amount required to cleave 1µg DNA in 1h in a 50µl reaction. You are adding 5 units in 20µl. Overnight incubation is too much)
Deactivate the enzyme after the reaction.
Just run a little bit of sample from one tube in the gel to see if digestion has happened. After confirming digestion simply use the PCR purification kit. You can pool your tubes.
Optional: Elute in Tris-Cl pH 7.5 instead of water or use warm (60⁰C) water.


What sort of biofiltration is best for a small, portable, biofiltration unit?

Any kind of sponge and pump filters will breed nitro bacteria to remove organic content. Added to a drip filter made from pure mineral sands and clays, you'd have a bacterial sponge and plant aquarium plus a sand filter.

You can make you own activated carbon too.

Urine requires at heavy plant growth to purify. You already have a tank, volume not given so I'll say it's 125 L. Here's a two stage bio filter: one with an incoming and circular bacterial filter to filter incoming water in graded sponges up to about .05 - 1 mm finest incoming particles for foods and stuff.  Use 2 divisions in the tank, one of 100 L, one of 25 L that you can prepare 10 L from every day.

Use 2 fish filters AC of 7 - 20 watts (?) or 12 V (DC) pumps similar to fish ones. Use 500 ml - 1L volume of filter sponges with fast access so you can squeeze out the bacterisl mats periodically because they will fill with nitrogen and phosphate and oxygen based pond organisms.

If you can fill the 100 liter tank with algea, it's ideal.

Put a valve to keep 2nd 25 L tank separate. Filter final 10 L drawn daily through mountain mineral sand from places with great spring water, i.e. dolomites / chalky to add trace elements. It's recommended you use sunlight and lots of plants in the first tank.


Evolutionary advantage of F plasmid in bacterial conjugation

F plasmids allow for the genetic exchange of material between cells, it's the closest thing to sex for most bacteria. Parts of the F plasmid are homologous to the chromosome of E. coli (mainly the transposons present on the plasmid) and through homologous recombination they can pick up bits of the chromosome. A lot of studies have been done where bacteria acquire traits such as galactose or lactose utilisation through these genetic exchange. They therefore allow fitness enhancing DNA to spread quickly through a population or species barriers [Ref].

Antibiotic resistance is not carried on F plasmids but there are many conjugative plasmids that do carry resistance genes (R plasmids). The F plasmid does carry a toxin/antitoxin system (ccdB/ccdA) [Ref]. If the cell loses the plasmid it will not be able to replicate its DNA because the toxin protein is very stable while the anti-toxin is rapidly degraded. So besides the evolutionary advantage there is also the possibility that it is simply 'selfish DNA' (see Richard Dawkins the Selfish Gene for details on this).

There are certain circumstances under which the F plasmid does not transfer such as low temperature so it is possible for a bacterium to lose the F plasmid and not get it back by conjugation. Maintaining a relatively 'useless' piece of DNA does have its metabolic cost so loss might confer a growth advantage.


You can try to use IntAct Molecular Interaction Database. The data in this database is based on:

data from the literature or from direct data depositions by expert
curators
<300k binary interactions in 2011  developed by the EBI's
Proteomics Services Team
recent reference: Aranda et al. '10

This is also mentioned in the summary of the Aranda et al.'10 article:

  IntAct is an open-source, open data molecular interaction database and
  toolkit. Data is abstracted from the literature or from direct data
  depositions by expert curators following a deep annotation model
  providing a high level of detail. As of September 2009, IntAct
  contains over 200.000 curated binary interaction evidences. In
  response to the growing data volume and user requests, IntAct now
  provides a two-tiered view of the interaction data. The search
  interface allows the user to iteratively develop complex queries,
  exploiting the detailed annotation with hierarchical controlled
  vocabularies. Results are provided at any stage in a simplified,
  tabular view. Specialized views then allows 'zooming in' on the full
  annotation of interactions, interactors and their properties. IntAct
  source code and data are freely available

Further you can use the Evidence tab in String(I assume you have already tried this but in the case you did not):

You can then click on Experiments, then something like this will show up:

You can see how (e.g. Reconstituted Complex assay) and you can see from which article this interaction is coming from if you click on an item in the table:


Chart of intra-species genetic diversity across species / phyla?

You can look at the Heterozygous SNP rates in genome-sequenced species, which is a measure of within species diversity.

You have an example in Figure 4 here:
https://genomebiology.biomedcentral.com/track/pdf/10.1186/s13059-016-1090-1

You can see in the figure that endangered species are plotted (most of them with poor genetic diversity).

Also, I am afraid that your starting hypothesis is not very good. Our species is very poor in genetic diversity and has little phenotypic variation. The human species went through several major bottlenecks during his evolutionary history that reduced their diversity. Even gorillas or giant pandas are more diverse than humans. You have a bias because you are human and are good at differentiating individuals from your own species.

Also a single representative from each group won't suffice as the differences can be huge inside a group. Additionally phenotypic variation is hard to measure in certain groups.

Sorry for being a bit negative


Why is there an apparent reduction of reptile species near the Mississippi River?

The reptiles mostly were ploughed away and replaced with soy beans.

The low reptile diversity zone matches the Mississippi Alluvial Plain which includes the Mississippi Floodplain. The Mississipi drains nearly half of the USA's geographic area, so the flood plain is massive.

The Silt Plain is very flat, mostly has hills left by oxbow lakes and river meanders. If you put your hand in the ground, it consists of organic matter/silt/clay/mud/fine sand, and it is very fertile until it is depleted by modern agricultural practices.

It's one of the more productive agricultural regions in the USA, and it's mostly giant square fields and mono cultures.

zoom in: http://gokml.net/maps#ll=32.163208,-91.720681&z=11&t=h&q=winnsboro

Here is a quote from the Discussion at the end of this review:

  traditional agricultural landscapes, typically characterized by
  mosaic–like structures, intermediate levels of disturbance, and able
  to host great biodiversity levels (Bignal & McCracken, 1996), have
  undergone profound transformations in last decades. The rapid
  extension of intensively cultivated fields and the reduction and
  fragmentation of the original habitats have led to the creation of
  more uniform and depleted landscapes, with significant loss of
  biodiversity (Whittaker, 1975; Bull & Skovlin, 1982; Burel et al.,
  1998; Zechmeister & Moser, 2001; Moser et al., 2002; Pfiffner & Luka,
  2003). In accordance with these changes, our analysis of reptile
  assemblages in an agricultural area mainly devoted to the intensive
  cultivation of arable lands found the landscape to be relatively poor
  in biodiversity. Four out of five agricultural land uses hosted only
  one species, while most of the recorded reptiles occurred inside a few
  patches of semi–natural habitats and, above all, in the grid of
  vegetated buffer strips interspersed among the cultivated lands. In
  addition, during field activity, we observed only seven of the
  eighteen species of terrestrial reptiles reported for the province
  where the sites are located, and most records were ascribable to a
  single species.

Reptiles and Amphibians are at the top of the insect food chain, and studies have shown that they are sensitive to pesticides, especially when their numbers are low:

  By using three evaluation factors - (i) pesticide exposure, (ii)
  physiology and (iii) life history - a taxon-specific pesticide
  exposure risk factor (ERF) was created. The results suggest that about
  half of all evaluated species, and thus at least 1/3 of all European
  species exhibited a high exposure risk. Previously the region would
  have been host to a very tall high growth forests, because of the high
  temperatures, available water table of the area and fertility.

you can check pics 6 and 8 from this page to see the productivity of the region. It suggests that the reptile biomass was replaced with obese humans.

That forest has been reduced to the swamp forests where the roots are covered in stagnant water for most of the year, where some large aquatic reptiles take refuge, and which is completely different than the lost forests of the Mississippi plains.

The old forests would have perhaps been similar to florida's inland forest, and perhaps very different, because of the available water table, and much more productive silt, than florida's ground allows for. I didn't manage to find photos of the lost forests of Mississippi plain regions, they would have been dense, producing 3-7 times more biomass than normal forests.


Confusion about Photosystem 2 with regards to lysis of water

Generation of ATP via photons is the primary aim of the photosynthesis pathway, which is accomplished by the generation of a chemiosmotic gradient of $\ce{H+}$, which then drives the ATPase pump. All the other enzymatic setups are designed to just let this process run in the most efficient way.

  I would think that it is perfectly sufficient for PII to receive photons to excite an electron in the primary pigment reaction centre

While you are partially correct in assuming this, since the ETC also participates in creation of a chemiosmotic gradient (Plastoquinone), such a mecahinsm would not be able to run repeatedly. Without the replenishment of the electrons of the PSII, it will not be able to initiate another round of electron transport. Hence, the oxidation of water is crucial in providing PSII the electrons it passed onto plastoquinone, so as to allow another round of photon-absorption and continuation of the photosynthetic process.

  how is it controlled that the correct number of H2O molecules are lysed so that excess electrons aren't generated?

This is achieved by a complicated interplay of the enzymatic components within the PSII. In summary, utilizing the four stable oxidation states of manganese core in the redox center ($\ce{Mn}^{(2-5)+}$, four separate states of the center ($S1\rightarrow 4$) are formed. These states cyclically shunt one electron during each step, until a water molecule is bound to $S4$ which is then directly converted to $\ce{O2}$ by $P680+$, formed in PSII due to photon absorption, which is a strong reducing agent. Since the final step occurs only with water molecule bound to $S4$, which in turn is formed only by the cyclical transition between the various states of the redox center with systematic sequential loss of electrons, the overall process is very tightly constrained to extract only the limited number of electrons preventing any troublesome redox intermediates.

See here for some basic treatment of photosynthesis.


In the life-cycle of the HIV virus, how does the created DNA enter the nuclear membrane?

Some proteins are transported from cytoplasm to nucleus by the importin family through nuclear pore. These proteins have a specific sequence called Nuclear Localization Sequence (NLS) and the importin family recognizes NLS to import them. Recently it has been clear that the accessory protein vps which is translated from viral RNA and composes pre-integration complex (PIC) with viral DNA has atypical sequence like NLS.
So. it has been thought that DNA from HIV is imported into host nucleus by importin family with PIC.


A point mutation is a mutation causing the substitution, insertion or deletion of a single nucleotide.

An indel is a change in the number of nucleotides (either through insertion or deletion hence the name). When talking about indel most people (in evolutionary biology at least) refer to the insertion or deletion of a single nucleotide but some might refer to greater changes when talking about indels.

An indel which concern the insertion or deletion of a single nucleotide is a point mutation.


How many mosquitoes would it take to "drain" enough blood to put a person into shock?

This question falls into different subquestions:

1. How much blood does a mosquito take when feeding?

This is not so easy to answer, but there are publications which measure the volume of different mosquito species. Reference 1 lists volumes between 2.85 and 11.99µL per meal and mosquito. Reference 2 lists 3.07 and 5.71µL. To make the approximation a bit easier, let's assume that mosquitoes drink about 5µL per bite (which should be near enough).

2. How much blood does a human have?

According to Wikipedia, humans have around 77mL blood per kilogram of body weight. If we take a 70kg human, we get around 5L of blood.

3. How many mosquitos does it take to get a human into shock, and how many to suck him out completely?

According to the Medline, Hypovolemic shock occurs when a human loses about 1/5 (or more) of his blood volume. 1/5th of 5L is one litre. Since each mosquito sucks 5µL, this would take about 200.000 mosquitoes. To suck out all blood would take 1 million mosquitoes. (This is not possible since mosquitoes depend on an existing blood pressure, as reference 3 shows. If a capillary is empty due to massive blood sucking, they change to another.)

Besides this theoretical (but interesting) calculation, there are some real problems about getting biten by so many mosquitos. First, this is a question of available skin. The human skin is about 2 square meters in size, which would require 100.000 bites per square meter. To break this down further, a square meter has 10.000 square centimeters, so there would be 10 mosquitos which need to bite you per square centimeter. Rather unlikely.

Then each mosquito injects a mix of anti-coagulants, pain killers etc. prior to sucking to keep the blood from clotting and also to make sure you won't notice the bite immediately. As pointed out in the comments, this would already cause a lot of trouble and probably cause massive bleeding, since the effect of the anti-coagulants would sum up when biten by thousands of mosquitos. Additionally the body reacts by releasing histamines and since the amount would also be massive, this would cause real trouble and probably kill you.

References:

Regulation of blood meal size in the mosquito
La Crosse Virus Infection Alters Blood Feeding Behavior in Aedes
triseriatus and Aedes albopictus (Diptera: Culicidae)
Visualizing Non Infectious and Infectious Anopheles gambiae Blood
Feedings in Naive and Saliva-Immunized Mice


Can something cause both breaks and cross-links in DNA?

Cisplatin forms DNA-protein crosslinks (so DNA-protein-DNA by extension) in vitro [1] and a review [2] says that cisplatin leads to DSBs (although I can't access the primary source at the moment). But you know, with the exception of ionizing radiation, mutagens usually don't directly cause DSBs. It's caused by repair processes or things like stalling at replication forks because of the mutagen.

[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1874601/

[2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4047912/#!po=11.9919


Are prions an important driver in evolution?

It is proposed that prions are a good mechanism for "testing" phenotypic variation.

There are many identified proteins with prion-determining domains (PrD) in the yeast genome that can spontaneously switch between conformations with some low probability (eg: check SUP35 for one example, and [1] for a good overview of more). The theory is that:

the low probability of switching from non-prion to prion state allows for many more mutations and variations to accumulate -- generating greater genetic diversity than in standard expressed gene variability where most mutations are silent or detrimental
the prions provide a ready form of non-permanent inheritability that can be "trialed" by offspring and others in a colony of organisms -- this can be especially beneficial during say temporary changes in environment
if the prion phenotype is widely successful, selective pressure can easily mutate it into a more permanent fixture in the genome.

Check out the excellent paper published just last week in Nature exploring this this topic [2]. To give a sense of just how evolutionarily-advantageous prions can be, in the author's experiments and analysis they note that 40% of the prion traits they analyzed were beneficial to growth (eg:  in the paper strain UCD939 gains additional resistance to acidic conditions from the prion [PSI+]).

Assuming these hypothesis, prions would thus play a significant role in the evolution and variability of organisms.

[1] Crow, et. al. 2011. doi:10.1016/j.semcdb.2011.03.003

[2] Halfmann, et. al. 2012. doi:10.1038/nature10875


If you have some knowledge of python, you can do a lot of things with the ETE toolkit.

Disclaimer: I have used an older version of it, but in a very limited manner.


How do the quantities of ATP formed during aerobic and anaerobic respiration compare?

You means fermentation and respiration?
In aerobic,1 mol glucose trough respiration and get about 38 ATP
In anaerobic, 1 mol glucose through fermentaion and get 2 ATP


Number of transcription factor genes in the human genome

Here I will assume we are talking about eukaryotic sequence specific transcription factors (ssTFs) and try to answer your first and part of the second question. There is in any case not definitive answer yet.

An estimate of ssTFs genes in humans is given in the 2009 Nature Reviews Genetics paper by Vaquerizas, JM et al, A census of human transcription factors: function, expression and evolution.

An excerpt from the abstract:

  Here, we present an analysis of 1,391 manually curated sequence-specific DNA-binding transcription factors, their functions, genomic organization and evolutionary conservation.

The numbers are somewhat higher now. Wingender et al. have counted 1,558 human genes in their TFClass database 2013 NAR paper. In their 2014 NAR paper they included 1,557 human, 1,147 mouse and 1,105 rat orthologs.

Another way to look for this information is to see the number of entries listed in TF databases, like for example JASPAR. This has the advantage of including other species. However, the coverage here depends on the availability of position weight matrices (PWMs) for the binding specificities. Many uncharacterized TFs may not be found.

To try to answer your third question, that is, what is the proportion of TFs in the different species, a naive approach would be to divide the number of predicted TFs by the number of predicted genes in the target genome. For example, taking the latest estimates above with the predicted number of coding genes from Ensembl database (version 78) will return these percentages:

# Human
100 * 1557 / 20364 = 7.64%
# Mouse
100 * 1147 / 22606 = 5.07%
# Rat
100 * 1105 / 22777 = 4.85%

This suggests humans have a slightly higher proportion of TFs than rodents. However, these differences are not too big and may be dependent on the accuracy of the different estimates on TFs and gene numbers. An in itself, these numbers are not so interesting.

A much more interesting question is whether TF families have expanded more or less in different species (that is, whether the number of  proteins within each family has increased, regardless of the proportion to the total number of genes in the genome). I could find at least one paper where this has been done systematically for several eukaryotic species, covering animals, plants and fungi, and focusing on TFs common to the ones found in plants. The main conclusion of the paper is that some TFs families have expanded more in plants than in other organisms. Quoted from the abstract:

  To investigate if differences exist in the expansion patterns of TF gene families between plants and other eukaryotes, we first used Arabidopsis (Arabidopsis thaliana) TFs to identify TF DNA-binding domains. These DNA-binding domains were then used to identify related sequences in 25 other eukaryotic genomes. Interestingly, among 19 families that are shared between animals and plants, more than 14 are larger in plants than in animals. After examining the lineage-specific expansion of TF families in two plants, eight animals, and two fungi, we found that TF families shared among these organisms have undergone much more dramatic expansion in plants than in other eukaryotes. Moreover, this elevated expansion rate of plant TF is not simply due to higher duplication rates of plant genomes but also to a higher degree of expansion compared to other plant genes.


What causes the elongation of Genome down the evolutionary time line

DNA misreplication events can lead to accidental duplication of DNA (even the entire genome), misalignements in recomibination events, integration of DNA from extracellular sources e.g. viruses. All these events can lead to large scale changes in the genome size of an organisms, smaller scale changes can be insertions and deletions in the DNA from repair pathways such as non homologous end joining.


Why is hydrofluoric acid so dangerous if it is a weak acid?

The confusion arises from the term weak, which has only to be interpreted in chemical terms.

Weak acid, as you say, just means that the acid does not readily dissociate, not that its effects are weak! Just to say one, HF corrodes glass, something that not even smoking HCl does.

Wikipedia has a nice summary of HF toxicity (see also the references in the article itself):

  Hydrofluoric acid is a highly corrosive liquid and is a contact poison. It should be handled with extreme care, beyond that accorded to other mineral acids. Owing to its low dissociation constant, HF as a neutral lipid-soluble molecule penetrates tissue more rapidly than typical mineral acids. Because of the ability of hydrofluoric acid to penetrate tissue, poisoning can occur readily through exposure of skin or eyes, or when inhaled or swallowed. Symptoms of exposure to hydrofluoric acid may not be immediately evident. HF interferes with nerve function, meaning that burns may not initially be painful. Accidental exposures can go unnoticed, delaying treatment and increasing the extent and seriousness of the injury.
  Once absorbed into blood through the skin, it reacts with blood calcium and may cause cardiac arrest. Burns with areas larger than 25 square inches (160 cm2) have the potential to cause serious systemic toxicity from interference with blood and tissue calcium levels. In the body, hydrofluoric acid reacts with the ubiquitous biologically important ions Ca2+ and Mg2+. Formation of insoluble calcium fluoride is proposed as the etiology for both precipitous fall in serum calcium and the severe pain associated with tissue toxicity.


Is there a hormone combination that makes humans grumpy?

This is a hard question to respond to.

Many things might make someone grumpy.  There are also individual temperaments, making grumpy hard to quantify - a Grumpy to one person might barely be a blip on another individual's scale.  Hormones like cortisol reflect stress, and can make people in general irritable, but I doubt any one combination of hormones would always cause grumpiness.

But I thought I'd venture an answer since I did see this paper today:  "Low glucose relates to greater aggression in married couples" doi: 10.1073/pnas.1400619111

Being hungry will do this for lots of people, so maybe a bit of an answer for you. There are lots of different kinds of signals that mediate hunger though, so still a tough call.

Update: here's an additional article that specifically talks about parts of the brain involved in aggression and grumpiness as response to a drop in glucose.


Perhaps the question may also be phrased, "Why is it common for plants to produce chemicals that possess pharmacological or toxicological effects in man and animals?", and to that question it is often reasoned that plants, being sessile and otherwise defenceless food sources for predators, produce compounds that affect the physiology of animals in such a way as to make it not beneficial for a predator to consume them, which is close to your 3rd hypothesis. Remember that pharmacological benefit is largely anthropocentric, and relative at that. For instance, a plant compound that lowers blood pressure could be used as treatment of hypertension, but if the plant were to be consumed in its native state in appreciable quantity, it could put the eater into shock, cardiac arrest, etc.

Most pharmacologically active compound from plants comprise a class of compounds known as secondary metabolites: metabolic intermediates that are not appreciably involved with functions of growth, respiration, etc. (often interpreted as evidence for a defence mechanism).

Try this wikipedia article and see what you think: http://en.wikipedia.org/wiki/Plant_defense_against_herbivory

The major classes of secondary metabolites in plants are: terpenes, which are polyisoprenoids, phenolic compounds, including the polyphenolic compounds, which are a popular study in natural products research, and alkaloids (along with other nitrogenous compounds).


On Neuroimaging Analysis

  But being highlighted means being active (at least more active than other regions)

This is not the case in functional connectivity analysis, or indeed not necessarily the case in any sort of functional neuroimaging analysis. The colormap highlighting in such images as you referred to (see the primary reference for that particular image) reflect statistic scores, commonly z- or t-statistics. Correlation simply means that time-courses behave similarly over time, and the color coding tells you how strongly they correlate with the “common profile” of the cluster. This makes no direct statement regarding the total “activation level“ over time, as represented by e.g. the area under the curve of the timecourse. In fact, such a metric would be meaningless, since fMRI signals are de-meaned so that they fluctuate around zero (as seen e.g. in the timecourses depicted here). Functional connectivity networks thus do not imply in whatever fashion a higher level of activity in highlighted networks. For further visual clarification you can consult Figure 1. of this article showing that functional connectivity networks can be and often are active at the same amplitudes and have similar levels of “total activity“ as visually inferred from the integral of the power spectra. This integral analysis is not presented, however, as it is meaningless.

On Inhibitory Functional Networks

Whether functional connectivity networks are implied to be excitatory depends on the exact mode of analysis. If the analysis is truly based only on detecting large correlation scores, identified networks will not resolve inhibitory projections, as such connections would cause anticorrelation rather than correlation. It could still be that a functional connectivity network is based on multiple areas receiving strong inhibitory input from an upstream node, yet that node would not be part of the network. Consequently, proficient functional connectivity analysis will identify networks via methods such as independent component analysis (ICA), which are able to group both strong correlation and anticorrelation together, as seen here.

TL;DR

Yes it can, it often is, and it's generally highlighted in blue.


Methods of nuclear transfection - nuclear transport

My attempt to find an answer has suggested that no-one knows how the DNA gets into the nucleus.

This fairly recent paper reports attempts to track the pathway of DNA entry and transfer to the nucleus.

  Le Bihan et al. (2010) Probing the in vitro mechanism of action of cationic lipid/DNA lipoplexes at a nanometric scale. Nucl. Acids Res. 39:1595-1609

The technique used was transmission electron microscopy. Complexes of plasmid DNA + cationic lipids (lipoplexes) were labelled with silica-based nanoparticles to allow visualization.

The authors describe a transfection pathway with five steps:

  (i) binding of the lipoplexes to the cell surface;
  (ii) entry of the lipoplexes into the cells mainly via endocytosis (a direct fusion with cell membrane cannot be excluded);
  (iii) DNA release into the cytosol;
  (iv) transport through the cytosol; and
  (v) entry of DNA into the nucleus and nuclear transcription.

The authors were able to follow each of the first four steps but:

  our data show nanoparticles close to, but not within, the nucleus.

They speculate about what this might mean, but they do not refer to any previously published data. My conclusion is that the answer to your question is, as I said at the beginning of my answer: no-one knows how the transfected DNA enters the nucleus.


What does it exactly mean to sequence the genome of a species?

Sequencing a "species" builds a reference genome that is considered to be a good "representative" of the species. Of course there will be genetic variation between the reference and healthy specimens in practice (usually SNPs), however it should be minimal.


Why are sushi proteins called "sushi"? What are the origins of this name?

Because their shape reminded researchers of rolls of Sushi (Ichinose et al, 1990):

  These repeats were initially called GP-I structures because they were first identified in $\beta_2$-glycoprotein I. More recently, they have been called short consensus repeats or sushi structures because of their shape.


This is purely an anatomical definition: right dominant is defined as coronary circulation where the PDA (posterior descending artery) is a branch of the RCA (right coronary artery) and left dominant is defined as coronary circulation where the PDA is a branch of the LCX (left circumflex artery). The Wikipedia article on coronary circulation is a reasonable reference for this question.

There's nothing else special about the statement "dominant" and it doesn't have any other importance for cardiac function, except that someone who is left dominant would have more serious issues if there is a blockage in their left main or LCX.

Typical human coronary artery anatomy consists of two ostia off the aorta, right and left. The "left main" branches fairly early on into the LAD (left anterior descending) artery, which follows the septum between left and right ventricles down the anterior side, and the LCX, which follows the 'top' of the left ventricle counter-clockwise (if looking down at the top of heart and rotating the heart so the atria are on top; in an actual human heart the atria actually point towards the midline a bit more than other species). The RCA travels in roughly mirror fashion, following the 'top' of the right ventricle in clockwise fashion. The RCA and LCX nearly meet on the other side of the heart, at the posterior septum.

In a majority of people, the RCA continues and follows the septum down to the apex (kind of like the LAD but on the opposite side). In a non-negligible minority, the supply of the posterior descending artery is either shared by RCA and LCX or is completely supplied by the LCX.


Can compounds be predicted from Polyketide synthases gene clusters?

I would say that for type I polyketide synthases (PKS), this is possible. These proteins are variations on fatty acid synthases which have modules, each of which adds a two carbon unit as well as a chiral methyl group to an extending chain which may be reduced to give anything from a ketone, an alcohol to a completely reduced carbon chain.  In the illustration below you can see these 3 options, but double bonds are also possible.

Other sorts of PKS pathways (type II and III PKSs) have proteins which are harder to predict in terms of what they produce since a single protein does the extending of the polyketide chain to cyclize it, typically into an aromatic compound.  All this happens in a single protein site, so careful modelling would be required and I'd be suprised if this has been done accurately.

Note the last arrow there 'tailoring steps' - accompanying the PKS genes themselves are often a slew of acetyl and methyl transferases, additional reductases, coupling enzymes, even delivery proteins... the list goes on and on.  These steps would be hard to predict because the substrate for an o-methyl transferase isn't easily determined.

I think there are several companies trying to leverage 'best guess' bioinformatics here.  They are likely to get a good idea of the backbone, but maybe won't place every methyl and acetyl group correctly.

There are definitely people out there who think this could work to deliver diverse candidates to drug discovery.  see Radiant Genomics as well.


Regarding the Papers referenced above:

If the authors maintain that the evidence at the site of fusion is not clear and that explanations as to how this happened are flawed that is possibly concedable.   They would need to do more homework than these papers.  The discussion of vestigial centromere sequences and telomere motifs being inverted is interesting, though contrary views have been written up elsewhere.  I'm not going to review that evidence as I think its not primary to the question at hand...

I would point out that the centromere and telomere sequences are highly repetitive - they are so repetitive that they are often associated with unreliable sequencing in a typical genome build.  While its possible some will be found in future builds of the human genome, such sequences are just as likely to have been excised during mitosis or by mutation.  There would be strong selection pressure for them to be excised quickly; having two centromeres on one chromosome would probably be a fatal trait and the same is probably true for telomerase susceptible sequences in the middle of a chromosomal arm is too.  A lot has happened at the point of fusion and 150 kB of DNA seems to have included itself which is not from the original Chr 2A or 2B.

I think there is some confusion here: The fusion models examined do not predict the fusion from the local configuration of bases.  The main evidence for fusion has always been the fact that the two pieces of human chromosome 2 are nearly identical to chromosomes 2A and 2B of apes - typically 96-98% identical.  The genes are almost entirely in the same order, the inter-genic regions are very similar All along the 2A/2B length - millions of bases.  The site of fusion ad models for its occurrence is merely confirming what we already - there are two chromosomes somehow stuck together.  Since both papers focus on the site of combination and do not adequately address this primary piece of information, they seem to be missing this point.

The chances are infinitesimal that human chr 2 were to resemble those of other primates at random.   This is what you say in science when you mean 'impossible'.  One simply doesn't see a segment of DNA the size of Chr 2A and 2B being so similar for such a length when we look at rats, dogs, worms or any more distantly related living thing.  But for every primate the relationship corresponds to humans the same way.  In addition studies show that these highly similar blocks of DNA sit right next to the site of fusion and show a crossover where the fusion probably occurred.  Some recent hominids - Neanderthals and Denisovans had the chr 2 fusion as well.

I have to say is that there's always a chance that chromosome 2 fusion did not happen though in my view there's a tremendous amount of evidence that it did.  The second most likely explanation is that all the other apes had their chromosome 2 break into 2 pieces at some susceptible site.

I don't quite agree that chromosome 2 fusion is an indispensable or even leading piece of evidence that means that humans and the other primates are interrelated.  That question is a different kettle of fish and the relationship between Human chromosome 2 and the chromosomes of other primates is just one contributing point.  All the other chromosome sequences in primates are the same, and nearly every gene in human beings is closer to primates than to other animals.  If they had not found chromosome 2 fusion in the genome sequences few if anybody would have worried about it.

As to your last question - I don't know if its necessary that chromosomal fusion must occur in every living thing, but it appears that it has.  In fact what we see as we look at all the diverse chromosomes being sequenced, is that most chromosomes have been merged or rearranged over and over again.  Over long periods of evolutionary time, a typical chromosome looks like a patchwork quilt stitched up from pieces of other chromosomes.  These relationships are called synteny, which reaffirm the thesis that all living things came from a single point of origin, if you go back far enough.  Really, the fusion point of Chr2 is interesting because its a relatively new event; by picking through the pieces we might find some understanding of something that appears to be a common phenomenon in genome dynamics.

The above image comes from a review of methods to identify syntenic regions.  It identifies regions of human chromosome 7 and similar regions of mouse chromosomes, identifying regions on mouse chromosomes 6, 9, 11, and 12 with substantial similarities as well as a little bit of chr 2.  Hu chr 7 is 158 million bases long, so even a small band (> 1/1000th of the full length) on this chart means 100,000s of bases.

If all these syntenic relationships are considered together they can construct chromosomal rearrangement events that compare with the phylogenetic tree and typically verify speciation events that separate the two organisms being compared.

Whoops - just found this.  Take a look at this Biology.SE question: it refers to Robertsonian translocation where the long arms of several of the chromosomes chr 14, 15, 16, 21 and 22 are known to sometimes fuse, resulting in viability.  The answer there is useful - these variants don't tend to produce offspring, but it only takes one time.  Its only happened once in the past 5 million years or so.  So another point of view there.

That should't discourage the authors from trying again.

All this being said, as a scientific question I'd rather have a discussion like this, based on evidence and facts that anyone can evaluate.  The authors did quite a bit of homework and read some of the literature that is out there.  This is the right direction some of the creationists are taking here and I personally hope that they keep at it.

If science is to have any merit (or fun) at all, its because any idea can be called into question and be re-evaluated at any time by anyone.


Where can I get a file/list of the common and scientific names of species?

Maybe not a direct answer to your question, depending on what you mean with "unencoded data file", but the Global Biodiversity Information Facility (GBIF) has an API where you extract data for species names. Their database includes common names (aka vernacular names) when they have that, and often common names from different languages. Using this API, you can extract data and construct a name file for a particular taxa that you are interested in.

As an example, this is the list of the first 20 vernacular names found for Passer domesticus (House sparrow):

{
   "endOfRecords" : false,
   "results" : [
      {
         "language" : "",
         "sourceTaxonKey" : 100220560,
         "source" : "Global Invasive Species Database",
         "vernacularName" : "English sparrow"
      },
      {
         "language" : "",
         "sourceTaxonKey" : 100220560,
         "vernacularName" : "Europese huismuis",
         "source" : "Global Invasive Species Database"
      },
      {
         "vernacularName" : "Gorrion domestico",
         "source" : "Global Invasive Species Database",
         "language" : "",
         "sourceTaxonKey" : 100220560
      },
      {
         "source" : "Integrated Taxonomic Information System (ITIS)",
         "vernacularName" : "GorriÃ³n casero",
         "language" : "spa",
         "sourceTaxonKey" : 102101640
      },
      {
         "vernacularName" : "Gorrión Común",
         "sourceTaxonKey" : 123213203,
         "language" : "spa"
      },
      {
         "language" : "spa",
         "sourceTaxonKey" : 101186844,
         "source" : "The European Nature Information System (EUNIS)",
         "vernacularName" : "Gorrión Común"
      },
      {
         "language" : "spa",
         "sourceTaxonKey" : 114130266,
         "source" : "Colaboraciones Americanas Sobre Aves",
         "vernacularName" : "Gorrión casero"
      },
      {
         "vernacularName" : "Gorrión casero",
         "source" : "Yanayacu Natural History Research Group",
         "sourceTaxonKey" : 119245200,
         "language" : "spa"
      },
      {
         "vernacularName" : "Gorrión casero",
         "source" : "Catalogue of Life",
         "sourceTaxonKey" : 119950016,
         "language" : "spa"
      },
      {
         "language" : "swe",
         "sourceTaxonKey" : 101186844,
         "vernacularName" : "Gråsparv",
         "source" : "The European Nature Information System (EUNIS)"
      },
      {
         "vernacularName" : "Gråspurv",
         "language" : "dan",
         "sourceTaxonKey" : 123213203
      },
      {
         "vernacularName" : "Gråspurv",
         "language" : "nob",
         "sourceTaxonKey" : 123213203
      },
      {
         "language" : "deu",
         "sourceTaxonKey" : 116795880,
         "vernacularName" : "Haussperling",
         "source" : "Taxon list of animals with German names (worldwide) compiled at the SMNS",
         "country" : "DE"
      },
      {
         "language" : "deu",
         "sourceTaxonKey" : 100483595,
         "source" : "Belgian Species List",
         "country" : "BE",
         "vernacularName" : "Haussperling"
      },
      {
         "language" : "deu",
         "sourceTaxonKey" : 123213203,
         "vernacularName" : "Haussperling"
      },
      {
         "sourceTaxonKey" : 101186844,
         "language" : "deu",
         "source" : "The European Nature Information System (EUNIS)",
         "vernacularName" : "Haussperling"
      },
      {
         "source" : "The Clements Checklist",
         "vernacularName" : "House Sparrow",
         "language" : "eng",
         "sourceTaxonKey" : 113987294
      },
      {
         "vernacularName" : "House Sparrow",
         "source" : "Taxonomy in Flux Checklist",
         "language" : "eng",
         "sourceTaxonKey" : 100159046
      },
      {
         "source" : "Colaboraciones Americanas Sobre Aves",
         "vernacularName" : "House Sparrow",
         "language" : "eng",
         "sourceTaxonKey" : 114130266
      },
      {
         "sourceTaxonKey" : 102101640,
         "language" : "eng",
         "vernacularName" : "House Sparrow",
         "source" : "Integrated Taxonomic Information System (ITIS)"
      }
   ],
   "limit" : 20,
   "offset" : 0
}

Using this type of search: api.gbif.org/v1/species?name=Passer%20domesticus, you can look for all info for a particular species, starting from either a scientific name or a common name (in example, Passer domesticus).

GBIF includes information in 1,643,948 species (and counting), but I don't know for what proportion they have common names (or where there are common names).


This is the Sarcastic fringehead fish (Neoclinus blanchardi). [Source2]


Is it correct that the nicotinic acetylcholine receptor has nothing to do with Dopamin?

Let's simplify your question with correct terminology: you have a presynaptic neuron and a post-synaptic neuron. The presynaptic neuron can release multiple signals (neurotransmitters) into the synaptic space, or cleft. The postsynaptic neuron can be equipped with multiple sensors (receptors) that are specific to detect certain signals.

The signal and the sensor don't have to match, although this is costly if it's poorly tuned. Most neurons that are entirely unresponsive are pruned. Darwinian selection makes circuits much more efficient than what pure chance alone would produce, but remember that nature can be quite imperfect and stochastic.

However, you can have neurons that have a dopamine sensor (receptor) and provide an acetylcholine signal (neurotransmitter) and vice versa.

Acetylcholonergic and dopaminergic neurons can be connected. Here is an example.

Also, most people forget that neurons not only form chemical synapses but electrical synapses as well. That means the circuitry does not rely on ligands and receptors.


The question is quite unclear but I'll try to say a few words that may help you.

You seem to be considering evolution as an individual that decides what is good and what is not. You seem to be considering the evolution as determing at any time point what will be good for a given species. That sounds very wrong.

Evolution is much more than Natural Selection (NS) but for the purpose of this answer I will talk only about NS. NS is a differential of fitness. Fitness is a function of both the expected reproductive success and expected survival of an individual. The environment is part of what determines the fitness of an individual.

So the question, you might be willing to ask is why is having white fur advantageous for a polar bear. The answer is on this post. In short, polar bear live in a very cold climate and their white fur is actually made of clear tubule which let the sun get through and reach their black skin. If it is unclear for you why dark matter warms up faster than lighter matter, you might want to follow a short physics lecture on light.

I would recommend that you have a look at a very introductory class to evolutionary biology such as Understanding Evolution by UC Berkeley for example. It is pretty short (much shorter than reading the book you're reading and you will learn so much more about evolution).

EDIT

I will not be able to explain you the basics of evolution theory entirely as it would not fit in a single post. So, I am reacting to your first comment but for the follow-up questions, please just have a look at an introductory source of information first and we will all gain lots of time. (No aggressivity here, I just want to avoid spending my day on this single post). Once you've finished an introductory course you are very welcome to ask further questions. Btw, evolutionary biology is a very big field. There are a large number of researchers (me and other users on this website included) who work during their whole to further our understanding of evolutionary processes.

  Natural selection must wait for these painstakingly slow changes to provide a large variety of options for it to choose from

This is wrong for two reasons. 1) NS tends to be a relatively fast process for rising the frequency of beneficial mutations. 2) NS does not give options to chose from. It is even the opposite NS remove options to keep only some of them. Mutations create options. In more correct terms, mutation increase the genetic variance while NS (and genetic drift that I haven't talked about yet) remove variation.

A1 allele is a very simple software for students in evolutionary biology that help the to simulate the action of NS and genetic drift on an already polymorphic locus. You might not understand what is meant by "polymorphic locus" but this just mean you need to have a look at an introductory course to evolutionary biology.

  if random changes in the cellular chemistry can suddenly alter the colour of hair from black to white, why cannot they change the colour of the hair from black to blue or red or crimson or violet or green, how did cellular chemistry know that what was needed in the arctic climate was only white?

Well, again the hairs aren't really white!

Mutation are random (although this statement can be misleading because there is variation in mutation rate). A mutation is just a "mistake" done during the replication of DNA. An organism does not make mutations to achieve a particular goal. It just make mutations. This is why the vast majority of mutations are deleterious (=decrease the fitness of the individual carrying it).

Now, some mutational effect (in terms of phenotype and not fitness) are more likely than others. For example, a polar bear may already produce a number of pigments that it could "easily" use for colouring its hairs. For example, a polar bear already produces dark pigments (such as melanin) and it is reltaively likely for that a single mutation could darken the fur of the polar bear. If having darker fur was beneficial then this mutation would increase in frequency in the population(assuming no genetic drift which is wrong but this is a story for another time). On the other hand, a polar bear does not produce violet pigments (to my knowledge). As a consequence, it would take a much larger number of mutation (each of which aren't necessarily beneficial) for a population of polar to have a light violet fur (and we would need to assume that having a light violet fur is beneficial).


According to PDB (protein data bank — a repository for protein structures) the chromophore must be protected from interaction with water molecules to fluoresce.

  The chromophore is found right in the middle of the [protein], totally shielded from the surrounding environment. This shielding is essential for the fluorescence. The jostling water molecules would normally rob the chromophore of its energy once it absorbs a photon. But inside the protein, it is protected, releasing the energy instead as a slightly less energetic photon of light.

This means that denaturing the protein will result in quenching of the fluorescence1, so you are unlikely to see significant signal on a denaturing gel.  In fact, as WYSIWYG has pointed out, fluorescence has been used as a marker of renaturation of GFP1.

Reference:
1: R.Y. Tsien (1998) The green fluorescent protein. Annual Review of Biochemistry 67, 509-544.


Shimadzu explains peptide mapping as follows:

  Peptide mapping involves selectively cleaving the individual target [proteins] using an appropriate enzyme or chemical and analyzing the peptide fragments obtained using HPLC [high-performance liquid chromatography] or another suitable method. [... I]dentification of the peptide fragments separated by LC [...] [can be done] using amino acid composition analysis, N-terminal amino acid sequence analysis, or mass spectrometry.

As such, it does not provide a sequence of amino acids. Instead, you get a specific set of peptides of different sizes, dependent on the method used, that in turn can be used for protein fingerprinting.


If a person is infected with an RNA virus what percentage of the RNA in the blood of the person contains RNA of the virus?

I think your question is:

  Can you diagnose someone with an RNA virus by looking for that RNA in their blood?

The use of nucleic acid tests, or NATs in diagnosis has been around for a long time. The specific for profit company you mention is not the first to use them. Almost all NATs work by first amplifying the genetic material with PCR or other methods, so there does not need to be a large proportion of pathogen RNA vs total RNA in a sample in order to use a NAT.

NATs, rather than culture or antigen/antibody based tests, provide the definitive diagnosis for many viruses, RNA viruses included. As the CDC describes, NATs (among other tests) are also used to screen donated blood for RNA viruses (HCV, HIV, and West Nile).

Incidentally, the for profit company you mentioned does NOT detect all bacteria and DNA-viruses in the sample as you said. It screens for a large number of specific pathogens in their

  proprietary micro-organism reference database


Which cells are responsible for the extracellular matrix remodeling?

Taken from The role of matrix metalloproteinases (MMPs) in the pathophysiology of chronic obstructive pulmonary disease

  Metalloelastase (MMP-12) is (as the name suggests) capable of
  degrading elastin, as well as other extra-cellular matrix components.
  It is produced predominantly by infiltrating macrophages and appears
  essential for macrophage migration through extra-cellular matrix

Matrix Metalloproteinases in Cancer Cell Invasion gives a more thorough description of the various MMP and TIMP types

  MMPs are mainly produced by nonmalignant stromal cells in malignant
  tumors. Tumor cells also secrete factors, such as extracellular MMP
  inducer (EMMPRIN), which enhance the expression of MMPs by stromal
  fibroblasts (see Toole, in this book). In addition, growth factors and
  cytokines secreted by tumor-infiltrating inflammatory cells as well as
  by tumor or stromal cells modulate MMP expression.


What "algorithm" are carnivorous larvae using when foraging?

I'm going to assume that when you say algorithms, you mean the forms of innate behavior an organism may have relating to their senses (e.g. when sunlight is detected by a worm through the photoreceptors in their skin, it will move towards the opposite direction of the source of light to stay in their preferred environment).
These mentioned species of insects are very different taxonomically, but their number of sensory organs are for most part similar including during larval stages.
Examples of innate behavioural responses seen in invertebrates include taxis and kinesis.
Taxis is a change in movement in response to an environmental stimulus – either towards (positive) or away (negative)
Kinesis is a change in the rate of activity in response to an environmental stimulus
So, when talking about rough algorithms, when a larva detects a particular stimulus (e.g. chemicals of prey via chemoreceptors),  The organism will either have a 1 or a -1 value for Taxis response (e.g. it runs towards or away from the prey), and a rate of activity relative to taxis which represents kinesis (e.g. it gradually moves faster towards the prey as the chemical stimulus becomes stronger (meters per hour for example).
So, you could say that the theoretical formula/algorithm for hunting prey relating to the chemoreceptors as an example would be:
Taxis ('1' or '-1' to symbolize moving towards or away from a prey) multiplied by the number of 'prey' chemicals received by the chemoreceptors equaling the strength of the larva's response which could be (as an example) translated to the velocity of larva
Of course all the other senses such as photoreceptors and the chordotonal organ (vibration sensor) must be considered and I couldn't find any actual algorithm for how these species hunt. This is just a way to percieve how insects both in and past their larval stages respond to stimuli through their innate behaviour.


I am going to assume you have a count table that you are starting with. Every tool you decide to use is going to have its own respective instructions so let me get you pointed in a direction to find one that works for you.

I wrote a simple R package for my lab awhile back but there are much better ways to put together Co-occurrence networks (in no particular order):

SparCC
CoNet
MENA
Spiec-Easi
MDiNE

Now speaking specifically about "hubs", "connectors", and other keystone organisms, I would recommend reading more about what they are and how they were developed. Again, I have a brief summary here but the original "hub" came from a paper on bee pollination networks


How long can a plant generate oxygen from its own carbon dioxide, produced during nighttime?

For how long could the plant generate $\ce{O2}$ from its own $\ce{CO2}$, produced during night?

Plants do not generate $\ce{O2}$ from $\ce{CO2}$.

Photosynthesis consists of two general steps, one that requires light and one that does not. The first step occurs in the thylakoid membrane, and splits water into oxygen, hydrogen ions, and energy. The second step is the carbon fixation step, which occurs in the chloroplasts and uses energy to convert the carbon dioxide into carbohydrates.

Step 1: $\ce{2 H2O + light → 2 H+ + O2 + energy}$

Step 2: $\ce{3 CO2 + 6 H+ + energy → C3H6O3-P + 3 H2O}$

The more detailed chemical equations can be found on the Wikipedia Photosynthesis page.

Since the first step which produced oxygen is light-dependent, it occurs mostly during the daytime. To keep growing during the night, the plants break down the carbohydrates they produced and stored during the day. This cellular respiration uses up oxygen and generates carbon dioxide just as animals do.

Will the plant eventually run out of oxygen at night?

As mentioned, plants require oxygen for cellular respiration, which occurs both at day and night. The difference is that during the night, they are not producing oxygen via photosynthesis. Assuming the plant is in sufficient light and temperature conditions during the day, the plant will not run out of oxygen at night. Plants can survive in sealed environments for very long times. A fun example is a reportedly 53 year-old bottle garden. In a bottle garden, which is essentially the system you are creating, the only difference from a plant out in the environment is that the same oxygen, carbon, and hydrogen molecules are constantly being recycled via photosynthesis and cellular respiration.


Recommendations for textbooks on statistical and quantitative genetics, and genetic epidemiology

For statistical genetics, take a look at:

Likelihood, Bayesian, and MCMC Methods in Quantitative Genetics. Daniel
Sorenson and Daniel Gianola. (2002. Springer).

Warning: heavy on math (calculus). If that doesn't scare you, it's excellent guide to non-frequentist statistical methods applied to problems in genetics.


I saw an excellent public science talk a few weeks ago. The speaker presented 5 questions which, if you answer yes to, you can only come to the conclusion that evolution exists. Firstly though we should define evolution: Evolution is the change in the inherited characteristics of biological populations over successive generations.

It was one of the best arguments I've seen put forward so I'll try to recreate it here. Put this to them and see what they say - and just in case they say no to any, I've put answers in for you ;) There is no hard evidence for the first four points because they are so damn obvious that if people say no, even after a logic based argument, then all they will ever say is no, they shouldn't need a scientific paper.

1) Do individuals reproduce?

The answer to this is undeniably yes, you were the result of reproduction. Reproduction exists.

2) Is there variation among individuals?

Yes, again this is undeniable. Do we all look and act the same? No. Are some people taller than others? Yes. Some more physically fit than others? Yes. Is everyone's hair or eye color the same? No. See, undeniable. Variation exists.

3) Do some individuals die before they get to reproduce?

Obviously yes. Children unfortunately die (of natural causes) which means they do no get to reproduce. Just go look in a cemetery or open the obituaries page of you newspaper and you'll likely find some one who died before they could have reproduced. Some people also never reproduce, because of life choices or fertility problems. Variance in reproductive success exists.

4) Do offspring resemble parents?

The answer to this is also yes, when two humans reproduce they (normally) produce something that resembles a human. And when that human reaches maturity they will likely look a more like their parents than a random stranger. Personally I was looking at old family photos recently and I honestly though I had found a picture of me marrying my mother, that's how similar my dad and I look. Heritability of variance exists.

5) Does heritable variation lead to differences in reproductive success?

If you've answered yes to all of the above then you really should be answering yes to this one too. As a hypothetical illustrative scenario, imagine two male deer. One has big antlers and one has small antlers. The size of antlers is largely genetically determined. The male with big antlers is seen as more attractive by a female. She chooses to mate with him. She gives birth to his offspring (n=2, 1 male 1 female) who inherit his genes for large antlers. This repeats with several females in the population (n=10). The smaller male has fewer mating events (n=2) and therefore sires fewer males in the next generation. The next generation contains more males with large antlers (n=10) than small antlers (n=2). This is evolution, the change in the inherited characteristics of biological populations over successive generations.

Another example is humans. We know some men have low sperm counts leading to low probability of successful mating. Further, we know that male infertility can be genetically caused for example by Y-linked genetic defects. Therefore we can expect that males with low sperm counts, caused by Y-linked defects, will have fewer offspring than a healthy male (given equal opportunity to mate) and because all males inherit their fathers Y chromosome they too will have low sperm counts. They will be represented at a lower level in the population's next generation. Again, this is evolution.

Speciation:

It then doesn't take much to jump from this to speciation. It involves the introduction of isolating mechanisms. These can be things like geography (allopatric speciation), or sympatric mechanisms like morphology, behavior, or any trait which prevents one group of individuals mating with another.

I'll illustrate first, and take the more difficult type - sympatric speciation. Again imagine our deer population. This time there is variance in sperm morphology, and female reproductive tracts. Males can produce two different types of sperm, one (male type S) is a slow moving but more resistant to the hostile female reproductive tract (because it is resistant to all types of antibody the females can produce), the other is faster (male type F) but less resistant (because it is resistant to only some of antibody the females can produce). Female reproductive tracts vary in the number of different antibodies they produce, one produces "all" that can be produced (female type R) and the other only a subset of the full array (female type W).

What will happen is that type S males will be more successful when mating with type R females because their sperm survive (whereas type F males have no sperm fertilizing the egg). However, type F males will be more successful in sperm competition than type S when mating to type W females. Repeated over many generations, these incompatibilities will cause distinct mating groups which do not overlap, i.e. species.

In reality it is much simpler to demonstrate this with allopatric speciation. Here two groups of one species become isolated by a geographical feature, like a river. Over time these populations evolve differently (because genetic mutation is random and selection might differ on opposite sides of the river). When they get the opportunity to mate after X generations, they can't because they have evolved genetic incompatibilities (offspring fail to survive, eggs can't bee fertilized).

One of the absolute classic examples is an experiment using fruit flies by Diane Dodd.   In her experiment she reared a population in two groups, one on starch based food, and one on maltose based food. After many generations (35 I think) the two groups showed mating preference, which is a reproductive isolating barrier, within their groups (mating pairs were more often formed from within treatments). Here is the paper.

Picture from http://evolution.berkeley.edu/


Meiosis does not determine sexual form. Eukaryotes use meiosis and fertilization to recombine genes to form new combinations.  Meiosis does produce haploid cells from diploid cells, but that has nothing much to do with the sexual forms involved.

In the case of the algal genus Chara, the organism's life cycle is entirely haploid except for the single-celled zygote formed during fertilization; this is called a haplontic life cycle.  Being haploid does not require an organism to be of one sex (or any sex), so there is no difficulty to being monoecious and having both male and female structures on a single organism.  The reason for having two kinds of gametes, sperm and ova, is simply practical: the specialized job of sperm is to move to another gamete, adn the job of the ova is to provide a maximum amount of nutrition for the future zygote (which means larger size and hence limited mobility).


Is sex linked inheritance independent of dominance?

Drosophila follow the same sex determination as in humans, XY for males, XX for females. The eye colour is sex linked, that is, the genes for eye colour are only carried on the X chromosone in this case, not the Y (there are other linkages that are only carried on the Y, but that's not the case here). The wild-type colour, red, is dominant over the white eye colour. When speaking of inheritance of eye colour in drosophila males specifically, you don't need to consider dominance or recessiveness as males only get one copy carried on the X - either the wild type red, or white, there is no interaction between alleles. The dominance and recessiveness only comes in to play with the eye colour of females, as they get two copies, one on each X they get from the parents, in which case the heterozygous will appear red eyed, as will the homozygous for the red eye allele.

For the image: In this cross we have a heterozygous red eyed female (XWXw) crossed with a white eyed male (XwY). In the offspring you see that half of the females would be heterozygous for red eyes, thus presenting as red eyed, and half would be homozygous for white. In the males half would be red eyed and half white eyed as there is no dominance or interaction between alleles as they only have the single copy on the single X chromosome they have inherited.

Hope this makes sense!

With all that in mind, you are right, you will only get white eye males in the F1 generation if the mother in a cross is heterozygous for the eye colour trait.


Let me first clarify the difference between anaerobic respiration and fermentation.
Literally respiration refers to breathing, but its definition has been extended to include cellular metabolism that leads to ATP generation.

Fermentation, as you said depends on substrate level phosphorylation. Anaerobic respiration on the other hand just means ATP synthesis in the absence of oxygen- in other words anoxic. This happens in several cases in which the terminal electron acceptor is not oxygen but some other chemical species such as $Fe^{3+}$ or fumarate.

E.coli can carry out ETC mediated ATP synthesis both in the presence and absence of oxygen. At high oxygen concentration it uses $O_2$ as electron acceptor, mediated by cytochrome-d. At low oxygen concentration other kinds of cytochromes accumulate and the cell uses fumarate or nitrate as the terminal electron acceptor with the help of fumarate reductase and nitrate reductase respectively. This is an old article but is still quite informative. Check it out.
Fumarate and nitrate reductases are regulated as a part of what is known as FNR regulon. FNR is an oxygen-sensitive transcription regulator. In the presence of oxygen it is inactivated. In the absence of oxygen it activates the fumarate and nitrate reductase genes.

Perhaps in the absence of these alternate electron acceptors, the bacterium totally depends on SLP.


CRISPR guide RNA design and primer synthesis

A quick check with BLAST returned the following result:

Homo sapiens huntingtin (HTT), mRNA
Sequence ID: NM_002111.7Length: 13669Number of Matches: 1
Related Information
Gene-associated gene details
GEO Profiles-microarray expression data
PubChem BioAssay-bioactivity screening
Range 1: 267 to 286GenBankGraphicsNext MatchPrevious Match
Alignment statistics for match #1

Score           Expect  Identities  Gaps        Strand
40.1 bits(20)   0.017   20/20(100%) 0/20(0%)    Plus/Minus
Query  1    GGAGGCCTCGGGCCGACTCG  20
            ||||||||||||||||||||
Sbjct  286  GGAGGCCTCGGGCCGACTCG  267

The sequence you have is 5'-3' and it matches the Minus strand on the Human genome. You don't need to reverse the sequence!


Are there any enzymes in cytoplasm to help the newly-synthesized polypeptide to form tertiary structure?

There are several types of proteins that do this, all of which fall under the category of molecular chaperones. In particular, chaperonins such as GroEL/GroES complex in E. coli, sequester newly-formed polypeptides to allow them to fold their tertiary structure and avoid aggregation. Another widely studied class of these proteins are heat shock proteins (Hsps): these are involved generally in acclimating cells to stresses (such as heat), and some of these Hsps have been specifically implicated as chaperones. I'm a new user, so I can't post a 3rd link, but just google Heat shock proteins and you'll find plenty of information.


What is this fossilized claw found in a Belgian forest?

Looks like the proximal end of a rib of a large mammal (cow, horse, deer). Without information about how large it is, it is not possible to get closer to an identification. It's not a claw and very likely not a fossil. It just looks old and dirty.

Here's a horse rib cage (from https://www.rodnikkel.com/content/saddle-tree-blog-from-shop-and-desk/the-rib-cage/):

Ribs in the 4-7 range seem to be a good match for shape but not as much for roundness.


How does an excessive amount of beta carotene affect skin colour?

How much beta carotene does it take to change someones skin colour?

To turn the skin yellow, rather than orangish, a person would have to eat about 10 carrots a day for a period of at least two weeks, consuming at least 51 grams of beta-carotene each day. The average carrot contains about 5 to 6 milligrams of beta-carotene

What is the reason behind this?

A very high diet of food which contain carotenemia (such as carrots, squash, sweet potatoes and others) can cause skin discoloration. The skin, and especially the palms of the hands, turn yellow, rather than orange. This change in skin colour fades and eventually disappears when the individual's diet changes back to normal.

  Carotenoderma is deliberately caused by beta-carotenoid treatment of certain photosensitive dermatitis diseases such as erythropoietic protoporphyria, where beta carotene is prescribed in quantities which discolor the skin.

What does an excess of carotenoids do?

  An excess of carotenoids, being eliminated via sweat, may cause a marked orange discoloration of the outermost skin layer. This benign and reversible condition – which is most easily observed in light-skinned people and may be mistaken for jaundice – is known as carotenosis or carotenoderma.

sources:

https://en.wikipedia.org/wiki/Carotenosis
http://www.webmd.com/vitamins-supplements/ingredientmono-999-beta-carotene.aspx?activeingredientid=999&
http://umm.edu/health/medical/altmed/supplement/betacarotene
http://emedicine.medscape.com/article/1104368-overview


How much of the genetic differences between humans and chimpanzees are due to genetic drift?

The easiest way to track whether a particular protein-coding gene has diverged between two species because of drift or actively maintained selection is to look at the ratio of synonymous to nonsynonymous mutations within that gene. A synonymous mutation is one that doesn't change the identity of the amino acid within that protein; a nonsynonymous mutation is one that does. Synonymous mutations are neutral by definition; their presence gives us an idea of how much time has diverged and how frequently mutations in that protein coding region change over time.

A dN/dS (Nonsynonymous mutation to Synonymous mutation) ratio of 1 suggests that the primary driver of change between species is purely neutral change. That usually means that it doesn't matter what is going on with that protein and is a little unusual--I would primarily expect to see something like that in a gene that is on its way to becoming a pseudogene.

A ratio of less than one means that synonymous mutations are much more likely to persist in that region than nonsynonymous ones. This is usually a sign that purifying selection is happening--for whatever reason, it's important to the function of both species that those proteins stay relatively similar.

A ratio of more than 1 means that there is diverging or directional selection happening, and that that protein type is changing between the two species because selection is actively modifying one or both proteins.

Here is a paper specifically analyzing whole human and chimpanzee genomes using this metric.


Does CoA always bind to organic molecules through a thiol bond?

This is coenzyme A (CoA). As you can see, it has an -SH group at its end. So when it interacts with other reagents, it forms thiolesters. CoA is just shorter.


I don't think that all leads are available.

I looked at the Signals combobox for different databases. This combobox seems to be the list of all available leads.

For example, take a look at iafdb (Intracardiac Atrial Fibrillation Database). It will plot you an ECG containing leads II, V1 and aVF and some other leads.

Another example is the EEG database eegmmidb (EEG Motor Movement/Image Dataset) which contains many leads.

Look also at the mimic2wdb/39 (MIMIC II waveform database, version 3 part 9) which contains 4 ECG leads and some other parameters like breath rate.


What is the spacing between stop codon and transcription terminator?

In general, there is no need for a spacing between stop codon and terminator. They can be right next to each other.

When transcribed, transcription terminator forms a hairpin-like structure which interacts with the RNA polymerase to stop the transcription. Usually, the upstream sequence will not interact with the terminator and it will be transcribed normally. In a rare case the coding sequence might contain sequences that extend the hairpin and might result in interrupted translation. This can be avoided by doing a thermodynamical inspection of the secondary mRNA structure, but this is usually unnecessary.


RNA or ribosome, which one moves during translation?

Here's an example in which the ribosome is fixed:

During co-translational translocation, the ribosome is essentially anchored onto the ER membrane through the Sec61 complex. It certainly cannot move along the mRNA. The mRNA is fed through the ribosome and the nascent peptide traverses into the ER lumen.


Why do genes with closely related functions often reside on different chromosomes?

The thing we must remember is that during evolution, there occurs many events that may result in genomic reshuffling.

Considering your example of MHC, when we look into the evolution of the complexes

  The classical human MHC contains 224 genes, .... Antibody and T cell mediated immune responses against invading pathogens are initiated through MHC class I and class II molecules. These main components are not only missing from invertebrates, but are also not present in primitive jawless fish, such as hagfish and lamprey. MHC class I and II molecules do, however, exist in all jawed vertebrates, including the cartilaginous fish.

Now that tells us something in itself. If you observe the universal evolutionary tree, we can conclude that the hagfish and lamprey are most ancestral, especially compared to telostii. This is crucial when speaking in terms of evolution, as

  this demonstrates that the separation of the MHC class I and class II loci is characteristic of teleost fish, which represent half of all vertebrates. Since the genes of the immune system were present in the common ancestor of tetrapods and teleosts, the differences in their genomic organisation may be the result of lineage-specific chromosomal events such as duplications, inversions, deletions and translocations.

You can read more about the MHCs here:

Sambrook, Jennifer G., Felipe Figueroa, and Stephan Beck. "A genome-wide survey of Major Histocompatibility Complex (MHC) genes and their paralogues in zebrafish." BMC genomics 6.1 (2005): 152.

And thats usually the reason for the major changes you see. Often other changes occur, due to transposons, which cause pseudogenes to form and/or neofunctionaliation to occur. You can read about them here:

Feschotte, Cédric, and Ellen J. Pritham. "DNA transposons and the evolution of eukaryotic genomes." Annual review of genetics 41 (2007): 331.

I am fairly certain, that this applies practically to majority of the genes, that are not linked strongly genetically (http://learn.genetics.utah.edu/content/pigeons/geneticlinkage/).


Why do you retch when you see something disgusting?

Physiologically speaking, your body is reacting to something you have known associations learning. An extreme form of this phenomenon is seen in drug addiction.  After chronic use of a substance there are certain cues a person associates with the drug effects. Whether that be a certain group of people, a sound, a place, or an object the stimulant is eventually associated with the drug effect. After a certain amount of time a physiological reaction occurs with just the introduction to the stimulant without the drug. Often, if an addict receives a stimulation without a drug they are, at first, excited, calm, or feeling whatever the drug effects caused. But then, if no drug is received, the withdrawal effects come into play and makes the addict feel worse and crave the drug more intensely.

Anyway, so when you see something you associate with being gross or awful, your bodies physical reaction is essentially prepping you for the event.The biological and cellular effects of associative learning are regulated in the central nervous system (brain). The main theory is that the initial effect of the stimulus is regulated by dopaminergic channels, and the learning and associations are regulated by serotonergic channels. However, it is more like a complex network of synaptic channels at work in various parts of the brain. The regions known to be apart of associative learning are the emotional cortex of the brain are the amygdala, prefrontal cortex, and hippocampus.

For gastrointestinal upset the stimulus is most likely associated with an event that caused GI upset previously. For example, let's say you went out to a party and had too much to drink. You throw up everything you've eaten that day and you just generally feel awful and 'sick to your stomach.' Now, every time you see, smell, or taste that brand or flavor of alcohol you consumed, you immediately gag because your body is remembering the previous event and associates that stimulus with the vomiting and sick feeling. Does that make sense? Let me know if you would like more clarification.

Sources:

Drug Addiction Drug Habituation - Profiles in Science
Control of cocaine-seeking behavior by drug-associated stimuli in rats: Effects on recovery of extinguished operant-responding and extracellular dopamine levels in amygdala and nucleus accumbens
Neural and psychological mechanisms underlying appetitive learning: links to drug addiction
Physcopharmacology by: Meyer and Quenzer (ISBN 978-0-87893-510-9) (best source)


Why are smaller mammals more prone to cancer and tumors

The topic is called Peto's paradox, you can find references to studies on the wiki page, here's a summary:

A rat cell is more likely to get cancer than an elephant cell in the same time span. Mice have cancers in 2 years as often as humans have in 60 years.

Studies find that 4 ton elephants have only 4 times more blood cells than a 12 gram shrew. They have big mammal cells that divide at a slower rate. Rats can double their body weight every 10 days when they are teenagers, as if a puppy with a lot of appetite could become an adult dog in 30 days.

It is thought that the genetic safeguards that have evolved to protect large mammals against cancer would slow the growth and reproduction rates of small mammals. For example, an elephant has 14 copies of the cancer suppression gene TP53, humans have three copies, hyraxes and manatees have one copy.

Evidence for the paradox began to emerge in the 1970's. Studies from zoos on many mammal species have confirmed that big animals are protected from higher cancer rates.

https://en.wikipedia.org/wiki/Peto%27s_paradox


Why do some animals and fungi prefer asexual reproduction?

Here is a quite intuitive and straight forward possible explanation:

The key is to rephrase "if the conditions are bad" into "if the focal individual don't fit its environment" or "if the genome of the focal individual is not fit" or "if the focal individual is not fit".

If an individual has a high fitness, it has better to create clones which will be fit as well.

If an individual is not fit, it has better to take the risk to reproduce sexually hoping that some of the offsprings will be fit thanks random recombinations and mutations (there are usually much more mutations during meiosis than during mitosis).

Note:

Sex allocation and evolution of sex is a very broad subject. Your question is linked with discussion on sex allocation. You might be interested by these books:

Eric Charnov
Stuart West
Perrin and Beukeboom

But you might simply have a first look through wikipedia sex allocation, Muller's ratchet or have a look to the diversity of reproduction. You could also have a look to specialized literature, the work of S. Otto for example. Usually introductory books on evolutionary biology contain a chapter on the evolution and diversity of sexual reproduction.


Do all multiple sequence alignments employ global alignment algorithms?

It is dangerous to generalize, as different multiple sequence alignment (MSA) programs may well employ different algorithms. However as the objective is to align many sequences along their whole length, and all MSA programs of which I am aware present the results as such, it is difficult to envisage anything other than global alignment being employed.

For the widely used Clustal W and X, this is certainly the case. Clustal employs a progressive alignment algorithm which involves the heuristic assumption that the most closely aligned sequences by pairwise alignment are a valid basis for the order in which progressive multiple alignment is performed. The initial pairwise alignments (which are used to produce a guide tree) use dynamic global alignment, as does each progressive alignment step, although this alignment is to a profile of previously aligned sequences, and uses context-dependent scoring.

There is an extensive Wikipedia article on MSA and one of the original Clustal papers is freely available on-line. The excellent book by Durbin et al., Biological Sequence Analysis, contains a chapter on the topic.


Could hydrogen replace oxygen in cellular respiration?

No, hydrogen could not replace oxygen because it has entirely different characteristics. The most important one is probably its electronegativity - oxygen 'pulls' electrons much 'stronger' than hydrogen.

Basics: Reduction potential

Oxygen is the so-called terminal electron acceptor of the electron transport chain in eukaryotes. You can see "reduction potential" as a kind of stored "energy" which molecules have, similar to the power stored in batteries (very similar actually). To make this text a bit shorter I'll call it "RP" from now on.

One maybe confusing detail is that a substance with low RP has "more energy" than a substance with high RP, so it is the opposite way of thinking.

In very generalised terms, metabolism means that molecules with a low RP (glucose) are oxidised (burned) and turn into molecules with much higher RP (CO2). Coupled with this, a different molecule with very high RP (oxygen) is reduced and becomes a molecule with slightly lower RP (H2O). (You may have heard this before - it's called a redox reaction.) *

The important part is that the RP "released" by the oxidisation (burning) is larger than the RP "taken up" by the reduction. The surplus leaves as energy - heat and light if you just burn the glucose. This is a spontaneous process, meaning it will occur just by itself - even if it takes a long time if nobody drops a match on it.

The idea of metabolism is to let that process happen - but use as much of the energy it releases as possible. This works by not just letting it burn, but intercepting that burning process at different stages so that at each step a bit of the RP can be taken off and stored in something else. This "something else" is NAD which I'm sure you've encountered before. Each step that glucose is burned down, another bit of NADH is made, which then has a respectable reduction potential.

NADH (leaving out NADPH here which is a bit different) is channeled into a process called oxidative phosphorylation which retrieves the reduction potential in an actual form of energy.

Basics: Terminal electron acceptor

Finally, the reduction potential I've been talking about all the time is really just electrons, involved in bonds which are "happy" to react. Passing down the reduction potential as I've explained is really a passing down of electrons into more and more stable, less reactive bonds. That's why it's called "electron transport chain". At the end of oxidative phosphorylation, those electrons are dropped onto O2 and make it into H2O. That's why O2 is called the "terminal electron acceptor".

Why Hydrogen can't replace Oxygen

Now to come back to why hydrogen cannot perform oxygen's function in our body. We use glucose as our source of reduction power and oxygen as our terminal electron acceptor. O has a high electronegativity (3.5) so it pulls electrons strongly towards it. H's electronegativity is only 2.1, so it's much weaker. O as a terminal electron acceptor works because it pulls them much stronger than H when they bond, so an O-H bond is almost like giving oxygen an electron. In order for hydrogen gas (H2) to perform the same function, it would need to be possible to drop electrons onto hydrogen in a bond where it pulls them much stronger than the other partner. They do exist, and such compounds are called hydrides. But the catch is: unlike H2O, these are normally strong reducing agents, meaning that hydrogen would rather not be in that bond. This not a feasible option for cell respiration, at least in humans, because it requires a lot of RP input. Making oxygen into H2O does not require a lot, it's a very cheap electron acceptor.

I hope I was able to put this in understandable terms. Let me know if I need to clarify anything.

--

*It works with other molecules than glucose->CO2 / O2->H2O too, many prokaryotes do that and in fact that's how batteries work


Fisher's Fundamental Theorem of Natural Selection

I don't think that you need to look further than the Price equation, which is basically a proof of a generalized version of Fisher's fundamental theorem. Price had a series of papers in the 70's that derived and applied the Price equation (e.g. Price, 1970; Price, 1972a), but most relevant for your question in probably Price (1972b).

A nice summary of Price's legacy can be found in Frank (1995).


Do human visual functions degenerate due to genetic factors or by external factors?

Vision deteriorates for both reasons, but I'm not quite sure how to separate the effects of aging from wear and tear.

Cataracts are the leading cause of blindness in the world. Ways in which environment (which falls under the category of wear and tear in my book) affects cataract formation:

UV light: people living at high altitudes (e.g. Tibet) have more cataracts 2° to increased UV light than those at lower altitudes (sunglasses with UV protection delays the process)
lead exposure increases cataract formation.
infections in infancy and childhood (rubella, toxoplasmosis, other)

Macular degeneration is another cause of vision loss. Environmental factors include:

smoking: speeds up age related macular degeneration.
diet: diets low in antioxidants, and obesity increase degeneration.

Retinal damage caused by diabetic retinopathy:

Juvenile onset diabetes has long been thought to be associated with viral infections from coxsackievirus B, cytomegalovirus, adenovirus, rubella, and mumps.
Type II diabetes is influences by obesity, lack of exercise, certain medications, (nicotinic acid, some diuretics, anti-epileptics, psychiatric drugs, and drugs to treat HIV (can impair beta cells or disrupt insulin action); Pentamidine (used to treat a type of pneumonia) can cause pancreatitis and diabetes; glucocorticoids/steroid hormones may impair insulin action.

Corneal opacities:

infections: (Chlamydia trachomatis) bacteria that are spread by close contact with an infected person or by flies, especially common in Africa.
recurrent injury (soot and pathogens from indoor smoke, a dusty, windy environment).
vitamin A deficiency

Nearsightedness:
- near-point work: reading, working with a computer all day, etc.

Glaucoma:
- diabetes, obesity, near-point work, other.

Nonenvironmental causes would be genetics and illnesses associated with aging.

genetic predispositions associated with diabetes, nearsightedness and farsightedness
decreased lens plasticity with age
strokes secondary to hypertension, etc.
amblyopia (“lazy eye”), strabismus (when eyes are aligned in different directions), astigmatisms
hereditary causes of glaucoma and age-related macular degeneration
retinitis pigmentosa, (degenerative disease of the retina)
innumerable genetic disorders (Marfan's, Tay-Sachs, Albinism, Cone-rod dystrophy, various autoimune disorders, etc.
retinoblastoma
predisposition to glaucoma

 Focusing on Vision Through an Environmental Lens
 Glossary of Eye Conditions
 Causes of Diabetes
 Inherited Eye Disease