I will clarify your question a little. We start with two men, Dave and John. We know Dave and John are related, either as brothers, or parent-child. Can we use genetics to work out their relationship?

If Dave and John are brothers they will have the same mtDNA, the DNA in the mitochondria, because mitochondria are maternally inherited. They should have the same Y chromosome, because they have the same father (the Y comes from the father, and males have one Y to pass on, therefore they each received the same Y).

If Dave (John) is John's (Dave's) father, then they should have different mtDNA because they have different mothers (assuming that Dave (John) didn't have a child with his mother or sister, and that mtDNA is variable within the population). They would have the same Y chromosome, because that is paternally inherited.

If Dave and John have the same X chromosome it would be indicative of the same mother (there is a 50% probability that two male siblings will have the same X chromosome, while the probability of a father and son having the same X chromosome would be determined by variability of the X chromosomes within the population).

For the autosomal part of the genome, each parent carries two copies of each gene. This means that, in each gene, there is the potential for four different alleles, with two of those being passed to the offspring. For example, at gene $A$ the mother may have alleles $A_1$ and $A_2$, while the father has $A_3$ and $A_4$. The offspring receives one copy from each parent, with equal probability. The probability that a son receives $A_3$ from the father is 50%. The probability that a second son receives the same $A_3$ allele is 50%. Therefore, both father-son and brother-brother relationships have a coefficient of relationship of 0.5.

In summary, the mtDNA will liekly be the best indicator, but it is only indicative, it is possible (but highly unlikely in most modern societies) for father and son to share the same mtDNA.

You could, in principle, work out whether Dave is John's son or his father. For example (a really over simplified example), look at the diagram below. You first look at Dave's sequence and one chromosome in a pair has the sequence AAAAAAAAAA (Red chromosome) while the other has GGGGGGGGGG (Yellow chromosome). You then look at John's sequence and find one chromosome with the sequence TTTTTTTTTT (Green chromosome) and one with the sequence AAAAGGGGGG (Red & Yellow Chromosome). John could have received the AAAAGGGGGG chromosome from Dave after Dave's red and yellow chromosome recombined, while it is not possible that John is the father of Dave. John's green chromosome came from his mother.


It means that 85% of its genome is coded for proteins (ORFs). The other 15% not, so these can be regulatory elements, repeats, or other.

You can measure that by measuring the total length of all ORFs, and compare it with the total length of the genome.


Is it possible to reduce maturity time of plants with biotechnology?

Perhaps investigate the families of YUC genes that synthesize the growth hormone auxin (ncbi.nlm.nih.gov/pmc/articles/PMC6941117) and ARF genes (ncbi.nlm.nih.gov/pmc/articles/PMC4737911) that respond to auxin. Auxin overproduction or changes to ARFs might speed growth. But some herbicides are synthetic auxins (e.g. 2,4-D) and work by exhausting and killing weeds (en.wikipedia.org/wiki/2,4-Dichlorophenoxyacetic_acid), so modifying these pathways may have unwanted side effects, depending on the crop.


How much pollen is needed to pollinate a flower?

A single ovule in a fruit is pollinated by a single grain of pollen. So, in theory, a fruit with n seeds can be pollinated by n grains of pollen. In reality, of course, not every pollen grain makes it to the ovules, but if we treat your assumption as true, then a flower can be fully pollinated by as many pollen grains as there are ovules in the flower.

If you plant your zucchini and cross your zucchini flower with pollen from spaghetti squash and orange-fleshed squash, you will end up with a zucchini fruit filled with seeds that are either half spaghetti squash or half orange-fleshed squash. If you planted the seeds from that zucchini, you would end up with some individual plants that have spaghetti-squash traits and some with orange-fleshed squash traits. You would not end up with any plants with both stringy and orange-fleshed fruit.


What does this biomass measurement mean and how to translate it to volume

50 g m-2 d-1 translates to "50 grams per square meter per day": the negative signs are negative exponents (check a math textbook). This is equivalent to writing

((50 g)/m2)/day

You cannot transform this into volume, doing so would lose the meaning: if you are talking about biomass growth of 50 grams per square meter per day, you are saying that there is 50 grams of new biological material produced within a square meter of land (say, a patch of grassland or forest). Talking about it in terms of volume doesn't make sense because the "height" coordinate doesn't produce additional biomass, since the source of energy is the sun.


Ideal lab glassware cleaner for molecular biologist

If you're just using it for hand washing, you probably don't need an ultra-concentrated solution. A very small amount of detergent goes a long way. (Think about it - what would you do with an ultra-concentrated solution? Probably squirt a small amount on the glassware and then add water.)

What I've seen done is to make your "dilute" solution of Alconox, put it in a squirt bottle, and then use a healthy squirt of it when washing. In fact, you probably find you don't even need a healthy squirt of it. A small amount of even the dilute solution is fine.

The approaches I've seen have been rather cavalier - basically just throwing a bunch of the powder in the squirt bottle and filling it with water. You quickly get a sense of how much will dissolve, and if you use a squirt bottle with a drop tube that doesn't go all the way to the bottom, you don't need to worry if not all of it dissolves.

Alternatively, as you you seem the fastidious type, you can fill another (non-squirt) bottle partway with Alconox, the rest of the way with water and let that sit (perhaps with occasional mixing). This should give you a saturated Alconox solution, which you can use to fill the squirt bottle, being careful not to transfer residual powder from the bottle. Then you can add more Alconox powder and water to the stock bottle, let dissolve, and you should be ready for the next time.

Again, this may only give you a 10-20% solution of Alconox in water, but that should be more than sufficiently concentrated for most usages.


Salbutamol's Pathways of Interaction and Classification

An agonist works with the receptor: a substance that initiates a physiological response when combined with a receptor; in the case of salbutamol (or albutarol in the US) they activate the beta-2 receptor on the muscles surrounding the airways. They are also known as sympathomimetics, as they imitate β2 adrenergics.

A blocker (or antagonist) is one that that blocks the action of endogenous catecholamines; for that reason, they are also called sympatholytic: antagonistic to or inhibiting the transmission of nerve impulses in the sympathetic nervous system.

It appears you have experienced a simple confusion in terms. Salbutamol/albuterol is definitely a sympathomimetic, used extensively on asthma and COPD.

Pharmacology and Therapeutics of Bronchodilators


What kind of spider is this from Sydney, Australia?

Good news is that this is definitely not a funnel web spider (Atracinae), which, by the way, is not that dangerous✻.

The image doesn't have a good resolution, but that seems to be a spider from the Family Lycosidae, known as wolf spiders, more specifically Venatrix pictiventris.

Here is an image for comparisson:

Source: http://www.findaspider.org.au/find/spiders/497.htm

This is the distribution of Venatrix pictiventris in Australia, going from Tasmania to Queensland, with most observations in New South Wales:

✻ I advocate for the protection of sharks, spiders, snakes, bats etc. So, whenever I can, I try to demystify arachnophobia. People love saying that the funnel web is deadly and so on, but for you to have a better idea, moths (e.g. Lonomia) kill more people than spiders.


Is it known how the first viruses formed?

One of the main points of contention in the study of virus evolution is whether or not they appear before the last universal cellular ancestor (LUCA) or afterwards (commonly accepted: genes that "escaped" from host organisms aka the escape hypothesis or vagrancy hypothesis).  Basically though, the LUCA is the most recent ancestor that all organisms living on Earth are derived from.

Increasing evidence support that ancestry of viruses may predate the LUCA, for example an idea is that there "was an 'ancient virus world' of primordial replicators that existed before any cellular organisms and that both RNA (first) and DNA (later) viruses originated at this time, donating some features to the first cellular organisms.  However, "a competing theory is that RNA cells existed before the LUCA and that RNA viruses were parasites on these RNA cells that later evolved DNA as a way of escaping host cell responses."

So basically, some theories support the pre-LUCA ancient virus origin and some support post-LUCA.  Because it's impossible to replicate conditions from billions of years ago, several approaches using evolutionary genetics and probability models are recommended by the author of the paper, referenced below.  He also discusses the specific supporting criteria for the theories that you can read in greater detail.

Holmes, E. C. (2011). "What does virus evolution tell us about virus origins?" J Virol 85(11): 5247-5251.


Are CoA and CoAS the same thing in a compound?

To understand the nomenclature here it is very helpful to think about how Coenzyme A works. It has a thiol group (-SH) which can form a thioester bond to an acyl group.

So the sulphur in "CoA-S-R" is part of the CoA, and in "CoA-R" the sulfur is just not explicitly named. Those two mean exactly the same thing: Coenzyme A linked to R via a thioester on the thiol group.

One specific variant that is very important in biology is acetyl CoA. The chemical formula you mentioned (CH3C(=O)CoA) is acetyl CoA, and here the same as above applies and the sulphur is explicitly mentioned in the second one and implied in the first one.


Does the mutation CCR5-delta 32 increase the genetic info?

Whether or not a mutation changes the 'amount' (meaning the size of the genome) of genetic information present in an individual depends on the type of mutation and is independent on which gene is affected.

In general there are 3 types of mutations:

point mutation: this is the change of one base pair to another (e.g. A to C). The total amount of information/the size of the genome is unchanged.
deletion: this means that a certain stretch of DNA is missing, likely disrupting what was there before. The total amount of information/the size of the genome is reduced.
insertion: this means additional DNA was added at a certain place in the DNA and probably disrupts something that was there before. The total amount of information/the size of the genome is increased.

The CCR5-delta32 mutation is caused by the deletion of a few (only 32) base pairs, however this deletion causes a frame shift in the gene and therefore leads to an early stop codon, which renders the protein inactive.


No, it's only a very rough approximation.

I actually made a spreadsheet to figure this out.

The rows represent the composition as described by the quote.  I translated each into its appropriate chemical formula and converted all measurements to grams.  Then I found the atomic weight of each.  The gray area represents the grams of each element made up from that particular description, which are summed up in the first summary line.  The second summary line are the values as specified in The Last Word's link, which are based on a 70 kg (154 lb) person.

You can see that while some of the numbers are in the right ballpark, most are still off by significant amounts (the bottom row is percentage error - negative means the anime was too low, positive that it was too high).


Is the rate of photosynthesis higher than the rate of respiration?

The net exchange of gasses in any area will be different depending on the number of plants and what plants they are.  This is because it depends on the number and size of leaves, and because chlorophyll is essential for photosynthesis, it also depends on the amount of chlorophyll in the leaves. Therefore that part of the question is very broad.

Overall, photosynthesis (oxygen production) is higher than the rate of respiration in plants during a year.

Aerobic respiration continues all the time in plant cells (in light and in darkness), using up oxygen and making carbon dioxide. Photosynthesis, in contrast, occurs only in light and uses up carbon dioxide and makes oxygen. The more light there is, the more oxygen is produced.

There is a light intensity at which respiration and photosynthesis cancel each other out. This is called the compensation point. Below this level carbohydrates are used up and the plant cannot grow.

This and more can be read in this document from the Royal Society of Chemistry


DP is the total number of read bases spanning a particular position. If you add up the different AD, you should get a number close to DP, the difference being merely in how the reads are filtered in either set of numbers.


Can fructose take multiple forms ? Which of these structures of fructose is correct?

The two structures on the left are correct; the one on the upper left is the alpha-D-fructofuranose form, while the one on the lower left is the beta-D-fructofuranose form.
Fructose is a ketohexose (a six-carbon sugar with its carbonyl group present as a ketone group in the molecule's open-chain form); the carbonyl carbon (the 2-carbon, to be precise) is optically inactive in open-chain fructose, as the oxygen and two carbons bonded to it adopt a flat trigonal planar geometry, but, when the carbonyl group is attacked by the 5-carbon's hydroxyl group to form the cyclic fructofuranose (fructose in a five-membered ring) configuration, the 2-carbon changes from being part of a (trigonal planar) carbonyl to being part of a (tetrahedral) hemiketal, introducing an additional stereogenic center that wasn't present in the linear form.  The arrangement of the substituents around this new stereogenic center is essentially a random crapshoot, with half of the new fructofuranoses having the hydroxyl pointing in direction 1 and the hydroxymethyl pointing in direction 2 (the alpha form), and the other half having the hydroxymethyl pointing in direction 1 and the hydroxyl pointing in direction 2 (the beta form).
There are, by the way, eight other configurations that fructose can take; three of them (plus the two you've already drawn) are for D-fructose (the naturally-occurring-in-the-vast-majority-of-naturally-occurring-fructoses form), while the remaining five are for L-fructose (which occurs only very rarely in nature and is essentially useless for most living organisms), which has the hydroxyls on the 3-, 4-, and 5-carbons pointing in the opposite direction.1

The alpha-D-fructopyranose and beta-D-fructopyranose forms have a six-membered pyranose ring, rather than the five-membered furanose ring; these are formed when the hydroxyl group attacking the carbonyl is that attached to the 6-carbon, rather than the 5-carbon, and are actually energetically much more favourable than the fructofuranose forms, making up essentially 100% of crystalline fructose and 70% of fructose in aqueous solution.
The open-chain D-fructose form is acyclic, with the 2-carbon actually being part of a carbonyl group rather than a hemiketal.  It is present in only minuscule concentrations in aqueous solution, but serves as the intermediate between all of the various cyclic forms of D-fructose.
L-fructose can adopt the alpha-L-fructofuranose, beta-L-fructofuranose, alpha-L-fructopyranose, beta-L-fructopyranose, or open-chain L-fructose forms, which are essentially equivalent to their D-fructose equivalents apart from their opposite chirality.

1: In the L-fructofuranose configurations, this takes the form of the hydroxymethyl group hanging off the 5-carbon pointing down rather than up.


What is the difference between phylogenetic tree "construction" and "reconstruction"?

There is no difference! In both cases, they refer to the building of a phylogenetic tree from data.

The expression 'phylogenetic tree construction' is less common.


What makes humans omnivores, and not herbivores?

As the answers given already point out, humans are generally considered omnivores that are able to use food sources available to them opportunistically. Apart from that, there actually is not much to debunk in the PETA statement - it is just a slightly one sided view on the history of human diet. Just as one sided as the claims that humans would not have evolved a really big brain without consuming animal products. Especially the canine teeth cannot be seen as evidence for prehistoric hunting, as in great apes the size of canine teeth is ridiculously well explained not only by defensive but mostly by mating behaviour; apart from that, humans do not even have those, and that most likely is caused by the trend towards monogamy which reduces inter-male aggression.

However, coming back to the actual question, in the relative short history (approx. 200-300ky) of our species there is evidence for 'several transitions towards or away from a vegetarian diet in humans' (Nielsen et al., 2017).

And in fact, there even is a human-specific evolutionary derived haplotype (younger than the Human-Neandertal split) that shows signatures of positive selection and is associated with increased efficiency in the synthesis of long chain fatty acid from plant precursor molecules - which would not really be necessary for meat eaters, as these fatty acids are readily available in animal products (Ameur et al., 2012). More specifically, the genes lying on that haplotype belong to the FADS cluster that seemed to have had adaptive value - also for synthesising long chain fatty acids from medium chain plant precursor fatty acids - in African populations even more recently (approx. 85 kya, Mathias et al. 2012).

This finding has been supported by a more recent study by Kothapalli et al. (2016). They investigated a 22bp-indel allele in the FADS2 gene that is associated with both higher blood levels of long chain fatty acids and exhibits high frequency (signature of positive selection) especially in South Asia and Africa where there is long tradition for plant-based diet.

Conclusion:

Modern humans (and this is relevant, as diet varies strongly between species and therefore the species comparison does not need to be very informative) appear to have changed diet frequently but there is evidence for human-specific molecular adaptations towards plant-based diets.


Why does the wavelength in curly hair differ?

My hypothesis when the curls are left ungroomed they will form knots. These knots form a barrier that works similar to woven wool. Unlike strait hair the mat of knots (dreadlocks) collect dirt and form denser material that insulates against direct light and mosquitoes better than strait material. The wave length does play a part as well. The smaller the wavelength the tighter the knot. The tightest knots are commonly found in places that have the most sun light per year.

Strait hair tends to keep heat in more and ice builds up less on it.


Why are vegetables either red or yellow?

A lot of fruit and veg are green when unripe and become brightly coloured when they are ready to eat (obviously not true for all, but most fruit/veg does).

This is probably deliberate as a mechanism to signal to birds and animals that it is ready to eat, so that they can disperse the seeds inside.

Red and Yellow are bright colours not usually seen on plants except of fruit/veg, and flowers (which are brightly coloured to attract bees and whatnot), so it makes sense these could be used as signals.

http://www.rosincerate.com/2015/07/colour-changing-fruits-and-veggies.html


The human body can not store Proteins (technically).
BACKGROUND :
PROTEIN is a very broad term and there are hundreds and thousands of proteins.[1]
Proteins are heteropolymers consisting of amino acids held by peptide bonds.
Amino acids :
There are 9 amino acids which we need to intake.

Phenylalanine, valine, threonine, tryptophan, methionine, leucine, isoleucine, lysine, and histidine.

Amino acids our bodies can produce:

These five are alanine, aspartic acid, asparagine, glutamic acid and serine.

These amino acids combine in different arrangements to give those thousands of Proteins. This process is carried out by Ribosomes (cook) and mRNA (recipe) inside every* cell.
Protein metabolism in humans :
During human digestion, proteins are broken down in the stomach to smaller polypeptide chains via hydrochloric acid and proteaseactions. This is crucial for the absorption of the essential amino acids that cannot be biosynthesized by the body.
Trypsin and Chymotrypsin as Trypsin and Chymotrypsinogen are the enzymes  necessary.
.
MAIN ANSWER  :
The excess Amino Acids are broken down into Glucose ( carbohydrate like stuff ) and the Nitrogen moiety is converted into Urea / Uric acids. This is then excreted by kidneys.

Amino acids can be broken down into precursors for glycolysis or the Krebs cycle.
Amino acids can also be used as a source of energy, especially in times of starvation. Because the processing of amino acids results in the creation of metabolic intermediates, including pyruvate, acetyl CoA, acetoacyl CoA and so on; amino acids can serve as a source of energy production through the Krebs cycle.

Therefore excess protein is simply used to make energy like carbs and the Nitrogen part is excreted. Now the excretion process can strain the kidneys due to increased work load, and prolonged stress can lead to malfunctions.
Also,
Our body is very concerned with conserving nitrogen levels, since our body can't fix nitrogen gas (N2) into ammonia (NH3). but, we can't just store huge amounts of ammonia because it's toxic. sugars and fats aren't toxic, so we can store them. because of this, our body either quickly utilizes excess ammonia to make nitrogenous compounds like amino acids and nucleotides, or it excretes it via Urea in our urine.
Problem with Protein storage :
If our bodies had to store proteins, it would need several sophisticated mechanisms and specialised storage cells.( Like we have adipose tissues short fats and lipids storage ).
if you examine the structure of amino acids, they are very similar to many of the carbon-hydrogen-oxygen metabolic intermediates. for example, alanine is an amidated pyruvate, glutamine is an amidated alpha-ketoglutarate, etc. many are easy to make, and most don't cost much to do so, so the body would rather use these intermediates to either:

Create acetyl-CoA, NADH, FADH2, and ATP for energy. this would happen during exercise or starvation.

Create glycogen, fatty acids, nucleotides, NADPH, and other metabolic compounds. this would occur after a big meal, during sleep, and when energy is not needed in high amounts. these compounds are very expensive ATP-wise.

So there's no need to store whole Amino Acids because they can be immediately used for whatever the body needs and then remade when necessary.
We do not store amino acids because we don't need to.
Right dose of Proteins :
Research shows:

A total of 80 g of whey protein was ingested in one of the following three conditions: 8 servings of 10 g every 1.5 h; 4 servings of 20 g every 3 h; or 2 servings of 40 g every 6 h. Results showed that MPS was greatest in those who consumed 4 servings of 20 g of protein, suggesting no additional benefit, and actually a lower rise in MPS when consuming the higher dosage (40 g) under the conditions imposed in the study.

Check here for the interesting results ( this is very relevant to your second question )
Therefore distributed intake of right amount of protein is important!
Scientific literatures :
Proteins:
https://en.wikipedia.org/wiki/Protein_(nutrient)
https://en.wikipedia.org/wiki/Amino_acid
Protein Metabolism:
https://opentextbc.ca/anatomyandphysiology/chapter/24-4-protein-metabolism/
Protein intake and storage:
https://newsnetwork.mayoclinic.org/discussion/are-you-getting-too-much-protein/
https://www.self.com/story/what-protein-does-in-your-body


Why are children and adults so different?

GREAT QUESTIONS!!!
Why delay sexual maturity in the first place?
-I believe it is also related to "the best-used" of resources. Firstly, it is unnecessary and impossible for children to have sex (biologically and evolutionarily), they don't have the physicality to sustain sexual intercourse or the ability to bear a children inside their body. Secondly, it is to focus resources on growth. Children uses lots of energy on growth. Human body does amazing jobs on allocating body resources or material so that we are in the best shape possible. If they don't do sex, they can focus more on growth.

Why tie sexual maturity to a host of other changes? For example, why aren't babies born with adult hair patterns? (Yes, because hair growth responds to sexual hormones, but the response could be different.)
- This one is a hard one. I believe it is just how biologists categorize human growth. We can study how human bodies develop in each stage, which is I believe it's really important on morphology.

Why the different body proportions?
-Evolutionary advantages!!! It is believed that baby has a greater head portion than adult. That's why people say children learn better than adults. Human values their brains more than other organs of the body, developing intellectual capacity as early as possible allows them to win in natural selection.

Why lose play behaviour and learning ability as adults?
If I understand you correctly, you are asking why adults lose their play behaviour and learning ability as they grow up. For learning ability, I believe it is caused by degeneration, just like the other organs of the heart. We have a mortal body and so once the body hits its maximum growth capacity, it will start going downhill unfortunately. For play behaviour, I believe it is a human behavioural changes due to life experience, social expectation and peer interaction. We lose interest of 'games' as we grow up because they are considered to be childish, silly and not useful.


Is there any species (subespecies?) whose DNA or RNA contains only in stem-loop structures?

The existence and importance of stem loop structures is well documented.

I'm not sure what the second question means exactly. If you mean 'an organism that has at least one stem loop, try HIV. The MS2 system is also a stem loop binding protein that's used as a tool a lot in biology, I suggest googling it.


Why do meristematic cells have prominent nuclei and dense cytoplasm?

Because meristamatic cells are the ones who are undergoing mitosis to increase the height of the plant, and diameter of the plant . They undergo continuous division. So y hey don't mature. They only form the primary cell wall.
I wrote another a answer.  Perhaps this will answer the question


When the pain receptors are fully loaded then it's not possible to excite these receptor greater. However the perception of pain has a large psychological component and is not well understood. Your brain could modulate your perception of pain naturally or due to illness.


The answer lies in the question. Liver cirrhosis constrains hepatocytes into small fibrous spaces limiting regeneration, hence the nodular pattern.
However,fibrous degeneration occurs in specific patterns. It can be located mostly around portal regions (centrolobular pattern) or diffusely through the whole lobule.

So basically, it is all good that hepatocytes can regenerate, but the limiting factor is not that. It is the structural impairment of the liver lobules and drainage system that will impair regeneration.

Moreover, most cirrhotic patients could not tolerate halving of their residual hepatic function. Not to mention the extensive surgery required. It would kill them swiftly.


Absorption of digested food in small intestine

In general:

Hydrophilic/polar/charged molecules require some kind of assisted transport across a membrane
Hydrophobic/nonpolar molecules can easily diffuse across a membrane

Glucose, galactose, and amino acids are hydrophilic. Fructose, fat-soluble vitamins, and short-chain fatty acids are hydrophobic.

Glucose and galactose have similar structures (aldose/pyranose) and are both hydrophilic. Fructose has a slightly different structure (ketose/furanose) which affects the way it is transported. Basically, it has a ketone (rather than an aldehyde) so it is relatively less reactive/polar. Because it is hydrophobic, it can diffuse across a membrane more easily.

"Since the concentration of fructose is higher in the lumen, fructose is able to flow down a concentration gradient into the enterocytes, assisted by transport proteins." (Wikipedia) Based on this statement, it seems that the lumen maintains a higher [fructose], relative to the enterocytes.

As explained in your link, glucose is mediated via SAT to ensure one direction of transport: we want glucose going only INTO our bloodstream. The [glucose] in lumen decreases after a meal, but we want glucose to keep being absorbed (hence SAT).. Also, unlike fructose, glucose and galactose are highly regulated for use in glycolysis, so it is important to keep glucose in the appropriate cells. In particular, because of its structure, fructose enters glycolysis after the "rate-limiting" phosphofructokinase step in glycolysis.

Quick notes on fat-soluble vitamin and short-chain fatty acids: they're both relatively small and hydrophobic. Short-chain fatty acids can easily diffuse across a membrane, which is also made of lipids. (I recommend reading about hydrophobic effect if you want to know more about this).. Larger fatty acids require shuttles because of their size.

Regarding "reabsorption" into the small intestine:
Diffusion is the result of the random motion of particles. The more collisions in a higher concentration region eventually leads to a net movement "down a gradient." Using this logic: at some point, yes, the molecule may go back out into the lumen or go back in ("reabsorb") because it basically follows the gradient.

(I may come back to this post after learning more about it in a few months.. I used most of my answer based on what I learned in nutrition, o-chem, biochem)

Read more here about fructose metabolism


What regulates these two methods of splicing?

As Alan Boyd said, this process is called trans splicing where exons of different RNAs are joined together. Physical proximity is conducive for trans-splicing. This study shows that trans-splicing frequency is higher if the genes are proximal. Proximity not only means closer in the genome but also the 3D proximity governed by chromosomal interactions.

Now, what factors  promote trans splicing is not properly understood.


How are non-glucose sugars metabolized in the body?

Where is this occurring in the body?

Almost totally in the liver.

To leave the liver as a sugar, it would have had to been converted to glucose, right?

Correct, but it's not a direct conversion.
Fructose is metabolized almost completely in the liver in humans, and is directed toward replenishment of liver glycogen and triglyceride synthesis...
...Increased concentrations of DHAP and glyceraldehyde-3-phosphate in the liver drive the gluconeogenic pathway toward glucose-6-phosphate, glucose-1-phosphate and glycogen formation. It appears that fructose is a better substrate for glycogen synthesis than glucose and that glycogen replenishment takes precedence over triglyceride formation. Once liver glycogen is replenished, the intermediates of fructose metabolism are primarily directed toward triglyceride synthesis.
So, Fructose is almost entirely made into something else first, and then that something (Glycogen or the Glycerol from triglycerides) gets broken down into Glucose or an intermediate.
Fructose stays in the liver because Fructokinase has a pretty low Km (0.5 mM) compared to Glucokinase (12mM) for Fructose, so almost all of the Fructose that enters the liver is phosphorylated into F1P - which cannot leave.


Why are there nail growth differences  between humans and other mammals?

Cat claws are growing all the time, like horse hooves, or human nails. However, cats and horses usually use their claws/hooves, so they get shortened through mechanical action.

An indoor cat may need their claws trimmed if it doesn't use them enough (that's why cats will want to scratch everywhere), or if has supernumerary toes that don't normally touch the ground. Similarly, cattle that doesn't get to move will suffer from hoof overgrowth, which appears to be very uncomfortable to the animal.

Consequently, if you were to use your fingernails more often for digging and scratching, you wouldn't have to trim them all the time.


Why is oxaloacetate made in the mitochondria?

Got it.  The ratio of [NADH]/[NAD+] is about 100000 lower in the cytosol than it is in the mitochondria.  The conversion of malate to OAA reduces a molecule of NAD+ to NADH, and that NADH can be used for the later step in gluconeogenesis: the conversion of 1,3-bisphosphoglycerate to glyceraldehyde 3-phosphate requires a molecule of NADH.


How many (taxonomic) families are there?

The NCBI Taxonomy statistics page displays the following information:

There are currently 73540 genera, 331418 species, and 23127 taxa of higher order. Since the number of taxa decreases with the genericity of the taxon, there are probably around 20000 families, give or take a few thousand.


Apparently, both are true.

  ...Individual differences exist in both odorant production and
  odor perception. The biological basis for the inability to produce the metabolite in detectable quantities is unknown, but the inability to smell the odor is associated with a single nucleotide polymorphism (rs4481887) within a 50-gene cluster of olfactory receptors. Pelchet et al. 2010

It's an open access paper (yay!), but to cut a long story short:

Pelchet et al. asked subjects to provide 'before-eating-asparagus'
and 'after-eating-asparagus' urine.
The subjects then acted as
urine-smellers for their own and others samples, and were asked to
choose between two unlabeled flasks which contained the 'before'
urine and which contained the 'asparagus' urine.
Most subjects produced 'asparagus' urine in which an odor was perceived
significantly more times than expected by chance, and
Most subjects perceived 'asparagus' urine correctly significantly more times than
expected by chance, however
~8% of subjects were non-producers, and
~6% of subjects were non-smellers.
Finally, looking at the actual amount of successes in perception: for
Caucasian subjects, one third of the variation in the amount of
correct odor perception was related to the A allele of rs4481887
(having AA or AG rather than GG). There was no connection between
this allele and production.

Pelchat, ML, C Bykowski, FF Duke, and DR Reed. 2010. Excretion and perception of a characteristic odor in urine after asparagus ingestion; A psychophysical and genetic study. Chemical Senses doi:10.1093/chemse/bjq081


Phyta means plant... The different 'phytae' mark different levels in the taxonomy...

Example:

Streptophyta from the Greek strepto, for twisted, i.e., the morphology of the sperm of some members and phyta (plant), a group including land plants and some algae

Embryophyta - land plants

Tracheophyta - vascular plants (from Ancient Greek τραχεῖα (trakheîa, “windpipe”) + -ophyta)

To answer your question... Phyta is a part of many plant taxonomy levels... It is not one type of plant but it marks the membership of a group to the kingdom of plants.


Yes, muscles do work as brakes; it's a process called eccentric contraction.

The energy balance of an eccentric contraction is a pretty difficult question. Some fairly recent research (Linari et al., 2003) found that a low velocities more energy is consumed (i.e. released as heat) even during eccentric contraction, while at high velocities, the muscle does store some energy from the eccentric motion. In frog muscles, at least.

So muscles do work a regenerative brake... in some conditions.

It's an active research topic where exactly this (non-heat) energy gets stored. Current models (in the previously cited paper) cannot account for all of what's measured experimentally; only 34% of it could be explained.


Can Alzheimer's disease be caused by Slow Prion infection?

Dr Yong in the paper titled Prion, The unconventional slow Infectious agent states that the formation of amyloid plaque which is a major contributor to Alzheimer's disease is a unconventionally slow infectious disease (Prion). Some papers have also pointed out the similarities between Alzheimers and prion disorders (reference) Cerebral amyloid plaques have also been identified in scrapie which is caused by a Prion. Discovery of a novel prion disorder (reference) with peripheral symptoms have led researchers to believe that protein misfolding, is the basis for most neuro-degenerative diseases, including Alzheimer's disease and Parkinson's disease.

With regard to your question, Alzheimer's has not been completely classified as a prion disorder as of now, but seeing that amyloid plaque formation (reference) and Creutzfeldt-Jakob disease (CJD) (a form of dementia) (reference) have been identified as being part of Prion disorders, it is highly likely that Alzheimer's is too.


It turns out sphingilipids have many functions in humans, many of which might still remain unknown. I will discuss here only the general, known functions  of sphingolipids, not about specific sphingolipids (as it'll make the answer too long).

Sphingolipids are believed to protect the cell surface from harmful external factors by forming a mechanically stable and chemically resistant outer leaflet of plasma membrane lipid bilayer.
Certain complex sphingolipids are known to be involved in cell signalling and cell recognition. It has been suggested that ceramide on the cell surface of one cell can be recognized by proteins on another cell's surface. Also, antibodies have been created which recognize the ceramide on a cell's surface1. All this suggests that sphingolipids play an important role in cell-cell interactions which lead to cell recognition and cell signalling.
Some simple sphingolipids, like ceramide and sphingosine-1-phosphate, have recently been shown to be mediators in signalling cascades involved in apoptosis2, proliferation3, necrosis4, inflammation5, autophagy6, senescence7, etc.
Ceramide-based lipids self-aggregate in cell membranes and form separate phases less fluid than the bulk phospholipids. These sphingolipid-based microdomains, or lipid rafts were originally proposed to sort membrane proteins along the cellular pathways of membrane transport8.
Studies indicate that proper sphingoid base synthesis is required to control protein phosphorylation events that are crucial for endocytosis and overexpression of protein kinase C1 (PKC1) and PKH1 or PKH2 (ortholgues of mammalian protein-phosphoinositide dependent protein kinase 1 or PDK1) restores the actin localization defects in the lcb1-100 mutant9,10. A suggested pathway representation would be like this11:

Decreased levels of ceramide and increased levels of sphingosine-1-phosphate are known to be mechanisms of tumor progression and drug resistance in cancer cells, and are hence being targeted in pharmacological experiments as possible cancer cures12.
Sphingolipid (mainly sphingomyelin, ceramide and gangliosides) reorganization and interaction with proteins within cellular membranes is suggested to cause many neurodegenerative disorders13.
Sphingolipids are also known to play an important role in microbial pathogenesis since in the context of bacterium- and virus-host interaction, the host is typically the source of sphingolipids, whereas in the context of the protozoan- and fungus-host interaction, both host and pathogen sphingolipids are involved14.
Sphingolipids also act as immune response modulators. Exogenously added sphingolipids (especially sphingosine) changed the receptor expression in immunological synapses, including CD3, CD4, CD8, CD45, CD54, etc. disrupting T-helper cell differentiation and prevelance of Th2 cells over Th1 cells. Sphingolipids activate macrophage function via elevation of receptor F4/80 expression and chemokine production. Fumonisin B1 regulates memory cell formation and secondary immune response, and inhibits the DNA synthesis in normal lymphocytes in response to mitogenes, more effective in T cells compared with B cells15.
Sphingosine-1-phosphate (S1P) level in lymphoid tissues, especially in thymus, is lowered as compared to blood. This creates S1P gradient that attracts lymphocytes and promotes S1PR1-dependent egress into the blood. When T cells are ready to exit the thymus and enter the blood, S1PR1 is re-expressed so that T cells can respond to the chemotactic effect of high S1P levels in circulation. When T cells re-enter the blood, S1P downregulates S1PR1. Increased lymphoid tissue S1P. blocks egress of lymphocytes by disruption of the S1P gradient or desensitization of S1PR1 on T cells. See the diagram below for representation16:

References:

 1. Gerrit van Meer, Sandra Hoetzl, Sphingolipid topology and the dynamic organization and function of membrane proteins, FEBS Letters, Volume 584, Issue 9, 3 May 2010, Pages 1800-1805, ISSN 0014-5793, https://doi.org/10.1016/j.febslet.2009.10.020.

 2. Hannun YA, Obeid LM (July 2002). "The Ceramide-centric universe of lipid-mediated cell regulation: stress encounters of the lipid kind". The Journal of Biological Chemistry. 277 (29): 25847–50. doi:10.1074/jbc.R200008200

 3. Spiegel S, Milstien S (July 2002). "Sphingosine 1-phosphate, a key cell signaling molecule". The Journal of Biological Chemistry. 277 (29): 25851–4. doi:10.1074/jbc.R200007200

 4. Hetz CA, Hunn M, Rojas P, Torres V, Leyton L, Quest AF (December 2002). "Caspase-dependent initiation of apoptosis and necrosis by the Fas receptor in lymphoid cells: onset of necrosis is associated with delayed ceramide increase". Journal of Cell Science. 115 (Pt 23): 4671–83. doi:10.1242/jcs.00153

 5. Snider AJ, Orr Gandy KA, Obeid LM (June 2010). "Sphingosine kinase: Role in regulation of bioactive sphingolipid mediators in inflammation". Biochimie. 92 (6): 707–15. doi:10.1016/j.biochi.2010.02.008.

 6. Lavieu G, Scarlatti F, Sala G, Carpentier S, Levade T, Ghidoni R, Botti J, Codogno P (March 2006). "Regulation of autophagy by sphingosine kinase 1 and its role in cell survival during nutrient starvation". The Journal of Biological Chemistry. 281 (13): 8518–27. doi:10.1074/jbc.M506182200

 7. Venable ME, Lee JY, Smyth MJ, Bielawska A, Obeid LM (December 1995). "Role of ceramide in cellular senescence". The Journal of Biological Chemistry. 270 (51): 30701–8. doi:10.1074/jbc.270.51.30701.

 8. Brown DA, London E (June 2000). "Structure and function of sphingolipid- and cholesterol-rich membrane rafts". The Journal of Biological Chemistry. 275 (23): 17221–4. doi:10.1074/jbc.R000005200

 9. Friant S, Zanolari B, Riezman H. Increased protein kinase or decreased PP2A activity bypasses sphingoid base requirement in endocytosis. Embo J. 2000;19:2834–2844.

 10. Friant S, Lombardi R, Schmelzle T, Hall MN, Riezman H. Sphingoid base signaling via Pkh kinases is required for endocytosis in yeast. Embo J. 2001;20:6783–6792.

 11. Rao, Raghavendra Pralhada, and Jairaj K Acharya. “Sphingolipids and Membrane Biology as Determined from Genetic Models.” Prostaglandins & other lipid mediators 85.1-2 (2008): 1–16. PMC. Web. 5 May 2017.

 12. Oskouian, Babak, and Julie D. Saba. “Cancer Treatment Strategies Targeting Sphingolipid Metabolism.” Advances in experimental medicine and biology 688 (2010): 185–205. Print.

 13. Elena Posse de Chaves, Simonetta Sipione, Sphingolipids and gangliosides of the nervous system in membrane function and dysfunction, FEBS Letters, Volume 584, Issue 9, 3 May 2010, Pages 1748-1759, ISSN 0014-5793, https://doi.org/10.1016/j.febslet.2009.12.010.

 14. Heung LJ, Luberto C, Del Poeta M: Role of sphingolipids in microbial pathogenesis. Infect Immun. 2006;74(1):28–39. 10.1128/IAI.74.1.28-39.2006

 15. Sphingolipid modulation of immune cell function: The Association of the Sphingolipidologists

 16. Maceyka M., Spiegel S. Sphingolipid metabolites in inflammatory disease. Nature. 2014;510:58–67. doi: 10.1038/nature13475.


Does a gene code for protein molecules or a DNA codes for protein molecules?

Your understanding is correct in that DNA encodes RNA, and this is a one-to-one relationship generally (although there are exceptions, see link below).  However, a given RNA can encode myriad proteins via translation.  This is because of different translation start sites and splicing of RNA.  You can read about this relationship between DNA/RNA/protein (the 'central dogma' of molecular biology), here:

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

But in the title of the quesiton you also ask about whether a gene or DNA encodes protein.  A gene is comprised of DNA; if someone talks about a gene, this just means a transcribed sequence, i.e. a region of DNA that is made into RNA.  Whether or not this is then translated does not impact its definition as a gene.  If it is transcribed, you could call it a 'protein-coding gene', otherwise you can call it a 'non-coding gene'.


What is the Cordil that Edward Topsell describes?

Your link says:

  [...] whereof the Latines derive or rather borrow their Cordulus, and
  Cordyla [...].

Wikipedia says about this:

  The genus Cordylus (Sauria: Cordylidae) includes a wide variety of small- to medium-sized spiny lizards from Africa, collectively called girdle-tailed or girdled lizards.

Tropical girdled lizard (Cordylus tropidosternum)
Source: Wikipedia


How does LDL leave the circulatory system and enter the interstitial fluid to deliver cholesterol to cells?

Many biologists had the same question for a number of years. In the 1950s, Nobel Laureate George Palade identified small vesicles in endothelial cells and postulated a mechanism whereby these vesicles would take in macromolecules from the luminal side of the endothelial membrane and transport them across the cell to release them to the tissues. His hypothesis has been tested, confirmed, and is now well documented.

Endothelial cells have LDL receptors that bind LDL in the capillary lumen, cause the cell to form a vesicle, and then transport it across to the membrane facing the tissues. There, the vesicle fuses with the tissue facing membrane, and LDL is released for uptake by peripheral tissue.

This process is called transcytosis. Endothelial cells use receptor mediated transcytosis to deliver many different large molecules to peripheral tissues in a regulated manner. You can read about this in some detail here (also the source of the figure), and more generally here.


Starch vs Cellulose. What are the differences between Alpha and Beta glucose ring structure in them?

The reason the monomer units are shown as alternating orientation in the cellulose case and not for starch is due to the angles required for the bonds between the atoms involved.

Note that in α-glucose the OH groups of the #1 and #4 carbons are shown on the same side of the ring.  When these two groups are changed into a single O joining two α monomers into starch, they have to remain in the same position.  When a single O joins them together, that oxygen requires the angle between the bond be less than 180 degrees, so the two glucoses have to be on one side of the oxygen.  That's fine in the drawing because in α glucose both OH groups are pointing down.

On the other hand, in β-glucose the OH groups of carbons 1 and 4 are on opposite sides of the glucose ring. Joining two β monomers to make cellulose requires that these two OH groups point in the same direction so that when changed into bonds to the single O, the angle which the oxygen requires can be provided.  To get the two OH groups pointing the same way requires one of the two β-glucoses to flip relative to the other.  Hence you get the monomers of cellulose alternating in orientation.

Part of the problem may be trying to visualize these 3-D relationships from the 2-D diagrams.  On this α-/β- glucose webpage there are some rotatable images of the molecules which may help visualize the relationships.


Why do some bad traits evolve, and good ones don't?

During the process of selection, individuals having disadvantageous traits are weeded out. If the selection pressure isn't strong enough then mildly disadvantageous traits will continue to persist in the population.

So the reasons for why a trait is not evolved even though it may be advantageous to the organism, are:

There is no strong pressure against the individuals not having that trait. In other words lack of the trait is not strongly disadvantageous.
The trait might have a tradeoff which essentially makes no change to the overall fitness.
Not enough time has elapsed for an advantageous mutation to get fixed. This doesn't mean that the mutation had not happened yet. It means that the situation that rendered the mutation advantageous had arisen quite recently. Consider the example of a mutation that confers resistance against a disease. The mutation wouldn't be advantageous if there was no disease. When a population encounters the disease for the first time, then the mutation would gain advantage but it will take some time to establish itself in the population.
The rate for that specific mutation is low and therefore it has not yet happened. Mutation rates are not uniform across the genome and certain regions acquire mutations faster than the others. Irrespective of that, if the overall mutation rate is low then it would take a lot of time for a mutation to arise and until then its effects cannot be seen.
The specific trait is too genetically distant: it cannot be the result of a mutation in a single generation. It might, conceivably, develop after successive generations, each mutating farther, but if the intervening mutations are at too much of a disadvantage, they will not survive to reproduce and allow a new generation to mutate further away from the original population.
The disadvantage from not having the trait normally arises only after the reproductive stage of the individual's lifecycle is mostly over.  This is a special case of "no strong pressure", because evolution selects genes, not the organism. In other words the beneficial mutation does not alter the reproductive fitness.
Koinophillia resulted in the trait being unattractive to females. Since most mutations are detrimental females don't want to mate with anyone with an obvious mutation, since there is a high chance it will be harmful to their child.  Thus females instinctually find any obvious physical difference unattractive, even if it would have been beneficial.  This tends to limit the rate or ability for physical differences to appear in a large & stable mating community.

Evolution is not a directed process and it does not actively try to look for an optimum. The fitness of an individual does not have any meaning in the absence of the selection pressure.

If you have a relevant addition then please feel free to edit this answer.


Do electric eels produce current as they just move about, and how/why?

You are right - the 800 Watts are not constantly produced:
There are three types of electrical discharge: (i) low voltage (ii) high voltage doublets or triplets and (iii) high voltage high frequency.
(i) low voltage allows the animal to orient itself in its environment [b].
(ii) high voltage doublets or triplets are used for hunting: By discharging a high voltage doublet or triplet the electric eel induces involuntary twitching in the prey animal. Since this twitching is producing a weak electric field, this allows the electric eel to locate its prey. See Figure 3 of [b].
(iii) high voltage high frequency is used to incapacitate the prey. It's about 400Hz at up to 600V [b]. Wikipedia [c] states that these electric eel can produce about 1Amp of current. That's in the region of 800Watts the narrator is speaking of. Edit2: The pulse duration is about 1ms [e]. With a frequency of 400-500Hz this leads to a surprisingly high ~50% dutycycle. The ability to keep the frequency stable depends on the age (=length) of your eel: The older the eel, the more stable the inter-pulse interval.

Caption: Fig3 from https://doi.org/10.3389/fnint.2019.00023, red=50cm, green=75cm, blue=115cm length of eel
In Figure 5 of [a] you can see that the electrical eel is able capture prey in ~5 sec. During these 5 seconds the electric eel is pretty much constantly producing high voltage discharges. These could be used to light a Christmas tree.
To summarize: Yes - electric eels are very much in control of when and how they discharge. This can be quite clearly seen (or rather heard) in [d] which is  Supplementary Movie 8 from [a]
[a] https://www.nature.com/articles/ncomms9638
[b] https://s3.amazonaws.com/vu-wp0/wp-content/uploads/sites/182/2015/11/Science.pdf
[c] https://en.wikipedia.org/wiki/Electric_eel
[d] https://static-content.springer.com/esm/art%3A10.1038%2Fncomms9638/MediaObjects/41467_2015_BFncomms9638_MOESM559_ESM.mov
[e] https://www.frontiersin.org/articles/10.3389/fnint.2019.00023/full


The genotype of a hybrid plant from a cross and its determination?

Real genetics is complicated

Biology is more complicated that you seem to expect. The answer very much depends upon the underlying genetics of the trait (and the underlying non-genetic factor affecting the trait; see here) as well as the genotype you are crossing it with.

Simplified model

But let's assume an extremely simple model of pure dominance / recessivity at a single bi-allelic locus. Let a be the recessive allele and A be the dominant allele. Let's assume the pure line you are using for the crossing is homozygote for the a allele (and let assume that we know it).

If the parent is AA, then all offspring will be Aa and all will have the dominant phenotype.
If the parent is Aa, then 50% of the offspring will be Aa and have the dominant phenotype and 50% of offspring will be aa and have the recessive phenotype.
If the parent is aa, then all offspring will be aa and have the recessive phenotype.

So, under this simple model, if you can produce a high enough number of offsprings to make good statistics, then yes, looking at the F1 generation is enough to determine the genotype of the parent.

Under a more complex model, it is not necessarily possible to only look at the F1 generation.


One example of what you may consider to be a macroevolutionary change is a whole-genome-duplication, or polyploidy event. These are not uncommon in plants, and can promote speciation due to a reproductive barrier arising between the polyploid progeny and the diploid parents. You can find many papers about this topic, here is one from 2009: http://www.pnas.org/content/106/33/13875.short


Why does K+ have more concentration inside of the cell compared to outside of the cell? Why is Na+ and Cl- the opposite?

Why nature has done it this way around is difficult to explain. What is certain, however, is that the membrane potential which results from the imbalance of these ions across the membrane is used for a variety of purposes, such as transport of other ions and molecules, action potential generation in neurons among many other things.

How it is accomplished is mainly through the Na+,K+-Atpase pump and secondarily through Cl- channels that exchange Na+ for Cl- to lift the amount of Cl- outside the cell.


Yes, it is possible to estimate the amount of repetitive DNA in a genome without sequencing. This was an important technique in the 1960s, referred to as C₀t analysis and pioneered by Roy Britten.

The approach taken is to study the kinetics of renaturation of heat-denatured genomic DNA (in a fragmented form). As you can see in this idealised Figure taken from the Wikipedia article on the technique there are components which renature rapidly whilst other components renature more slowly:

The interpretation of this is that repeated sequences renature rapidly because they are at a higher concentration than are single-copy sequences.

As stated at the linked Wikipedia article:

  ...it was through C₀t analysis that the redundant (repetitive) nature of eukaryotic genomes was first discovered.

And finally here is a quotation from Britten and Kohne's 1968 paper in Science:

  The rate of reassociation of the complementary strands of DNA of viral and bacterial origin is inversely proportional to the (haploid) DNA content per cell. However, a large fraction of the DNA of higher organisms reassociates much more rapidly than would be predicted from the DNA content of each cell. Another fraction appears to reassociate at the expected rate. It is concluded that certain segments of the DNA are repeated hundreds of thousands of times. A survey of a number of species indicates that repeated sequences occur widely and probably universally in the DNA of higher organisms.


Cousin Marriage from genetics point of view

The problem is that humans have 22 other pairs of chromosomes than just the sex chromosomes X and Y. Reproducing with your cousin (the son of your mother's brother is the son of your uncle which means your cousin) is generally looked down upon because of inbreeding.

Here's how it breaks down. Your mother and her brother (your uncle) each received 50% of their genes from your grandmother, and 50% from your grandfather. You received 50% of your genes from your mother and the other 50% from your father, who presumably is unrelated to the family. Therefore, you received 25% (50% of 50%) of your genes from your grandmother, and 25% from your grandfather. The same is true of your cousin - 25% from grandmother, and 25% from grandfather. The chances of some of your 25% and his 25% overlapping are rather high (for any one allele of a gene, it has a 1 in 4 chance of being the same as the cousin's). Combine that with 19-20,000-something genes, and that's a lot of overlap.

The problem with overlap/inbreeding is that any "hidden" (recessive) alleles may become homozygous. This may not be a problem for some genes, but a rather big problem for others (see my previous answer about Hunter Syndrome for an example.) There is a real potential of serious genetic diseases in any children resulting from such a relationship, which of course isn't fair to them.


What is the difference between sinew and tendon?

They get used somewhat interchangeably, which blurs the lines on the definitions.

When I had my anatomy classes, sinews were regarded as an inclusive class, which included both ligaments and tendons.

For the breakdown:

Tendon: Fibrous tissue that connects muscle to bone.
Ligament: Fibrous tissue that connects bone to bone.
Sinew: Includes both of the above.


How many rounds of TCA Cycle would a complete oxidation of a triacyl(15-Carbon fatty acid)-glycerol, give?

I am not too sure but this is my logic:

There would be in total of 18 molecules of Acetyl-CoA which means 18 TCA cycles. Propionyl-CoA gets converted to Succinyl-CoA which is a TCA intermediate (at about half of the cycle). If you do consider this, the 3 molecules of propionyl-CoA would only give you 3 partial rounds (or lets assume 1.5 rounds) of TCA cycle. Still 19.5; less than 22. Even if you consider the metabolism of glycerol, then 1 molecule of glycerol will give you 1 molecule of pyruvate i.e. 1 TCA cycle. So, the total is still 20.5 rounds i.e. less than 22.

I don't know what the other options are but "more than 22" is certainly not correct.


There are two questions here. 1) What is genetic variance? It is actually clearly defined. 2) How does sexual reproduction generate more genetic variation?

  What is genetic variance?

Assuming bi-allelic loci, just assign a value of 0 to one allele and 1 to the other allele. Then compute the variance! Average this value over all loci. Done! Have a look at any intro book in quantitative genetic for more info (see here)

  How does sexual reproduction generate more genetic variation?

You are right "sexual reproduction only "reshuffles" alleles, and doesn't generate new ones". It is a common misconception that sexual reproduction generate genetic variation. The details of whether it does or it does not depends upon the detailed distribution of dominance coefficient and distribution of epistatic effects.

There has been a lot of work on the subject and it is not an easy work to summarize it. Sally Otto does a great job to summarize this misconception in her speech On the Evolution of Sex and the Advantages of Recombination. You should definitely have a look at it.

Note however, in some species that preforms both asexual and sexual selection, it happens that sexual selection is coupled with higher mutation rate than asexual selection. In such cases, sexual selection does indeed increase genetic variance but only so because of tis correlated effect on mutation rate.


What is the direction of the processing of light by the (human) retina and how does it happen?

Short answer

Photoreceptors are the only cells in the retina that directly detect light; they can detect light through the other layers because those layers are so thin and effectively transparent: light passes right through to the photoreceptors.

Longer answer

The retina is fairly thin, and the bipolar/RGC layers don't contain much pigment. Have you ever looked at a thin slice of tissue under a microscope? You can do this and focus to different layers because single layers of cells are fairly translucent (remember they contain a lot of water): most light passes right through them. Some cells, such as red blood cells or photosynthetic plant cells, are harder to see through, but that's only because they are full of pigments.

The reason the photoreceptors respond to light in a way that can be detected biologically is that they contain special photosensitive pigments. In rods, this pigment is called rhodopsin and it is composed of a protein and a molecule of retinal. Most other cells in the retina don't have any such photoreceptors (there is a special class of retinal ganglion cells that is an exception, see for example here - these cells have a pigment melanopsin and contribute to light detection for circadian rhythms rather than vision).

Other cells in the retina respond to light only because they are sensitive to neurotransmitters released by photoreceptor cells and other retinal cells.

As far as why this is the arrangement, with photoreceptors in the back, it's really just a fluke of evolution and evidence that evolution and not design is the best explanation for diversity in biology. Eyes have evolved more than once in animals, however, and cephalopods like squid do not have their retinas arranged this way; in squid the photoreceptors are the most superficial layer.

Because the retina is so thin, this arrangement doesn't provide a large enough disadvantage to be selected against given the complexity in changing the organization. One exception to the thinness, however, is in the blind spot. The blind spot exists because all of the axons from the retinal ganglion cells have to exit the retina someplace. They exit in a big bundle, and there can't be any photoreceptors where that bundle is, so there is a spot where you cannot see. However, the position of the spot is not in the center of your vision, and that part of the visual field is usually covered by the other eye


You're misunderstanding a bit. Here are some definitions from Wikipedia, where I added some bold for emphasis:

Expiratory reserve volume: the maximal volume of air that can be
exhaled from the end-expiratory position

Inspiratory reserve volume: the maximal volume that can be inhaled
from the end-inspiratory level

In plain terms, ERV is how much you can still breathe out after you've breathed out all you normally would. You can try it out yourself: when you're finished breathing out and ready to start breathing in, try to blow out a bit, you'll find there is still air there. You don't need to breathe in extra to be able to breathe out this extra.
Similarly, IRV is how much you can still breathe in after you've breathed in all you normally would.
If you were to do a "fullest possible breath" that would include inspiring as much extra as possible, plus the normal breath volume, plus exhaling the last little bit you can:
IRV + Tidal Volume + ERV
There's still a little bit of residual air left over (RV), though, so:
IRV + Tidal Volume + ERV + RV
gives you the total capacity.


Simulating Migration in SimBit Software Program

In SimBit, no specific model is assumed as the user can very much chose for himself/herself what migration scenario to be simulated. The migration scenario can be set with the option --m (or equivalently with --DispMat).

There are four ways (what is called "Mode" in the manual) to indicate migration.
 A, LSS, OnePatch, Island and LinearNormal.

A

This mode stands for "All". This mode allows the user to enter a matrix with the migration rate between any two patches. Any migration scenario including the ones achieved with the below modes can be achieved with A. The interest of the other modes is to simplify the user's life esp. when dealing with many patches. I rather recommend using the other modes when these apply.

LSS

This mode stands for "Linear Stepping Stones". It allows the user to set linear stepping stones with any number of stones and potential asymmetry.

OnePatch

This is the default. It means no migration scenario apply as there is only one patch (or one deme if you prefer)

Island

This is a classical island model. The user must input the probability of not migrating.

LinearNormal

This is just like a linear stepping stone model except that the dispersal kernel follows a normal distribution.

Note also that the migration scenario (as well as the number of patches) is a time specific argument and therefore it can vary through time at will. You can have a look at the manual for more information.

Note that I have been working quite a lot on new versions that I have not put online yet, mainly because I was too lazy to rewrite the manual! The last version online is 3.69 but I am currently working on version 3.139! I will upload a more recent version in the coming week(s). Most notable improvement with the new version include:

Easier user interface; no need for all these quotation marks. Migration scenario will be given by the user as forward migration while it currently is backward migration which is a little less intuitive for the user.
More freedom on demography.
Possibility to simulate several species interaction with ecological relationships. One can simulate a whole ecosystem!


Equation relating probability of fixation and number of generations

From Hartl and Clark's 'Principles of Population Genetics' Third Edition chapter 7: Kimura and Ohta (1969) showed that the mean time in generations until the allele of frequency p is fixed (ignoring cases where the allele is lost) is:

$$t_1(p) = -4N[(1-p)log(1-p)]/p$$

The mean time to loss of the allele is:

$$t_0(p) = -4N[p \cdot log(p)]/(1-p)$$

Thus the mean persistence time of an allele is:

$$t(p) = -4N[p \cdot log(p)+(1-p)log(1-p)]$$

Hopefully I didn't make any typos there, but I reccommend this book to learn all the ins and outs of popgen. There is a PDF of the third edition online in an archive. For more book recommendations, please have a look at the post Books on population or evolutionary genetics?

You can also find these equations in the original article: Kimura and Otha (1968)


This is a question specific to the organism, assembly, and genes of interest to you. You can answer this yourself with a bit of elbow grease.

You could measure mean phyloP or phastCons conservation signal over UTR-annotated intervals, and compare it against the background mean conservation signal over random, mappable regions of the genome of similar length (i.e., calculate the mean and variance in UTR length and sample mappable regions of the genome for intervals with the same distribution).

At a very basic level, you could perhaps apply either the U-test or Wilcoxin rank-sum test, depending on your assumptions of dependence, whether your background does or does not include UTRs.

One source of phyloP and phastCons signals for various genomes and multi-genome alignments is UCSC Goldenpath. For example, here are phyloP 100-way alignments to hg38. You might get UTR annotations from Gencode, assuming you are working with human or mouse. To do interval overlaps and mapping/statistics operations, you might use gff2bed, bedops, and bedmap in the BEDOPS toolkit(*), and then use R to do statistical tests.

Disclaimer: I am one of the authors of the BEDOPS toolkit.


Is the cranial nerve blood supply encapsulated by the blood brain barrier?

I can't find a great answer to this either, but there is a known concept of a CNS-PNS transition zone, specifically as it pertains to myelination of cranial nerves. With the exception of CN 1 & 2 (which are effectively wholely CNS) the other cranial nerves are anatomically similar to spinal nerves, i.e. they're myelinated by Schwann cells and have an endoneurial blood supply. But they are also myelinated by oligodendrocytes for a short distance (varies by nerve) after taking of from their CNS nuclei before reaching that transition zone. According to this paper, that transition zone should mark the end of the astrocyte coverage which is necessary for BBB function. It's not a dead-ringer of an answer but this explanation makes as good physiologic sense as anything I've seen.

https://www.ncbi.nlm.nih.gov/pubmed/10697296


Identification of small fuzzy flying insect (pic)

To me, it looks like a male Aphid (males are winged, and have four wings) from the genus Eriosoma (wooly aphids). The white feathery substance is a wax secretion.

Have a look at Bugguide: Eriosoma, InfluencialPoints: Eriosoma and this page from the Uni of Minnesota for some more info.

A picture of a species from the genus:


How far do 2 ant colonies of same heritage have to be in space (and generation) in order to fight?

Space and generation don't directly affect whether ants fight, that's all regulated with pheromones. Some ant species are more tolerant of different smells than others (see the argentine supercolonies mentioned above) while some species of ant have 'rival' nests that they are particularly aggressive to.

So I guess the answer is 'it depends'. On pheromones produced by the queen, and species. And probably diet/weather/local food availability/ some other things I haven't thought of.

I don't think it's possible for some ants of a colony to fight and others not to, but I don't have any evidence to back that up specifically.


I saw this HHMI video today. It is called The Animated Life of A.R. Wallace, and it discusses the contributions that Alfred R. Wallace made to evolutionary theory. It is a little long for your stated time of 3-minutes. but it talks about how in fits of malaria he came up with his ideas on evolution.

HHMI also has a whole series of videos and modules on Evolution, though Wallace's came to mind as it showed his ambition and desire to solve the problem, even though he had not received formal training in the sciences.


Why does the amount of adipose tissue contribute the most to the total body water amount in humans?

Fat mass does not take up water.  It brings with it less water percentage than lean mass and so a person with more fat mass will have relatively less % body water.  Additional mass as fat contributed relatively less water than additional mass as lean tissue.

Consider a 50 kg individual who is extremely lean.  From your numbers, if this individual is 75% water (will will assume lean tissue is 75% water) that is 50 * .75 = 37.5kg water and 12.5kg nonwater body mass.

Now this 50 kg individual puts on 50 kg of fat.  The fat is 10% water (from your numbers) so an additional 10 kg of water.  This individual its now 47.5kg water and 52.5 nonwater; since this obese person weighs 100 kg now she has 47.5% water, similar to your example.

Suppose instead your 50kg person grew up into a 100 kg performance athlete.  Still no fat.  She is still 75% water because the lean tissue has 75% water.

It has to do with the % water each type of body mass brings with it.  This is with no special knowledge; using just the numbers in your example which is what your professor wants you to use.


How are dental cavities different from body injuries?

I disagree with some of these statements. Dental cavities are injuries and are treated like injuries warrent.

Unlike maybe trauma or cancer, dental cavities are a injury caused by decay of the enamel (the protective hard shell of the tooth). The decay is a result of the proliferation of bacteria, streptococcus mutants which releases an acid and breaks down the tooth.

When you have perforated enamel, other particles like food can get caught in the tooth and give rise to the growth of other bacteria. At this point you have a cavity.

Infection, the presence of certain toxins, and trauma all causes inflammation, a type of non specific immune reaction characterized by increased blood flow to the site of injury (which causes swelling, pain, redness).


What is the name of this about 10cm high, grey, "flat hat" fungus?

Based on the dark lamellae and the ring around the foot, I would bet on something in the Agaricus genus. The French Wikipedia gives quite some details about common species in this genus: https://fr.wikipedia.org/wiki/Agaric


One source says,

  Reactions cannot happen without water molecules.

It's not the most impressive source, but here's another source that has the same theme, with more details:

Cosmo Quest Forums

  The water molecule forms non-covalent bondings. It is bipolar and
  easily 'gets inbetween' other molecules which want to marry by charing
  their electrons more permanently. This makes water a great dating site
  where for example aminoacids quickly can try out their fit to many
  different parts of an RNA molecule. If they don't make good enough
  covalent bondings, water will immediately be there to separate them
  until the next one comes along for a try.

  Methane (on Titan) is as liquid as water and does transport stuff
  around. But it lacks the ability to interfer with how other molecules
  bond. Biochemical processes would be much slower in methane liquid
  than in liquid water.

Water is also a fabulous solvent; so many things can be dissolved in it. As others have mentioned, the simple abundance of water in the universe may be a factor.

However, I don't know anything about H2S' bonding ability or its power as a solvent.


Why does ostrich and other birds like pigeon swallow stones?

Birds do not have teeth so stones help in the process of grinding food.

Before even going to the stomach the food it starts to be processed in the "Crop". However is in the "Gizzard"  that the stones play a big role helping this muscular sack to mince and grind the food (the link sends you to an image of an open gizzard with pebbles inside).

Food and stones are present at the same time into this organ, therefore during peristaltic and contraction movements the friction between stones and food allow more efficient grinding.

Here you can a detailed description of the chicken digestive system that can be largely applied to birds in general.


Can cerebrospinal fluid deliver nutrients/drugs to neurons during sleep?

Only certain drugs can cross the blood brain barrier (BBB). However, there exist techniques to deliver drugs to the brain that otherwise cannot permeate through the BBB.
One such technique is called intrathecal delivery that injects drugs directly into the cerebrospinal fluid, avoiding the BBB problem and allowing the drug to reach cells, including neurons, in the brain. It has been used for certain kinds of chemotherapy, pain management, treatment of spastic cerebral palsy, and more recently for enzyme replacement therapy.
However with intrathecal delivery there is a risk of infection.

Having said that, if a drug reaches the CSF then your hypothesis should be correct. There is no experimental evidence for it yet.


I am not an expert in neurobiology, but this is what I have been able to find:

In general, the PNS (peripheral nervous system) does have remarkable neuroregeneration capabilities. However, the CNS (central nervous system), which includes the brain, has extremely limited neuroregeneration abilities. However, there are some interesting examples of CNS recovery:

  Children under six who undergo, unfortunately, a hemiectomy, whereby one half of their brain is taken out, are able to regain almost normal function because of the brain’s ability to rewire and literally take over the functions of the missing other half of the brain.

I am guessing one thing that can explain this is that in children, the CNS is still developing, and so if there is damage, the CNS can just entirely replace damaged parts (this might be different than "fixing" which is required in adults).

Again, I am not an expert on this and would be glad to hear a neurobiologist's opinion.


How to recognise the type of allele by pedigree analysis diagrams?

This question is a bit broad. You have to understand a lot of concepts to figure out the nature of the allele. I'll just point out some basics:

If an allele is dominant it should affect both males and females equally (not X-linked)
If one of the parents shows the trait (while other does not) then at least one offspring should show the trait (basic Mendelian segregation)
If both parents show the trait and one of the offspring does not then it means that the parents are heterozygous and the allele is dominant.


List of amino acid frequency of different foods?

A reasonable starting place could be the Food and Agriculture Organization of the United Nations:
http://www.fao.org/docrep/005/AC854T/AC854T03.htm#chI.I

This source looks by no means complete or easy to parse, but some simple web scraping may help you wrangle the data into a database.


Sodium hydroxide grade in library denaturation for NGS

The "molecular biology grade" is just a gimmick in many situations. The reagent grade NaOH is quite pure (≥98%). The usual impurities (major being Na2CO3; ~1%) are also chemically insignificant (See the Sigma-Aldrich products 1 and 2). For the product that you have, read the label for details. It should be more or less the same.

Just prepare your solution in MilliQ water and pass it through a 0.2µm filter.


What are the genus and species name of different breeds of dog?

All the different breeds of dogs - from Irish setters to greyhounds - are all part of the same species, canis lupus familiaris. The common, domesticated dog is actually a subspecies of the grey wolf. The different breeds do have different genetic characteristics (just as humans have, say, different eye or hair colors), but they're a all one and the same. The different names for different breeds are not like the scientific classifications of organisms via domain, kingdom, etc. They're just our choices.

References:

http://www.vetinfo.com/scientific-name-for-dogs.html
https://en.wikipedia.org/wiki/Dog_breed#Description
https://en.wikipedia.org/wiki/Subspecies_of_Canis_lupus
http://www.choosing-a-dog-made-easy.com/dog-types.html


A molecular marker for global protein synthesis

The answer will not satisfy you. The truth is no protein marker will do.

On one hand you seem to be looking at some individual, representative protein, which you could measure by immunoblot. But most proteins are in scant concentrations, just as many as required for their job, and go up and down depending on their specific roles, rather than on general metabolic trends. Even if some general control mechanism increases protein synthesis across the board, in a cell proteins are 20% actin, 20% tubulin, 0.0001% 4E-BP and 0.0001% p70-S6K (made-up numbers for the sake of example), any 1% total protein increase you'd like to measure would be 200,000 easier to detect in tubulin than in p70-R6K. In order to be a marker of general control of protein synthesis, the marker protein you'd want to measure should be a plentiful protein, with little to no specific control.

On the other hand, those are the characteristics of a house-keeping gene. So you won't be able to normalize such a "representative" blot! Normalizing house-keeping by house-keeping, you will have pretty much no change.

Embrace labeling experiments. Even there, the right normalization is debatable. If anything, the fact that everyone does those, rather than looking at protein X, should be an indication of how much you will struggle to prove points about protein synthesis rate using anything else.


You should have a look biological processes which are:

cellular respiration
photosynthesis

Loosly speaking, these two processes are just the opposite but deal with the same chemical compunds.

$C_6H_{12}O_6 + 6O_2 \xrightleftharpoons\  6CO_2 + 6H_2O (+ Energy)$

or in words...

glucose + Oxygen $\xrightleftharpoons\ $ Carbon Dioxide + Water (+ Energy)

From left to right is the process of respiration and from right to left is the process of photosynthesis.

Respiration releases energy from glucose (sugar). Therefore, animals, plants, fungi respire in order to get their energy from their food. More information on the chemical pathways on  Krebs cycle (or citric acid cycle). The main organelle involved in celullar respiration is the mitochondrion. Note: (Loosely speaking) the glucose is the end product of the digestion
photosynthesis allows organisms to create its own tissues from water and $CO_2$. But this cost energy. This is why plants use capture the energy form the sun with their leaves. More information on the chemical pathways on Calvin Cycle. The main organelle involved in photosynthesis is the chloroplast.

Note: In our lungs comes air which is a mixture of different gases (just like coke (Coca-Cola) is a mixture of different compounds). The two main compounds of air are Nitrogen (~78%) and Oxygen (~21%). We use only Oxygen. More info on the air composition here


How can I accurately measure glucose concentration in culture media?

The most common method of measuring glucose concentrations (in pretty much any sample) is an enzymatic assay based on the glucose oxidase enzyme. This method is reliable because the enzyme is known to be quite specific for glucose; it does not oxidize fructose, galactose, or any of the other common hexose sugars which can contaminate many other measurement methods. The enzyme can be coupled to other reactions so that the amount of glucose oxidized can be read out by a standard spectrophotometer. There are many kits commercially available based on this principle, like this one. A review of glucose oxidase from the glucose measurement perspective is found here.

Blood glucose analyzers are also based on glucose oxidase. Typically, they have disposable slips that contain glucose oxidase along with some electron-carrying chemicals that convert enzyme activity into an electrical current sensed by the device. It is possible to measure glucose in pretty much any solution with such insruments, but as mentioned in comments, you need to make a calibration curve for glucose in your solution of interest (culture medium, or whatever), as you cannot trust the readings from the instrument directly when measuring under different conditions. We have previously used this approach to measure glucose in mammalian cell culture medium, and it works fine in our hands.

It is also possible to quantify glucose by mass spectrometry or nucleic magnetic resonance methods, but unless you have such a facility and expert help, I guess that is not an option in this case.


I personally do not find the second part with the queries helpful without greater context.

The first part appears to be an accession number (more information on these can be found here: https://www.ncbi.nlm.nih.gov/Sequin/acc.html). By going to NCBI (https://www.ncbi.nlm.nih.gov/) and searching that accession number, you can get a lot of information quickly and easily.  Searching this particular number shows it to be a Asparagine-tRNA ligase from the fungal genus Leucoagaricus (https://www.ncbi.nlm.nih.gov/protein/KXN84633.1/).

If you simply have a DNA or protein sequence and no accession number, you can perform a BLAST (https://blast.ncbi.nlm.nih.gov/Blast.cgi).  This will search your sequence against a massive database of annotated DNA or protein sequences. The specific type of BLAST to run and the ideal parameters will take some reading on your part to determine.  However, if you're just starting out, nucleotide BLAST for DNA sequences, protein BLAST for protein sequences, and default parameters will often suffice. This search will provide you with the best "hits" to the database which you can then follow up on to get an idea of the function of your original sequence.


I could not find a concrete definition after searching several sources, but after reading a few papers I think the term Pure Odorant refers to its Olfactory Bulb profile. Peanut Butter will stimulate specific Olfactory nerves, and only that set of nerves, whereas impure Odorants may stimulate part of the profile and also other parts of the Bulb depending upon the impurity.

Basically, Peanut Butter has a unique smell that you can't replicate, and thus cannot mistake in either flavor or scent when compared to similar compounds. You may  not even be able to tell it was Peanut Butter at all if not for the scent.

A Lemon would not work the same way, as the major Odorant in a Lemon is Limonene - which is present in all citrus fruits. You would activate the same neuronal pathways for Lemons that you would with Oranges, Limes, and Grapefruits.

That's my best assessment.


Can a trait be too successful? Wouldn't overwhelmingly successful traits limit variability, which is one of the requirements of NS?

Yes, in neutral theory of evolution this is called fixation - when all the alleles (for a given locus) become identical. Note that it may happen, even if the gene does not have a striong selective advantage - due to the random effects.
If you are looking for the basic background in population genetics, Gellespie's book is a good starting point.


Is it possible to increase lifespan through controlled evolution?

I think this would probably work.  The grandmother effect, which is one of the main theories for human longevity after fertility might indicate that human lifespan would increase if the children come later.

Just have to disclaim here: We will never do this.  Many unthinkable consequences would result...

If you simply forbid anyone to have children before they are 40 or 45 (fertility doesn't drop until age 35 or so), forbid invitro fertilization and medical assistance to conception we would probably be looking at a prolonged lifespan.  Infertility rates in women at age 40 are not clear, but one estimate is that 40% of women can have children at 40 years of age.  If we want to seen an effect early, we would push the age up a year or two.  Forbidding in vitro fertilization and other medical assistance to offspring we could look like a 80-90% cut of people - lots of people would never have children.  This might make people unhappy an destabilize the social fabric.

Its not clear how long this would take.  The generation time would go to 40 years from about 20 now - 40 to get to childbearing age, but results would take 80 years - when we find out how the children would fare.  Given the C elegans longevity experiments and the fact that we are starting with 8 billion people, we probably would find some great late age breeders who may also live long.  But for the longevity phenotype to set in it would take several generations as we are looking for an indirect effect: later breeding causing longevity.  The Belyaev experiments which produced domesticated foxes by strong selective breeding took some 30ish generations to complete though they saw a significant effect in just 10.  It could take a similar numbers of selection rounds in this cse.  4-500 years. Ethical issues aside, this is why most geneticists study flies.

There would also be a lot of other negative socioeconomic consequences to this thought experiment.  One good thing is that the population of the earth would plummet - many people would be eliminated from the gene pool, though eldercare would be a major part of the world workforce.  Lots of work, not clear who is going to pay for it, but low unemployment and low low wages may result.

So you see Mister President, this is quite a distinct possibility, though some sacrifices would have to be made.

The science of human eugenics is not scientifically wrong, but selective animal breeding and lab experiments don't usually evaluate or care about the consequences of large peturbations in the gene pool.

You would also have a lot more autism and Downs syndrome and other congenital defects which tend to show up in offspring of older parents. These issues might improve with application of biotechnology which screens weak sperm and eggs without ruining the effect you are looking for, maybe not.

Since we are selecting against fecundity, the human race could be dogged by fertility problems or chronic genetic diseases which the genetic contribution of some of the more robust people in the gene pool being removed and the tendency to such age-related birth defects might not go away given the drastic selection pressure we are putting on the gene pool.

Other consequences you might not expect; some physical traits associated with longevity and prolonged fertility would cause us to look more alike and not necessarily in a good way.   Browse the internet; its probable that we would get shorter and possibly uglier?

There are many more direct ways to increase the human lifespan - better diet, exercise, the elimination of poverty, vaccinations, proper medical care, access to clean drinking water and a lower birth rate (fewer children not later) all are known to directly effect longevity, having more than doubled the human life expectancy in the past few hundred years.


What is the name of this red and blue striped spider (?) - Brazil, Rio de Janeiro

This appears to be some species of jumping spider (family Salticidae) in the genus Psecas.

For example, some red/blue striped species of Psecas:

]

 Sources: Top: Alchetron.com (image: Edwards, 2001)  |   Bottom: Tree of Life (image: Maddison 1994)

Wikipedia lists the following species from Brazil:

Psecas chapoda (Peckham & Peckham, 1894) – Brazil
Psecas chrysogrammus (Simon, 1901) – Peru, Brazil
Psecas viridipurpureus (Simon, 1901) – Brazil
Psecas zonatus (Galiano, 1963) – Brazil

Psecas chrysogrammus is my best guess given my limited knowledge of the specimen, this family, and arachnid literature.

We likely can rule out P. viridipurpureus (see here) and P. chapoda (see here) because of the longitudinal striping pattern of the dorsal abdomen of these two species.

I couldn't find any definitive or reputable sources regarding P. zonatus.

The sketch of P. chrysogrammus here seems to indicate that this specific species has the horizontal striping seen in the OP's specimen.

Salticidae.org provides these sources for P. chrysogrammus ID info:

M. E. Galiano 1963b. Las especies americanas de aranas de la familia Salticidae, descriptas por Eugene Simon. Redescripciones basadas en los ejemplares tipicos. Physis, Buenos Aires, 23 (66): 424, t. 32, f 14-18.
Simon E. 1901a. Histoire Naturelle des Araignees. 2(3-4) Paris: 460, f 528, 533(=H).


It looks like a Royal Poinciana tree with the scientific name Delonix regia..

Please refer to this link for more info


How do our eyes detect light at different frequencies?

Short answer
Action potentials generated to different colors are indeed similar throughout the nervous system and do not encode color as such. Instead, the different color- sensitive cells in the retina are connected to different neurons and these color-specific signals are kept segregated up until the higher visual cortical areas.

Background
Action potentials are indeed pretty similar throughout the nervous system. However, the color-sensitive sensory cells in the retina, called the cones, come in three flavors: red, green and blue. These colors form the RGB system just like in your LED TV and can together make all the available millions of colors. These three cones synapse ultimately onto color-specific secondary sensory neurons (Fig. 1).

Hence, R, G and B cones indeed generate identical action potentials in downstream neurons, the trick is they do so in different retinal ganglion cells, and at different firing rates depending on the intensity of light that particular cone is sensitive to. These different classes of retinal ganglion cells project onto different classes of neurons in the brainstem (lateral geniculate nucleus, or LGN) and ultimately onto different neurons in the higher cortical visual areas in the brain.

Fig. 1. Different classes of cones synapse onto different classes of secondary sensory neurons in the retina. source: Discovery Eye Foundation

The reason why we can differentiate millions of colors can be explained by the Hering model of color vision (Fig. 2). Basically, the different cones converge pairwise onto opponent color-sensitive cells. The red-green opponent system, for example, operates by weighing the amount of red and green in the incoming signal. This weighting results in an analogue system that can code millions of colors along the red-green axis (Fig. 3).

Fig. 2. Hering model of color vision. source: Webvision

Fig. 3. Red-green color axis. source: SO


What is the distribution of the number of heterozygotes in finite populations?

It is a multinomial (trinomial) distribution with $N$ trials, $p_{AA}=p^2$, $p_{Aa}=2p(1-p)$, and $p_{aa}=(1-p)^2$. The probability to get exactly $n_{AA}$ AA genotypes, $n_{Aa}$ Aa genotypes and $n_{aa}=N-n_{AA}-n_{Aa}$ aa genotypes is

$$P\left(N_{AA} = n_{AA}, N_{Aa} = n_{Aa}\right) = \frac{N!}{n_{AA}!n_{Aa}!n_{aa}!}p^{2n_{AA}}\left(2p(1-p)\right)^{n_{Aa}}(1-p)^{2n_{aa}}.$$


What is the difference between local and global sequence alignments?

The very basic difference between a local and a global alignments is that in a local alignment, you try to match your query with a substring (a portion) of your subject (reference). Whereas in a global alignment you perform an end to end alignment with the subject (and therefore as von mises said, you may end up with a lot of gaps in global alignment if the sizes of query and subject are dissimilar). You may have gaps in local alignment also.

Local Alignment

5' ACTACTAGATTACTTACGGATCAGGTACTTTAGAGGCTTGCAACCA 3'
             |||| |||||| |||||||||||||||
          5' TACTCACGGATGAGGTACTTTAGAGGC 3'

Global Alignment

5' ACTACTAGATTACTTACGGATCAGGTACTTTAGAGGCTTGCAACCA 3'
   |||||||||||    |||||||  |||||||||||||| |||||||
5' ACTACTAGATT----ACGGATC--GTACTTTAGAGGCTAGCAACCA 3'

I shall give the example of the well known dynamic programming algorithms.
In the Needleman-Wunsch (Global) algorithm, the score tracking is done from the (m,n) co-ordinate corresponding to the bottom right corner of the scoring matrix (i.e. the end of the aligned sequences) whereas in the Smith-Waterman (local), it is done from the element with highest score in the matrix (i.e. the end of the highest scoring pair). You can check these algorithms for details.

You can adopt any scoring schemes and there is no fixed rule for it.

Global alignments are usually done for comparing homologous genes whereas local alignment can be used to find homologous domains in otherwise non-homologous genes.


hummingbird feeders - is sugar water healthy for them?

Hummingbirds absolutely eat insects, and HONEY and BROWN SUGAR are a huge NO NO.
  The following is a statement from: http://wildbirdsonline.com/index.html

  Every year, as more studies are completed, we learn more about
  hummingbird life and diets. However, we find that some people think
  that hummers can survive on nectar alone. Nectar provides quick energy
  to sustain their extremely high metabolic rate and little else. This
  is important enough that the shape of the bills of hummers have
  evolved in partnership with the flower shapes that they frequent.
  Consequentially, there is a wide variety of hummingbird bill lengths
  and shapes among the more than 300 species that exist.

  There is another critical food source for the hummers. Essential
  vitamins, minerals, amino acids, proteins, oils and fats, fiber, etc.
  all come from the insects they eagerly consume, not the nectar. Their
  preferred insects include, but are not limited to: small beetles, true
  bugs, weevils, flies, gnats, mosquitoes, aphids, mites, leafhoppers,
  flying ants, and parasitic wasps. Their favorite insect food source is
  the spider and harvestmen (daddy long legs). Some ornithologists
  estimate that spiders are between 60% and 80% of their diet.

But there are lots of other resources for you to find accurate information about feeding hummingbirds.