Determining sequence of oligoribonucleotide

Here are a few hints which might help you:-

1) You get free UMP and CMP (in contrast to UMP + C or CMP + U) in the second experiment before alkaline hydrolysis.

2) There are two CMP in "N" oligoribonucleotide, and a free cytidine (and not CMP) in "M" and "Q".

3)Use the fact that all oligoribonucleotides were treated with phosphatase before being subjected to alkaline hydrolysis.

(Referring to your comment, I dont know why do you think consecutive cytidine is not possible).

These are a few hints that helped me solve this. If you want further clarification or the answer, tell me in the comments.

Answer for reverse derivation:- $5'-UACGCCGAC-3'$


Does gray/white hair turn gray/white from a normal hair? or does a gray/white hair actually grow gray/white originally?

It can actually be for both reasons and it more or less depends on the age what happens. The pigment of the hair is produced by pigment cells (the melanocytes) in the hair bulge and is then integrated into the growing hair (image from here).

The pigment melanin produced by these cells can be destroyed by reactive oxigen species which then leads to grey hair which can still be pigmented at the tip.

The other possibility is connected to the hair cycle. After growing for a while the growth stops, the hair falls out and the hair follicle goes into a resting state. In this phase the pigment cells die. When the hair follicle starts a new hair cycle, the pigment cell population in the hair bulb is renewed from the melanocyte stem cells in the hair bulge. Over time the number of the melanocyte stem cells gets lower until there are none left eventually. At this point new hairs will grow without pigment and be grey/white.

There are two interesting publications about this topic:

Oxidative Stress in Ageing of Hair
Melanocyte Stem Cell Maintenance and Hair Graying


Its not scientifically or logically possible to say 'this is impossible' but since this is a speculative question, I'll hazard an opinion.

I'd like to argue that, at Earth standard pressure temperature and atmospheric conditions, C H O and N are not really replaceable.  Throw water into the mix as the most common liquid and replacing any or all of these elements is hard to imagine.

One can think about this by looking at the formation of long hydrocarbon chains.  Silicon can form polymers, but they tend to fall apart. Silcone-oxide polymers [SiR2-O-SiR2-O-] are more stable, but do not resemble hydrocarbon polymers as readily.

Carbon is much more versatile, capable of forming either chain, or including sulfur, nitrogen in stable chains that don't seem to really have any length limitations.

At thousands of atmosphere's pressure, temperatures of 70 Kelvin or in a sea of sulfuric acid, its easy to imagine other sorts of chemistry would dominate - phosphate , arsenic chains or germainium lattices, but on Earth most of these would fall apart.

Even if/when life is discovered elsewhere , it will certainly feature chemistry that will completely amaze us; unlike anything here.  But even so, its hard for me to imagine it being completely exclusive of these four elements.  I just want to point out that by a wide margin, hydrogen is the most common element of the universe.   Nearly all the other light elements like C, O and N are the next most common.  This is simply because they take fewer nuclear fusion events to create.  Hydrogen is pretty useful no matter what chemistry you are looking at.  These four are probably going to be there somewhere - most planetary atmospheres have Ammonia, CO2 and methane in them as well - at least as far as we've seen.


What's the best way to measure/calculate the size of a light beam at the sample of a microscope?

Well you can always use a piece of white circular paper and draw the outline of the light onto it since it should be visible. This is a quick and dirty method that can be improved by taking a photo of the light with a camera if you have one and then comparing the distance of the edge of the paper measured with a ruler to that of the circle of light.


Why is cholera toxin added to certain culture media?

Empirically, it can improve growth of cell cultures (https://www.atcc.org/Global/FAQs/C/C/Cholera%20toxin-541.aspx).

It furthermore has the potential to make cell populations more homogeneous by selectively binding to gm1 containing cells that can arise from spatial inhomogeneities among cultured cells. Snijder er al. Nature 2009 (https://www.ncbi.nlm.nih.gov/pubmed/19710653)


What does probe number and segmentation mean in copy number variation (CNV) data

The data you posted looks like it was produced by GISTIC, a program commonly used by TCGA to detect copy number changes. Assuming the data really is GISTIC-produced, my understanding is that "Segment_Mean" refers to the average Log2 Ratio of the probes in that particular segment. Looks like the copy-number of your 4-probe segment in your example is slightly less than half the copy-number of the longer segment.

You can also try using the GISTIC Google-Group to learn more.


Why didn't the human Cerebrum evolve to have granule cells like the Cerebellum does?

By "cerebrum" I assume you really mean the cerebral neocortex, since the cerebrum includes other subcortical structures that themselves are quite distinct (e.g., the basal ganglia).

Simply, the neocortex and cerebellum have completely different functions. The cerebellum performs a particular class of computations that are very different from the variety of computations performed by the cerebral cortex. They have completely different laminar structures, with neocortex being a ~6-layer structure, the cerebellum has just 2-3. There are a much higher diversity of connections and cell types in neocortex compared to cerebellum.

It seems like an optimal configuration for the cerebellum is a very high cell density. More cells doesn't necessarily mean "better", because the more cells you have the less space you have for connections. There is no unused or empty space in the neocortex: if you packed in some more cells you'd have to lose something else.

Doya, K. (1999). What are the computations of the cerebellum, the basal ganglia and the cerebral cortex?. Neural networks, 12(7-8), 961-974.


Question about different gametes that can be produced

You are correct

Assuming that by linked, the question assumes perfect linkage (no cross-over ever happen), then your answer is correct! Good job!

Comments

Here are a few comments though...

  We have 5 traits, and each trait consists of 2 alleles.

There are 5 loci. A locus does not necessarily match to a single trait and a single trait does not necessarily match to a single locus. Actually, it is very very rarely (if ever) the case.

  To make functional gametes, each gamete must receive one of each allele so that it can survive.

This is not necessarily true. A "normal meiosis" (not leading to variation in copy number) may create a non-viable genotype and a "abnormal meiosis" (leading to variation in copy number) may create a viable genotype. But, it is true that we will only assume "normal meiosis" for this answer.


How do Streptococcus thermophilus and Lactobacillus bulgaricus precipitate the curd of swiss cheese?

lactic acid bacteria ferment the disaccharide lactose present in high amounts in milk to the three-carbon compound lactic acid, which acidifies the milk. this causes the proteins also present in milk to denaturate and coagulate, forming curdles. other causes/methods of curdling can be application of heat, salts or by adding the enzyme chymosin (rennin).


This article (DNA Topology: Fundamentals by Mirkin SM) probably defines and describes linking number better than I ever could:

  The fundamental topological parameter of a covalently closed circular DNA is called the linking number (Lk). Assume that one DNA strand is the edge of an imaginary surface and count the number of times that the other DNA strand crosses this surface (Figure 3). The algebraic sum of all intersections (which accounts for a sign of every intersection) is the Lk. Two important features of the Lk are evident from Figure 3. First, Lk is always an integer. Second, Lk cannot be changed by any deformation of the DNA strands, i.e. it is topologically invariant. The only way to change Lk is to introduce a break in one or both DNA strands, rotate the two DNA strands relative to each other and seal the break... Another characteristic of a circular DNA is called twist, or Tw. Tw is the total number of helical turns in circular DNA under given conditions. Since DNA is a right handed helix with 10.5 base pairs (bp) per turn, Tw is a large positive number for any natural DNA. Take a planar, circular DNA and try to locally separate the two DNA strands, i.e. to decrease the Tw. Since Lk cannot change, a decrease in Tw will be compensated by several positive writhes of the double helix (Figure 4). Writhing (Wr) is the third important characteristic of circular DNA, describing the spatial pass of the double helix axis, i.e. the shape of the DNA molecule as a whole. Wr can be of any sign, and usually its absolute value is much smaller than that of Tw. The above consideration can be formalized by the following equation: Lk = Tw + Wr. Note, that while Lk is an integer, neither Tw nor Wr should be such. Also, neither Tw nor Wr are topological invariants and their values easily change...

Linking number is simply the number of times one strand of DNA passes over the other. Compare this to:

Twist - the number of helical turns
Writhe - the number of superhelical turns

You can, perhaps, think of twist as the passing over of strands within the helix and writhe as the passing over of strands when the entire helix crosses itself. Both twist and writhe involve strands of DNA passing over the other and so both contribute to the linking number. In the absence of writhe, linking number and twist are equal and both describe the same thing: the number of helical turns. However, in the presence of writhe, twist alone is insufficient to describe the topology of DNA because it doesn't account for the passing of the entire helix over itself.

Since twist is the number of helical turns, actually counting it in your image is not necessarily difficult, just time consuming. The image already has the twists numbered, and I've put a red do at every turn of the double helix. I've also circled, in blue, every point where the double helix passes over itself (writhe):

In that image, in may be difficult to visualize (and even understand!) that the strands only cross over each other 36 times (Lk), even though there are 42 helical turns (Tw). While twist and writhe are different modes of strand crossing, it is important to realize that they are interchangeable without breaking the strands. Let's consider a simpler example, where Lk = -1 (Wikipedia: DNA Supercoil):

In the lower image, the strands do not form a helical structure (Tw = 0) but they do both pass over each other together (Wr = -1). Can you imagine that if you were to "unfold" the superhelix (Wr = 0), the two individual strands would still be linked together in a helical structure (Tw = -1)? Neither could I, so I made a video with my shoelaces:

https://www.youtube.com/watch?v=rI3LWIvptf0

I hope that answers your question. Let me know if I misunderstood what you were asking or if anything needs clarification. You may also find my shoelace video on the topology of helicase-mediated DNA unwinding informative.


Anopheles arabiensis lifespan and sporogony duration

What is the longest observed lifespan of a mosquito, especially of the species Anopheles arabiensis?

Mean lifespan calculations for Anopheles arabiensis range from 14 days (Karoki, 2013)* to 21 days (Yamada et al. 2014)**

*This Masters thesis tests efficacy of different drugs against An. arabiensis, 14 days is the mean control lifespan.
**These An. arabiensis are of a specific strain but no indication is given that the life span is different than normal An. arabiensis.

The CDC Anopheles mosquito page is another good source for information on Anopheles life spans:

  The adult females can live up to a month (or more in captivity) but most probably do not live more than 1-2 weeks in nature.

How long does it take for Plasmodium parasites to develop and move into the salivary glands of these mosquitoes?

US National Institutes of Health:

  Growth and division of each oocyst produces thousands of active haploid forms called sporozoites. After 8-15 days, the oocyst bursts, releasing sporozoites into the body cavity of the mosquito, from which they travel to and invade the mosquito salivary glands.

United States Air Force (USAF):

  The length of the developmental stage in the mosquito not only depends on the Plasmodium species but also the mosquito host and the ambient temperature.  This may range from eight days in Plasmodium vivax to as long as 30 days in Plasmodium malariae.

Wikipedia (Plasmodium falciparum) :

  Over the period of a 1–3 weeks, the oocyst grows to a size of tens to hundreds of micrometres... The sporozoites then migrate to the salivary glands and complete their differentiation. Once mature, the sporozoites can proceed to infect a human host during a subsequent mosquito bite.

US Center for Disease Control:

  After 10-18 days, the parasites are found (as "sporozoites") in the mosquito's salivary glands. When the Anopheles mosquito takes a blood meal on another human, the sporozoites are injected with the mosquito's saliva and start another human infection when they parasitize the liver cells.

Overall, it depends who you ask, but especially on the species of Plasmodium you're working with. I'd look for specific papers on the development cycle you're modeling and run with it.


I am a little confused that does the word "cooked" means ripe？If yes, then the question will be easy to answer. Fruit has a kind of ripener, ethlyene. Ethlyene will help fructose break down and make up more glucose. That is why you may taste a strong flavour when fruit is cooked.


Usually it is termed chlorosis, and comes about from an inability to produce chlorophyll. It can actually be determined by a whole range of things, and not just water shortage or waterlogged soil, including nutrient deficiencies, pathogen infection or unbalanced soil pH.

A lot of these factors relate to an inability of the plant root system to properly take up water. As you probably know, water enters the root system to be carried up into the shoot (through the xylem) mostly driven by transpiration, the water pressure caused by loss of water through the leaves. This water carries with it the soil-derived nutrients the plant needs to synthesise substances that can't be produced by photosynthesis. So if you change the water balance (for example by drying the soil) it becomes difficult for plants to get the nutrients they require to produce chlorophyll.

Usually this is mediated by reduced supplies of magnesium, iron or zinc, but because the precursor to chlorophyll is an amino acid, it can also be caused by shortages of nitrogen. pH comes into play because plants use a delicate balance of acidic ions to mobilise (make available to the roots) the nutrients in the soil, and if the soil pH differs too much this becomes untenable.

So in summary it relates both to shortages of key nutrients or changes in key soil characteristics, and the ability of the plant root system to uptake these key nutrients. It is mediated by these effects leading to an inability to produce enough chlorophyll, which leads to the yellowing leaves that you observe.


Our understanding of how life began on earth has indeed advanced substantially since Haldane, Oparin, Miller, and Urey. To learn about the latest ideas, I can't think of a better place to start than this excellent video series with Nobel Laureate Jack Szostack, who is currently doing some of the leading work on the subject.


What accounts for size variation in breeds of dogs?

This is a fascinating bit of genetics.

Dogs are especially variable in size and many appearance, behavioral and temperamental phenotypes.  It was long expected that variations in developmental genes were the reason that dog breeds were responsible for the amazing flexibility of dog sizes.  One early locus found was IGF1 (insulin like Growth Factor 1).

This 2011 PLOS paper actually review the specific genotypes of dog breeds and identifying loci that are strongly associated with breed phenotype supports this idea.

  ... (we scanned) the genome for signatures of selective sweeps in single breeds, characterized by long regions of reduced heterozygosity and fixation of extended haplotypes. These scans identify hundreds of regions, including 22 blocks of homozygosity longer than one megabase in certain breeds. Candidate selection loci are strongly enriched for developmental genes. We chose one highly differentiated region, associated with body size and ear morphology, and characterized it using high-throughput sequencing to provide a list of variants that may directly affect these traits.

Emphasis added.

This theory has an intuitive appeal as well - no dog breeds (I think) are larger than the wolf, the stock from which all dog breeds are descended.  All such breeds being derived from earlier developmental stages of the wolf makes an intuitive, if imprecise description of the effect here.

Regardless, dogs remain an important model organism for so many traits because relatively few genomic regions can cause so many important phenotypes, including size, but also behavioral and morphological variations.

In the below figure you can see how few genomic regions are responsible for the 46 breeds Vaysee et al. examined.


How do antioxidants affect human metabolism?

This mainly depends on which kind of antioxidants you're talking about.

Vitamin A and E are antioxidants acquired from the food
Superoxide dismutase, Catalase and the Glutathione system are enzymes produced by the cell.

Antioxidants keep the oxidative balance of the cell and quench free radicals which are generated by the mitochondrial respiratory chain. Very simplified: Antioxidants are thought to be anti-ageing compounds because free radicals destroy cellular compounds, which can be related to the ageing process.

I would be very careful with products claiming to contain antioxidants and be therefore anti-aging. This whole anti-ageing marketing is far from being scientifically proven.


Veritasium created an excellent video just on this topic, which I would recommend watching, but will summarize here.

A common misconception is that we lose weight when we digest food or burn calories. Keep in mind that that broken down food and those calories* aren't "going anywhere", so technically you shouldn't loose any mass (unless you get rid of the molecules by going to the restroom).

However, in the "informal" tests done by Derek Muller, he lost about 250 grams each night. Since during the night you sweat (which evaporates or gets absorbed into the sheets and blankets), he estimated that about 150 grams was lost through perspiration and breathing out water vapor.

The more surprising loss of mass, was 0.012 grams of carbon lost with each breath when breathing in oxygen, and then breathing out carbon dioxide. Although this seems like a tiny loss, assuming you breathe in and out about 7,680 times each night, that tiny mass loss adds up to almost 100 grams of weight loss through breathing alone.

I guess health magazines should start running articles like "Top way to lose more weight? Researchers say breathe more!"


Linkage Disequilibrium - What does it mean when D < 0?

Consider two bi-allelic loci, A and B with alleles A1, A2 for A and B1, B2 for B. Negative values for D means that A1 is more often associated with B2 than expected. Similarly, A2 is more often associated with B1 than expected.

More info on Wikiedpia > Linkage Disequilibrium or on any intro book to population genetics (see here for recommendations). If there is anything in particular you do not about the definition of LD, feel free to ask a question by highlighting what is unclear to you.


What is the rationale behind IgM being the default antibody?

When the Naive B cell gets activated and begins to secrete antibodies the affinity of the antibodies is low, as it hasn't yet gone through several cycles of affinity maturation. The increased avidity of the IgM balances the decreased affinity of these initial antibodies. If IgG were released at this stage, the body would have a much lower immune reaction to the antigen.

However after affinity maturation, the IgG has sufficient avidity and affinity to mount a stronger immune reaction than the initial IgM antibodies. If the body still produced IgM after affinity maturation, there would likely be a significant amount of crosslinking. This could potentially cause aggregates to form in the blood/lymph which could cause occlusions.

Edits:

  If the affinity of the antigen-binding sites in an IgG and an IgM molecule is the same, the IgM molecule (with 10 binding sites) will have a much greater avidity for a multivalent antigen than an IgG molecule (which has two binding sites). This difference in avidity, often 10^4-fold or more, is important because antibodies produced early in an immune response usually have much lower affinities than those produced later. Because of its high total avidity, IgM—the major Ig class produced early in immune responses—can function effectively even when each of its binding sites has only a low affinity.

Molecular Biology of the Cell

The claim on aggregation after affinity maturation is speculation based on the crosslinking that occurs with IgA antibodies (e.g. Phlegm) when there are only two high-affinity Ig molecules joined together rather than five.


How is the site of administration of a vaccine decided?

When the effectiveness of subcutaneous is comparable to intramuscular, then the choice is made based on the degree of discomfort and adverse reactions.

In many situations intramuscular will outperform subcutaneous delivery due to subcutaneous fat having poor vascularity which may result in slow mobilisation and processing of antigen(source).

Disclosure: I am not a biologist so this is outside my field of expertise.


Are these 2 procedures to fight cancer (cancer "vaccine", and cancer drugs which can attack all tumours) related?

The first source (Science Direct) says that the "vaccine" treatment stimulates T cells to attack cancer. In general, this treatment is intended for all tumors and has been very successful in studies in mice. Cancer.net and Cancerresearchuk describe cancer treatment vaccines in a bit more detail.

The second source (Telegraph.co.uk) mentions “tumor agnostic” or "tissue agnostic" drugs, which target tumors according to their genetic make-up, rather than the tissue from which they arise. This treatment is intended only for specific tumors with known genetic mutations. Examples of tissue-agnostic drugs are pembrolizumab and larotrectinib, which are approved by FDA for treatment of certain metastatic solid tumors.

So, these are two different ideas and most of these drugs are currently in a research phase.


Why are primary sensory cells considered neurons but muscle cells are not?

The quote from Quora has the correct answer; the distinction between neuronal and non-neuronal is an embryological rather than functional definition. Along those same lines, some of the other receptors you listed are considered sensory epithelia rather than neuronal. The retina is of neuronal origin, but hair cells in the cochlea are often not considered to be neuronal, despite the diagram you provided, nor are Merkel cells. The distinctions between epithelial and nervous tissue are often more difficult to identify because both derive from the same preceding embryonic tissues, whereas muscle is entirely separate.

In the end, these distinctions don't matter much unless you are interested in development or trivia (though I don't mean to discount the importance of development there, I just recommend that you don't worry too much about the distinctions if you are thinking only about final functions).


Ka/Ks (dN/dS) analysis module for Python?

Do you know about BioPython?

Here, on another website, someone already asked this question and a pretty nice answer was provided by Brad Chapman. He gives already written functions to perform this kind of analysis (I personally haven't tried the codes).

In Perl there is Bio::Align::DNAStatistics. You might adapt it to Python.

This might be useful as well.

I think there are plenty of possibilities that are offered to you. You can go through some others by doing google search with the keywords synonymous, non-synonymous and BioPython.


Molecular cause of cramps, spasms and strengthening in muscles? (incl. intro to muscle contraction)

I think a lot of your questions try to split the hair; is this happening at the chemical or the histological level and I do get what you're asking, but you should know that the distinction is often not worth making. Pretty much whenever a neuron's involved, the interesting biology is multi-scale.

  Is the membrane continuous along these tubules, or does the tubule just end somewhere inside the muscle fiber?

The membranes are continuous.

  When the muscle is twitching... is this neurological of nature, or is it related to a molecular cause in the muscle itself?

Most things you'd call a muscle twitch are at the whole-muscle-group scale, involving the coordinated contraction of many individual motor units, so it's basically neurological.

  When the muscle is cramping... I'm almost certain this arises in the muscle. What causes it? A malfunction with regard to the calcium ions?

A muscle cramp is a colloquialism for a couple of things that are quite different from each other. Overall, as with the previous question, if someone's experiencing a muscle cramp that means it's a fairly macroscopic phenomenon and it likely involves a whole group of muscle filaments, so it's neurological. Most spasms and cramps are neurologically mediated.

The connections with electrolyte balances (cramps from low sodium, potassium, magnesium, or calcium) also hint at the neurological basis because neurons act on each other (and on muscles) by forming or dissipating ion gradients. You may know that low dietary calcium can lead to muscle cramps; if this was relevant to the calcium release within the myocyte (from the sarcoplasmic reticulum) then the calcium-starved muscles wouldn't be expected to chronically contract (which requires calcium) but to chronically relax.

That being said, there's a lot of room for feedback mechanisms. So, let's say a person experiences a muscle tear; the tear is small enough that it doesn't compromise the function of the entire muscle group. In this case it's adaptive for the local damage to 'signal' to the rest of the muscle group to initiate spasm so as to stabilize the damaged structures as they're repaired. In this scenario the local damage would 'inform' a neurological (and/or endocrine) response that actually effects the spasm.

  Lastly, and on a slightly different subject, what are the microlesions in the muscles that occur during strength training, and what is the overcompensation that happens?

Last time I was updated on this (not my bag), there were some large questions remaining. The tricks used by growing muscle to establish large, regular arrays of contractile machinery, that is organized over many spatial orders of magnitude, are poorly understood. There are structures that monitor the overall organization and that detect any large deformations. Regarding overcompensation, let's play through a generic scenario. A muscle cell is loaded too much and becomes physically damaged. It has to stop taking orders (stop responding to contraction/relaxation signals) and to initiate repairs. The overcompensation results because muscle cell's not really capable of knowing how large it was before the damage, so the safe amount of repairs to do is extra. Probably there are epigenetic processes that let a muscle cell 'count' the number of times its been greatly damaged and to scale-up the response appropriately.

If you just consider two likely sources of damage -- mechanical strain and lactic acidosis -- you can see that there are widely different mechanisms that would be required to detect the damage and to initiate repairs.


Well, it's a type of firefly, belongs to the order of 'Coleoptera' (beetles), suborder of 'Polyphaga', family of 'Lampyridae' (firefly beetles). It's quite similar to the 'Photinus obscurellus' species (and probably the same species too), however it doesn't always have a black head like yours, however, articles have suggested that  firefly species in Brazil (Sao Paulo State) have 'adapted to mesophyl tropical forests, secondary growths, marshy areas, and open fields' (source = https://www.researchgate.net/publication/233574632_Fireflies_Coleoptera_Lampyridae_from_Southeastern_Brazil_Habitats_Life_History_and_Bioluminescence).

This adaption may have led to species having black heads as oppose the more colourful head of the Photinus obscurellus. However the bodies and the dimensions match yours very closely.

This image is from Google Images (more specifically : http://bugguide.net/node/view/194980/bgimage)


This looks like dried cholla cactus, although it will be hard to determine the species. It is sold commonly for fishtanks, so might even be found in places where it does not grow naturally if someone cleaned out their fish tank.

EDIT by Ilan: on this image you can clearly see that the tree identified right:


What is the name of this flower with purple leaves and orange inner part in NYC?

It's Echinacea. I've linked to one site but if you run an images search with Echinacea as the search term you'll see lots of examples.

And here is the WP page.

Supplementary

Echinacea are members of the Compositae. The flower (the head) in your picture is actually made up of lots of individual smaller flowers (i.e. it is a composite flower). The petals are formed by ray flowers, and the central part, the disc is made up of disc flowers. More details at the WP page I have linked to for Compositae.


What happens with the nitrogen in blood in membrane oxygenators?

It gets diffused out, like you expected.  Grist (2013) writes about this in relation to "the bends," which has already been mentioned by user1136.  He writes:

Cavitation of blood containing normal oxygen and nitrogen levels by mechanical heart valves after implantation generates bubbles that can be detected in the brain using transcranial Doppler ultrasound (2). These bubbles are mainly nitrogenous. Nitrogen is less soluble in water than oxygen. So during excessive turbulence, temperature changes, or pressure changes, nitrogen is the first gas to come out of the solution. (Ask any knowledgeable diver about the physiology of the bends.) We know these bubbles are mainly nitrogen because when the nitrogen in the patient’s blood is off-gassed by breathing 100% oxygen, the cavitated bubbles go away. In one study, the administration of 100% oxygen by facemask reduced the cavitation generation of GME by 98% (3). [Emphasis added]

Can't say it a lot better than that and the rest of the article.  When people are breathing de-nitrogenated air, it simply results in nitrogen being diffused out of the blood.  So yeah, basically the amount of N2 goes down to 0, at least if they are on it for long enough.
As for it being bad for you, not really, at least not perceptibly: though nitrogen is critical for body function, it's practically useless to the body in the N2 form; it has to be "fixed" to a more reactive form such as ammonia / other nitrogen oxide.

Sources

Grist G. 2013. Oxygen or Nitrogen: Which Is the Lesser of Two Evils? J Extra Corpor Technol 45(1): 61-63.

Sprent JI, Sprent P. 1990. Nitrogen fixing organisms: Pure and applied aspects.


How do physics notions of fluid dynamics relate to pressure gradients in circulation?

As far as we know so far, biology isn't able to break any laws of physics.
However, biology isn't passive: biological systems react to changing environments to maintain some level of homeostasis. Arguably this is one of the defining characteristics of life.
If you narrow the aorta, you will always get compensatory changes. Ultimately, the circulatory system is tasked with delivering sufficient blood to the body. It might be a bit of an oversimplification, but let's assume that blood flow stays constant, because flow is a good measure of the ability of circulatory system to deliver enough oxygen/nutrients to the periphery.
Blood flow is pulsatile, which also adds some challenges in understanding things simply, but let's simplify and think in terms of mean pressures. Again, this is wrong, but it's not terrible, kind of like when in a physics class you discuss a "uniform spherical cow" or something like that.
We can start with an equation you mentioned:
ΔP=Q*R
You write:

In this condition the radius of the blood vessel decreases which should mean that pressure decreases too

This is false. If we keep flow (Q) constant, but R increases due to a constriction, then ΔP, the change in pressure, must increase.
Consider:
ΔPaorta=Q*Raorta
If Q stays constant, but R (resistance) increases due to the decreased radius, then ΔPaorta must increase: there is a larger pressure drop. Perhaps you've confused the larger change in pressure with a "decrease in pressure" because there is this larger pressure drop?
Consider also that we can consider the rest of the parallel vasculature (all branches off the proximal aorta) in series with the aorta. If we think of the vasculature after the aorta as:
ΔPdistal=Q*Rdistal
then you can think of the whole system as:
(ΔPaorta + ΔPdistal) = Q*(Raorta + Rdistal)
If only the aorta is constricted and the distal vasculature keeps the same pressure and flow, then ΔPdistal must also not change. Therefore, the total pressure drop (equal to the difference in pressure between the aorta and great veins, the sum ΔPaorta + ΔPdistal) will be larger when ΔPaorta increases.

As far as Bernoulli:

This theorem and the fact that velocity has to increase to maintain a stable flow through the coarctation should mean that the pressure gradient drops. Moreover in every textbook I've found it is said that tension on the aortic wall increases too but this seems even more counterintuitive

Due to Bernoulli, if you go from large (A), to small (B), to large (C) diameter in some vessel, yes, you will have less outward pressure in the segment (B). You will also always have decreasing energy from A to B to C. However, think about what we were just talking about: if you want to keep the perfusion of the rest of the vasculature constant, that means you have to keep the energy at C (interchangeable with pressure in this context) constant, despite the constriction. You shouldn't be thinking about A B and C here when comparing a vessel with and without stenosis, you have to think about the non-stenosed case where you have large (X), large (Y), large (Z). In this case, you still have decreasing energy from X to Y to Z, but without the stenosis, you don't lose as much going through segment "Y". It is segment A that requires more energy/pressure/tension on the vascular wall compared to segment X.
There's some simplification here regarding vascular compliance, non-Newtonian fluids, and vascular permeability but these can be mostly ignored for these purposes. I think this website will help you a lot:
https://www.cvphysiology.com/Hemodynamics/H001
especially
https://www.cvphysiology.com/Hemodynamics/H012
for the part about Bernoulli's principle.


Are humans more adapted to "light mode" or "dark mode"?

A question that requires quite a lot of guts to ask on this site :) Nonetheless, and risking sparking a debate, there are a few arguments that spring to (my!) mind that can support the notion that we thrive better in 'day mode' (i.e., photopic conditions).

To start with a controversial assumption, humans are diurnal animals, meaning we are probably, but arguably, best adapted to photopic (a lot of light) conditions.
A safer and less philosophical way to approach your question is by looking at the physiology and anatomy of the photosensitive organ of humans, i.e., the retina. The photosensitive cells in the retina are the rods and cones. Photopic conditions favor cone receptors that mediate the perception of color. Scotopic (little light) conditions favor rod activity, which are much more sensitive to photons, but operate on a gray scale only. The highest density of photoreceptors is found in the macular region, which is stacked with cones and confers high-acuity color vision. The periphery of the retina contains mostly rods, which mediate low-visual acuity only. Since highest densities of photoreceptors are situated at the most important spot located at approximately 0 degrees, i.e., our point of focus, and since these are mainly cones, we apparently are best adapted to photopic conditions Kolb, 2012).
An evolutionary approach would be to start with the fact that (most) humans are trichromats (barred folks with some sort of color blindness), meaning we synthesize our color palette using 3 cone receptors sensitive to red (long wavelength), green (intermediate) and blue (short). Humans are thought to have evolved from apes. Those apes are thought to have been dichromats, which have only a long/intermediate cone and a blue cone.  It has been put forward that the splitting of the short/intermediate cone in our ape ancestors to a separate red/green cone was favorable because we could better distinguish ripe from unripe fruits. Since cones operate in the light, we apparently were selected for cone activity and thus photopic conditions (Bompas et al, 2013).

Literature
- Bompas et al., Iperception (2013); 4(2): 84–94
- Kolb, Webvision - The Organization of the Retina and Visual System (2012), Moran Eye Center
Further reading
- Why does a light object appear lighter in your peripheral vision when it's dark?


Can kit foxes and red foxes produce offspring?

Yes, a red fox and a kit fox could produce hybrid offspring, but it would be sterile.

Sterile red fox / arctic fox (V. lagopus) hybrids have been bred for the fur trade for decades (source).

Arctic foxes are quite closely related to kit foxes, and both species are equally distantly related to red foxes, so since one can produce hybrids then the other should be able to as well. Here's a screenshot from onezoom.org showing their relation. (Arctic fox = Vulpes lagopus)

Red fox / kit fox hybrids have not been observed in the wild, and kit foxes are not widely kept in captivity except in zoos, so I am not aware of any record of such hybrids. It would likely take intentional effort on the part of a fox breeder to produce them.


A good exemple should be the “harpoon” in cone snails (Conidae), which is created from a modified tooth inside their proboscis.

(Cone snail with proboscis, from KQED.org)
The harpoon is launched at prey at close distance, and is used to poison and stun prey, and later to pull them in. According to high-speed camera capture the harpoon is launched in just 200 microseconds, with an acceleration similar to a gun. The “harpoon“ structure is also very similar to a human made harpoon (see picture below)

(from KQED.org, Courtesy Manuel Jimenez Tenorio, Universidad de Cádiz)

(from KQED.org, Courtesy Joseph Schulz, Occidental College)
These harpoons are not re-used, and a cone snail can have up to 20 harpoons at different stages of development (see Cone snail toxicity).
It is also worth noting that the harpoon and its venom is a potent defence weapon also against humans. One cone snail can contain poison to kill about 700 people, and people stung by cone snails can get severely injured or even die (fatality reported to 15-75% according to Kapil et al, see below).
If you would include use of tools, in projectile use/shooting animals, apes and elephants are known to use stones as throwing weapons (see wiki-page linked below).
Sources:
https://www.kqed.org/science/1923898/watch-these-snails-stab-fish-and-swallow-them-whole
wikipedia: projectile use by non-human organisms  (with other examples of projectile use)
Kapil S, Hendriksen S, Cooper JS. Cone Snail Toxicity. [Updated 2020 Sep 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. www.ncbi.nlm.nih.gov


In humans, the amnion (amniotic sac) persists from the primitive amniotic cavity1.  One side of this is formed from the cytoblast (a prismatic epithelium) and the plasmodioblast.  Together these two layers are the ectoplacenta or chorion.  They are also referred to as Rauber's layer.  These replace the lining epithelium of the uterus, whereupon internal cells undergo atrophy to create the amniotic sac.2

The other side of the amniotic sac is formed of the epiblast/ectoderm (internally) and the hypoblast (externally).  Within the epiblast the other layer is comprised of prismatic cells whereas the inner layer are flattened (the hypoblast/entoderm).  This double layer forms the bilaminar blastodermic membrane.2

I'd really reccomend that you borrow the referenced books from your university library as I found the diagrams much easier to understand than the text.

1 Gray, Henry. "Embryology: Formation of Membranes." Ed. Robert Howden. Anatomy Descriptive and Surgical. Ed. T. P. Pick. 15th ed. London: Chancellor, 1994. 90. Print. Colloquially Gray's Anatomy

2 Gray, Henry. "Embryology: The Ovum." Anatomy Descriptive and Surgical. Ed. T. P. Pick and Robert Howden. 15th ed. London: Chancellor, 1994. 82-83. Print. Colloquially Gray's Anatomy


Why does immunity from the flu vaccine appear only after two weeks?

Most information here can be found broadly in Cellular and Molecular Immunology, 8th Ed.

Here's how the flu vaccine works: Scientists forecast months in advance which strains they think stand to cause the most problems. The vaccine is often trivalent, protecting against three different strains on flu: Two influenza A and one influenza B. You can read about the process directly from the CDC.

The two major viral receptors are neuraminidase and hemeagglutinin. They determine the serotype of the virus, such as H1N1. They serve as peptide antigens for immune recognition. Where influenza infects a cell, it starts to produce proteins essential to it's replication in the host cytoplasm.

The innate immunue system, upon realizing there's an infection, does quite a bit to try and mitigate things but it's a messy job. Looking at the link, lots of inflammation, damage and dead tissue. At that, there will be no memory of the same infection, and the same process happens over and over unless there's a better way to take care of things.

This is really where your adaptive immune system comes in, T/B cell, antibodies, etc. A wild type influenza virus stimulates the same adaptive response as the strains in a flu vaccine: Proteins such as the neuraminidase are picked up by macrophages or dendritic cells, and they enter transport to the closest lymph node. On the way, they chop up the viral protein into peptide antigens and load them onto MHC-II molecules, and export the complex to the cell surface, becoming antigen-presenting cells or APCs. T cells expressing CD4 coreceptor can interact with the MHC-II on APCs in a cascade of events that lead to effector T-helper (Th) cells. Th cells, in concert with follicular dendritic cells and recognition of cognate antigen by naive B cell can result in proliferation and differentiation of B cells to plasma cells that secrete antibodies specific to the viral antigen that was initially recognized.

The problem, is that this process takes time to ramp up plasma cells numbers and antibody production. The average time often denoted by literature is about 2 weeks.

Furthermore, with adaptive immunity you get memory cells that will remember a given infection and quickly resolve it with antibodies should you ever catch the same bug.

The difference between our wild type influenza and the ones in the vaccine is attenuation. The point of the wild type influenza people often catch is it's really good at infecting humans, and upon infection it causes a lot of damage. We can attenuate influenza's pathogenicity by growing the flu strains in tissue that is not human. Over a few generations, the virus adapts: it becomes more pathogenic/virulent in non-human tissue, but harmless to humans. You then remove the harmful parts of the hemeagglutinin and neuraminidase genes from a wild type strain to get inert HA and NA (so that you get the wild type immunogenicity), combine them with structural proteins from the attenuated strain, and combine them to form a new, live-attenuated vaccine strain that can be grown in the non-human tissue (see image below).

So also keep in mind that just because your infection resolved in under 2 weeks that the antibodies you produced wont help you from getting the same bug again. During flu season it tends to come at your from all sides and the antibodies that evetually get produced help a lot.


What is the name of the groove down the middle of an anther?

I think what you are looking for is the connective. Anthers are usually two-lobed and connected by a band of sterile tissue that also connects the anther with the filament - therefore the name, I guess (see Wikipedia article for stamen). It says

  Most commonly anthers are two-lobed and are attached to the filament either at the base or in the middle area of the anther. The sterile tissue between the lobes is called the connective.

Each anther lobe usually consists of two pollen sacs (see Wikipedia article for microsporangia). It says:

  Each anther lobe develops two pollen sacs. Thus, a two-lobed anther develops four pollen sacs situated at four corners of the anther.

And further (accentuation by me)

  The cells of endothecium possess fibrous thickenings. They remain thin-walled and constitute stomium (line of dehiscence) in the shallow groove in between the two microsporangia of the anther lobe.

This groove frequently is called by its orientation, i.e. longitudinal groove, even though I do not think this really is a well-defined technical term (but do a quick Google search for "longitudinal groove" anther and you will find several biology books using the term, e.g. this).


What is the difference between "cistron" and "gene"?

A cistron is a gene - here's how the word came about:

It's 1955. The proposed double helical structure of DNA has been published and the race is on to understand the implications of this for genetics. Geneticists have been working with genes for decades, but they don't know what genes are. Sanger has sequenced the two polypeptides of insulin, so the idea of a specific sequence of amino acids is established. The emerging molecular geneticists believe that genes will be explained by a feature of DNA, probably a sequence of nucleotides, but they don't know how. Crick and others are theorising about coding (i.e DNA > protein), but at this stage there is no genetic code, no mRNA or tRNA.

Seymour Benzer, at Purdue, is working on fine structure of a genetic region in bacteriophage and in this year he publishes a key paper with that phrase as the title. Without going into a lot of detail about his experimental set up, he is studying a region of the bacteriophage T4 genome called rII. Wild-type T4 can form plaques on E. coli B or E. coli K12. Mutations in the rII region cause a large plaque phenotype in E. coli B so it is easy to isolate them, but these phage cannot produce plaques on E. coli K12 which sets the scene for a powerful assay for rare recombination events.

Benzer used this system to do very fine mapping of thousands of rII mutations because he was able to use the system to measure recombination frequencies, but what matters in the present context is that he was able to do a kind of complementation test (he called this pseudo-allelism). He was able to assign the rII mutants into two groups according to whether, in a mixed infection, they produced lots of progeny. So if he mixed two phage with different mutations and didn't get many progeny he put these in the same group. On the other hand if he did get a lot of progeny he placed the two in different groups. He called this approach a cis-trans test.

  "The application of the phenotype test to pairs of rII mutants leads to the division of the region into two functionally separable segments."

This is as close as he dared to go to claiming to be studying genes. He refers to 'functional units' but never uses the word 'genes' because at this stage that word belonged to classical genetics in higher organisms. In 1957 he proposed the word cistron for the functional unit defined by this type of test, and the word caught on, particularly because of its incorporation into the operon model with the idea of polycistronic mRNA. His other coinings, muton and recon were not adopted.

The two T4 genes/cistrons in the rII region of the phage genome are now called rIIA and rIIB.

  Benzer, S (1955) Fine structure of a genetic region in bacteriophage Proc. Natl. Acad. Sci. USA 41:344-354


Why does the butterfly have a cocoon stage in its life cycle?

Holometaboly is believed to have evolved only once (Labandeira, 2011), but is arguably the most successful mode of development we know of in terms of species richness (Kristensen, 1999 - PDF link). Insects which have adopted this method are far more diverse than their hemimetabolous counterparts. A conservative estimate by Hammond (1992) is that holometabolous insects comprise more than 60% of all living organisms.

The subclass Pterygota (winged insects) is divided into (super orders) endopterygota (wings develop interiorly) which are holometabolous, and the exopterygota (external wing development) which are hemimetabolous.

Hemimetabolous insects (usually) develop from an egg to an adult through a series of immature forms (known as nymphs or instars) which are slightly modified (and usually slightly larger) forms of the preceding form. There are exceptions to this mode within the exopterygota including asexual parthenogenesis which is common in aphids. The general life cycle is well illustrated in the Dermaptera (earwigs). All stages inhabit the same ecological niche and so maintain the same general body plan.

Image file from Wikimedia Commons here

Although hemimetaboly is a more gradual process than holometaboly, it happens in a small number (often four or five nymphal instars) of discrete steps rather than the more continuous development of other animals such as mammals. Although all insects fall into either the exopterygote or endopterygote categories (i.e. wings either develop externally or internally), there are examples of intermediate processes which lie somewhere between hemi- and holometaboly. A notable example are the Cicadas. Cicadas are Hemiperans (true bugs) which lie in the exopterygota and so are, by default hemimetabolous. However there is a considerable difference between their immature and mature stages:

Illustration by Debbie Hadley, using drawings from Insects - Their Ways and Means of Living by Robert Evans Snodgrass, U.S. Bureau of Entomology. These drawings are in the public domain. From here.

During the immature stages, the larva (or nymph) will burrow underground, sometimes for many years. This requires strong front appendages, which they also use when they surface to grip onto a surface whilst they shed their final skin to become an adult. This differential niche exploitation is likely to have given rise to the morphological differences between immature and mature life stages.

Exploiting different niches during different developmental stages not only reduces intra-specific competition between young and adult, it also enables the insect to be more specialised to fulfill their specific role, which changes as they develop. The role of the immature is to grow, they do not yet need to be able to reproduce or disperse; whereas the role of the adult is to find a mate and reproduce. Young often develop below ground where there are fewer predators, adults often fly to enhance dispersal (further reducing competition and also decreasing inbreeding). These two activities call for vastly different body designs.

Some other common holometabolous insect orders are Coleoptera (beetles), Hymenoptera (bees, wasps, and ants), and Diptera (true flies), whereas hemimetabolous groups include Orthoptera (grasshoppers, crickets etc.), Mantodea (praying mantids), and Blattaria (cockroaches).

As for the chrysalis which Lepidoptera (butterflies and moths) have evolved to surround their pupal stage, the main role is likely to be protection. Larvae (caterpillars) are a highly nutritious and energetic food source and thus have adapted defensive mechanisms such as mimicry, warning colours, and dropping to the ground when disturbed. This drop would damage the metamorphosing pupa (the most vulnerable stage as it is usually relatively immobile), as the cuticle softens to allow for cell-rearrangement.

The process of insect development is regulated by juvenile hormone (JH), see Konopova et al, (2011) for more on this.

References

Hammond, P. (1992) Species Inventory. Global Biodiversity (ed B. Groombridge), pp. 17–39. Chapman and Hall, London.
Konopova, B., Smykal, V. & Jindra, M. (2011) Common and Distinct Roles of Juvenile Hormone Signaling Genes in Metamorphosis of Holometabolous and Hemimetabolous Insects. PLoS ONE, 6, e28728.
Kristensen, N.P. (1999) Phylogeny of endopterygote insects, the most successful lineage of living organisms. European Journal of Entomology, 96, 237–253.
Labandeira, C.C. (2011) Evidence for an Earliest Late Carboniferous Divergence Time and the Early Larval Ecology and Diversification of Major Holometabola Lineages. Entomologica Americana, 117, 9–21.


Does caffeine actually enhance cognition?

Caffeine response is dependant on the individual. Caffeine has a very similar chemical make-up to adenosine which your body uses to transfer the energy you eat into energy your body can actually use (chemical energy). When your body has enough adenosine, it begins what is called a negative feedback cycle that stops adenosine production and sustains homeostasis. The feedback loops works by delivering a signal to put the body in a regenerative phase upon further adenosine binding. However, caffeine, being the wonderful individual that it is, disrupts that negative feedback loop and continues the conversion of excess (eaten) energy to chemical energy. But where in your body its dispersed is dependant on the individual.

The conversion to chemical energy is indirect though. Since adenosine is a principal neuromodulator, it actually tricks your body into behaving as it would at your most natural wakeful state. For example: Glutamate, GABA, norephinephrine, serotonin and acetylcholine are all inhibited by adenosine build-up at A1 receptors (a type of adenosine receptor) but caffeine stops adenosine from inhibiting these neurotransmitters. These five neurotransmitters all assist in metabolism (Glutamate is an essential compound in cellular metabolism).

Caffeine will never give you energy, it just uses your energy faster, in fact it probably causes energy debt from the work your body does to flush out the toxin.

In short: Yes it can enhance cognition, if the extra ATP (energy molecule made from adenosine) is carried to the brain. As it is not a homeostatic process it's difficult predict.

When the body is constantly put out of it's homeostasis, it adapts the toxin into its homeostatic balance (kind of like a beat em' or join em'). In this way, an individual's body begins to need the caffeine to function normally. Caffeine dependance is very low however, since it has been around for centuries, we've evolved to know it as a toxin but to not depend on it.

References:

J Alzheimers Dis. 2010;20 Suppl 1:S3-15. doi: 10.3233/JAD-2010-1379.

http://thebrain.mcgill.ca/flash/a/a_11/a_11_m/a_11_m_cyc/a_11_m_cyc.html

http://pharmrev.aspetjournals.org/content/51/1/83.short


Are both B and Y ions required to determine the sequence of a protein by mass spectrometry?

In an MS/MS spectrum, difference between the successive peaks of a b or y ion series allows one to determine the amino acids making the series/peptide. Either one of them should be enough to give you the sequence. However, an MS/MS spectrum obtained from the mass spec instrument doesnt tell fragment types. Therefore it takes some expertise and tricks to spot y or b ion series. For example: if you are analysing a sample digested by trypsin, your C-term residue will either be K or R. So you can look for a Y1 ion if there is 147 indicating K or 175 indicating R. Also, Y ions tend to be highest intensity peaks in a spectrum. For more helpful tips on this there is an excellent tutorial :
http://www.ionsource.com/tutorial/DeNovo/DeNovoTOC.htm.

Also, in practice you seldom get all of the b or y ion peaks and there are often missing peaks. For this reason it is useful to have both b and y ions series so that gaps in one can be filled by the other. This is not only useful when you are dealing with denovo sequencing but also in a more typical shotgun proteomics experiment. In a typical shotgun proteomics experiment one searches their mass spec data with peptide search engines. These are software which use a protein sequence database which is in silico digested, based on the specificity of the protease used in the experiment, and from the resulting peptide sequences search engines make a library of predicted MS/MS spectra (this is done by fragmenting along the peptide backbone and listing all possible b and y ions). Then these predicted spectra are matched with the observed spectra to predict the peptide sequences that could result in the observed spectra. Again, not all of the peaks present in a predicted spectra will be found in an observed spectra. So it is best to have ions from both b and y ion series. More ions matched between the observed and predicted spectra, better is the score and confidence in identification.


How are synaptic vesicles brought to the synapse?

You are looking for a review on vesicle cargoing along the cytoskeleton. This open access article is the most recent I found on the subject.

From the abstract:

  How synaptic cargos achieve specificity, directionality and timing of transport is a developing area of investigation. Recent studies demonstrate that the docking of motors to their cargos is a key control point. Moreover, precise spatial and temporal regulation of motor-cargo interactions is important for transport specificity and cargo recruitment. Local signaling pathways Ca2+ influx, CaMKII signaling and Rab GTPase activity regulate motor activity and cargo release at synaptic locations.

M. A. Schlager, C. C. Hoogenraad: Basic mechanisms for recognition and transport of synaptic cargos. In: Molecular brain. Vol. 2, 2009, p. 25. DOI:10.1186/1756-6606-2-25. PMID 19653898. PMC 2732917.


Was the Okazaki fragment experiment ever replicated?

Formation of Okazaki fragments in polyoma DNA synthesis caused by misincorporation of uracil - Brynoff, et.al. Cell; Volume 13, Issue 3, p573–580, March 1978 one of many, but you only need one to disprove your professor.

You do not always need to replicate the exact same assays in order to validate a model. Replicate means reproduce the same experimental results in which to draw the same conclusion. Another person need not reproduce your work exactly, so long as your results were the results of experiments that you were able to reproduce on your own. Standards for Replication in Science


Calculation of saturation of carbon in surface waters

Take a look at Paragraph 2.

I'll outline it in more or less plain english (I hope).

for 37 lakes they used this method:

1) they took a sample of water from 0.1 to 0.25 m below the surface.  Using a thermos bottle.  This would minimize change of the gas composition of the water with a change of temperature.  The bottle was not sealed, but left out for a while in the air there at the lake (it was "equilibrated with ambient air").  If you were looking for issues you might or might not like this.

2) a sample of air 1m above the lake was taken.

3) they got a gas chromatograph to measure the CO2 in the air above the water sample, as well as in the air from above the lake.  They might have taken the readings right there at the sampling point, or not its not clear. They may have also sealed bottles up and taken them to the lab.  It sort of sounds like a point of sample measurement.

If the air above the water samples had more CO2 than the air above the lake, they called the water supersaturated as the water was emitting CO2.

This method does its best to simplify the question of whether fresh water bodies are saturated with CO2 and emitting it or if they might be absorbing it.  By not outgassing the CO2 in the water and trying to get an absolute content of CO2, they are able to get around the various organisms and minerals in the water and pH which would vary the amount of CO2 the lakes can hold.  they are just focusing on whether the water is giving off CO2.


How does a Na+/H+ antiporter drive osmosis in this "osmotic motor"?

Since posting, I did some more research using background refs from the intro (who knew?). The trick seems to be that when protons are pumped out, the cell regenerates them from water in order to maintain pH. So the solute concentration DOES increase inside the cell with more Na/H transport.


Calculating chromosome number in meiosis: Why is the crossbreed between a fox and a dog (dox) sterile?

This is not simply a question of math, just determining if the diploid number is even or odd. If it was that easy, all hybrids with an even diploid number would be fertile, and that doesn't happen. The problem is way more complex, and it has to do with chromosome pairing.

In the question described, we have the following numbers:

Canis lupus (dog): 2N = 78, therefore N = 39;
Vulpes vulpes (fox): 2N = 38, therefore N = 19;

Now, let's suppose, in an exaggerated simplification, that all 19 chromosomes in the fox's gamete find an exact homologous in the dog's gamete (again, this is very unlikely). So, in this oversimplified scenario, we would have 19 pairs of homologous chromosomes in the hybrid's cells.

However, even if that's the case, we still have 20 chromosomes in the dog's gamete that didn't find any homologue in the fox's gamete.

That mismatch, alone, is enough to block meiosis, particularly at the pachitene checkpoint.


What is the difference between vegetable and animal fats?

There is a subtle difference between oils and fats- oils are generally unsaturated (Carbon-Carbon double bonds) whereas fats are saturated (all single bonds).

  Are these two types of fat have equal influence considering their converting to fat tissue in humans?

No. There are some kinds of fatty acids that are synthesized only by plants (Essential fatty acids). However, these can be obtained indirectly from animal sources such as fish.

Fats have multiple roles- not just storage. They are also critical for making up the cell membrane.

  What are the converting pathways for vegetable oil fats to adipose tissue in humans?

The fatty acids in oils are absorbed in the intestine and esterified (wit glycerol) to form triglycerides. Then, they are incoporated in lipoprotein complexes. There are different types of lipoproteins- VLDL (Very Low Density Lipoprotein), LDL (Low Density Lipoprotein) and HDL (High Density Lipoprotein) which have different sizes and compositions.

When lipoprotein comes in contact with lipoprotein lipase in capillaries, the free fatty acids are liberated from trigycerides, which is taken up by adipose tissue.

The fats stored in adipose tissue depends on diet. This has been studied in rabbit but similar principles may apply to humans too. Fats can also be synthesized in the body. It is always saturated fat and is synthesized by the fatty acid synthase complex. The starting substance is Acetyl-CoA which is produced during catabolism of both carbohydrates and fats.

  if one eat Y of 2 meal if saturated and unsaturated fats, he/she (in equal conditions) will gain X gram if they were saturated fat and Z in a case of unsaturated fats?

By principles of mass balance, if both have equal rates of absorption and degradation then there will be equal gain. According to this study, absorption rate of unsaturated fats is higher. In that case if you eat $X$ grams of both types then the absorbed amount should be $Y_{sat}$ < $Y_{unsat}$

I am not sure about the degradation rates but I think it is higher for saturated fats because unsaturated has to be reduced to saturated before metabolizing via $\beta$-oxidation. Determining the exact steady state values will be tricky without a mathematical model.

NOTE: Dont confuse this with body weight gain (in the sense of obesity); it is a complex phenomenon. You have to consider a lot of things when predicting weight gain.


How do snakes determine the direction of prey from their thermal infrared sensing pit organs?

From Wikipedia:

The facial pit actually visualizes thermal radiation using the same optical principles as a pinhole camera, wherein the location of a source of thermal radiation is determined by the location of the radiation on the membrane of the heat pit. However, studies that have visualized the thermal images seen by the facial pit using computer analysis have suggested that the resolution is extremely poor

Individual pit organs act like pinhole cameras because they are arranged, well, like a pinhole camera: there is an invagination of tissue surrounded by heat-sensitive cells with a smaller hole to the outside world. From Sichert et al 2006 it looks like this:

The dashed lines here indicate heat originating from some distant point source. That point source covers some fraction of the heat-sensitive membrane. Points at different distances and directions will be picked up on different parts of the heat-sensitive membrane. For example, because this source is coming from below, only the top of the pit is illuminated; for a source coming from above, only the bottom of the pit would be illuminated, etc.
If you have access to the Sichert paper, they go into more detail about the mathematics that the pit organ geometry creates. In summary, for any cell you can map a receptive field of places in the world that can project to that spot, and through a summation of these receptive fields across the whole pit organ you can reconstruct a map of where heat is originating. At that point, the principles are no different from visual organs like the retina. The authors show that even with each individual detector having imprecise resolution, the combined activity can be decoded to form a clear image from a simple linear combination of the receptive fields.
Other studies like Chen et al 2012 show that vipers integrate retinal vision with their pit organ senses, because occluding a pit on one side and an eye on the other is worse for prey targeting success than occluding both on the same side. Neuronal evidence of this integration has been observed for quite some time, see for example Newman & Hartline, 1981.
Bothe et al 2019 is a more recent paper investigating some of the neural circuitry behind the processing of pit organ information and integration with vision.

Bothe, M. S., Luksch, H., Straka, H., & Kohl, T. (2019). Neuronal substrates for infrared contrast enhancement and motion detection in rattlesnakes. Current Biology, 29(11), 1827-1832.
Chen, Q., Deng, H., Brauth, S. E., Ding, L., & Tang, Y. (2012). Reduced performance of prey targeting in pit vipers with contralaterally occluded infrared and visual senses. PLoS One, 7(5), e34989.
Newman, E. A., & Hartline, P. H. (1981). Integration of visual and infrared information in bimodal neurons in the rattlesnake optic tectum. Science, 213(4509), 789-791.
Sichert, A. B., Friedel, P., & van Hemmen, J. L. (2006). Snake’s perspective on heat: reconstruction of input using an imperfect detection system. Physical review letters, 97(6), 068105.


Examples of intracellular parasites of medical or economic importance?

As Armatus pointed out above, all viruses are obligately intracellular, and their medical and economic importance cannot be overstated.

Many bacterial species live intracellularly. The arthropod specific Wolbachia has a wide variety of consequences for its host, including alteration of reproduction and sex ratios, induction of reproductive isolation possibly driving speciation, and conferring protection from some viral infections.

Eukaryotes can be intracellular parasites as well: Malaria is a well-known example. Toxoplasma gondii is another intracellular parasite that uses cats as a primary host, but can use other warm-blooded animals (such as humans, rats, and birds) as intermediate hosts. T. gondii infection has been shown to induce behavioral changes in rats, causing an attraction to cats (thereby increasing the chance that the parasite will infect the cat and sexually reproduce). There is also some evidence that T. gondii infection in humans causes behavioral and psychological changes such as decreased reaction times, and links to depression and suicide.


Until a better answer shows up...

A tool strain appears to be a mouse strain that is useful for making recombinant mice.  It has genes inserted into its genome to make detection of your manipulations easier.  In this case several phenotypes (luciferase, human SMN) can be observed as well as a tetracenomycin resistance marker is in place so that offspring with the gene can be easily estimated.

  These Tg(SMN2)89; Smn1+/-; Tg(SMNΔ7)4299; ROSA26rtTA; "old" Luci-TRE-SMN mice allow high levels of both luciferase and full-length human SMN expression to be regulated by the addition/removal of doxycycline. These may be useful as a fluorescent reporter and/or Tet-On/Tet-Off tool strain for doxycycline-inducible rescue of Type II (moderate) proximal spinal muscular atrophy (SMA).


I want to know the name of this water plant?

This is a water-primrose Ludwigia, probably Ludwigia peploides but I am not sure about the species (also because you didn't provide a location). Luwigia peploides and L. grandiflora are native to South america. However, in the rest of the world they are considered invasive weeds. In the European union L. peploides and L. grandiflora are considered "Invasive alien species of Union concern" This means EU member states should take appropriate action against these species.

Water-primrose has a high variation in the shape of the leaves, especially between vegetative and flowering sprouts. On the picture in the question the leaves are almost round. However, on the ground just left of the hand, there are lanceolate leaves, almost willow-shaped. This is the same species and the reason it is also called floating primrose-willow.


Fst Differences Between Mature Trees and Seeds

I will assume the claim Clearly there is genetic differentiation between population 1 and 2 in seeds, but not much in adult trees. is correct and that you have done your stats correctly.

A complete analysis of the situation depends of how you calculated Fst. Did you use Weir-Cockerham Fst or standard Nei's formulation? How did you average (with or without weights) over population and loci? But without going to these details, here is an extreme scenario that explain why you could observe such patterns.

Imagine, the migration rate from any population and to any population is 0.5. In such case, in absence of selection you would not expect any divergence between populations. However, if genotypes AA and AB both have seed survival probability of 0 in pop2 (but not in pop1), then pop2 will be fixed for A2A2 at the adult stage even though when looking at the seeds you cannot see any evidence of divergence.


Studying the epigenetic variability, can I use SNPs?

Starting from what appears to be your main question:

  Can I use SNPs associated with a gene's higher expression to compute the likelihood of that gene being expressed in the brain region?

I would strongly advise against using SNPs determine if genes are expressed (at all) in a given tissue.For one thing SNPs that affect expression (then often called eQTLs) will usually only have small +- effects on expression instead of switching it on/off and also have that effect in many/all cell types. Unless an (individual) SNP has clearly described /and validated effects on gene expression in a specific tissue/brain region, you should assume it has global effects.

Now, luckily for you gene expression in different cell types, tissues etc is a relatively well studied area and there are resources for gene expression in the brain available (brain atlas is probably closest to what you might look for).
You can uses these resources to determine which genes are expressed in your regions of interest and from there on check if SNPs associated with these genes correlate with certain structural brain features you are interest in.

One more thing you note:
The title of your questions (as well es comments) mention that you are interested in epigenetics. Neither gene expression nor SNPs/eQTLS are diretcly linked to epigenetics, so if this is your actual focus you should also look for availbale ChIP-seq data or similar and also include this into your analysis (correlation of SNPs with epigenetic marks is difficult but not impossible)


The fastest vaccine developed is a mumps vaccine, which took 4 years. Where is the hope that we will find a COVID vaccine in less time?

Expectations for accelerated vaccine development are based on two main points.

Groups have been working on vaccines for SARS-CoV-1 since 2003, and much of that work is applicable to SARS-CoV-2 (the COVID-19 virus). Here is a review article discussing work on SARS-2 vaccines based on work on SARS and MERS. One example, transgenic mice are available that express the human version of ACE2, the host receptor protein that allows SARS coronaviruses to enter a cell. These mice allow vaccine testing that is much more informative than cell culture tests, and weren't developed until 2006-2007. SARS was eliminated in 2004, so we can estimate it would take at least two years to develop an animal model for COVID if it wasn't already available.

Here is a diagram from the linked review showing timelines for traditional vaccine development and the accelerated SARS-CoV-2 vaccine development:

Several pharma companies have developed "plug and play" vaccine platforms which allow rapid manufacture of vaccine candidates once a molecular target is known. In this case, the target is the 'S' glycoprotein. Once the sequence that encodes for this target is known, it can be inserted into the platform and produced quickly.

Here is another diagram from the same review describing some of these platforms:

EDIT - I wanted to emphasize a third point: If you notice the "Production (at risk)" text in the accelerated development diagram, it means that pharma companies are producing large amounts of their vaccine candidate before testing is complete, and therefore running the risk that their warehouses full of product will be rendered worthless by bad outcomes in the clinical trials. Moderna had started production of their mRNA vaccine candidate by July 15 2020, so this gives them a several month head start if the trials turn out well.


This is an excellent question. You are on the right track with the random match idea. B-cells (as a group) develop receptors that bind every possible antigen and then get rid of the receptors that match antigens in our body. Some textbooks are a little more careful in their language, though, and say almost every possible antigen.

See Alberts

  The preimmune repertoire is apparently large enough to ensure that there will be an antigen-binding site to fit almost any potential antigenic determinant

I'd note, though, that we've yet to identify an antigen that can't be bound by an antibody.

The process by which an individual's set of B-cells is able to generate all these different B-cell receptors was discovered by Susumu Tonegawa. He was given a Nobel prize in physiology or medicine for the discovery in 1987. You can read about it at nobelprize.org.

In broad strokes, each B cell has multiple copies of different types of gene segments that make up the B cell receptor. When the B-cell develops, it selects one of each kind of segment at random and pastes them together. At the level of the human organism, this generates an awful lot of diversity, but not quite enough to produce receptors that bind every possible antigen. The additional diversity is produced by adding or deleting additional DNA bases at random.

This produces a new problem, though, because with B-cells that have receptors that would bind every possible antigen, we would end up attacking ourself. The details here are the answer to a new question, but the basic answer is that B-cells that would recognize self are selected against, leaving us with a complement of B-cells that have receptors that bind literally every possible antigen that is not self.

Lauren Sompayrac has an excellent introductory book on the immune system that makes these very difficult concepts much more approachable. It's called How the Immune System Works, and I highly recommend it.

Here's a diagram from that book, showing the random selection and pasting together involved in one of the parts of an antibody (the heavy chain):


What stops messenger RNA from binding to itself?

It does fold on to itself. There are secondary structures in RNA and some of these secondary structures also have regulatory functions (for example, riboswitches). Some of these structures can also inhibit translation (by different mechanisms such as the masking of the ribosome binding site or analogous eukaryotic sequences, or stalling of ribosome etc). Other non-coding RNAs like tRNAs and rRNAs fold into specific structures that are essential for their function.

Many assays have been developed to study RNA secondary structure in vivo. SHAPE and DMS-seq are some examples.

The translation initiation factor eIF4A has a helicase activity that helps in resolving some secondary structures and facilitate translation (despite this, some structures can impede translation).

Also check out ribosome profiling experiments.


Phenotype-Genotype for multi-hybrid crosses

In my opinion, the easier way is dealing with each trait separately, as if it was a simple monohybrid cross, and writing down each result:

Aa x aa → $\frac{1}{2}$ Aa;
BB x BB → 1 BB;
Cc x cc → $\frac{1}{2}$ Cc;
dd x Dd → $\frac{1}{2}$ Dd;
Ee x Ee → $\frac{1}{4}$ EE;

Now, simply multiply all the results:

$\frac{1}{2} * 1 * \frac{1}{2} * \frac{1}{2} * \frac{1}{4}$ → $\frac{1}{32}$

I don't know about your country, but in my country of birth all secondary books have a chapter for monohybrid cross and another chapter for dihybrid cross. I don't like that, it creates a nonexistent separation and it makes (some) students memorize concepts. Linkage apart, I like to say to my students to do not mind about dihybrid, trihybrid, tetrahybrid etc crosses, just treat them as individual monohybrid crosses combined.


Effects of selection on effective population size

From Conner and Hartl's A primer of ecological genetics:

  "Any variance in reproductive success among individuals greater than
  random expectations, a commonplace concurrence in natural populations,
  reduces effective population size."

So yes, selection does reduce the effective population size and for the reason you suggest - it removes some individuals from the mating pool/ reduces their contribution to the next generation. Mathematically it can be derived as

$N_e \approx \frac{ 8N_a}{V_m + V_f + 4 }$

where $V_m$ and $V_f$ are sex-specific variances of offspring production (males are often more variable in reproductive success than females).

They give an example of selection affecting $N_e$, in a population of deer 33 males had four times the variance ($V_m$ = 41.9) in reproductive success of 35 females where variance was $V_f$ = 9.1. Thus effective population size was

$N_e \approx \frac{ 8 * (33 + 35)}{41.9 + 9.1 + 4 } = 9.9$

The notation $N_a$ is the actual number of individuals in the population. This can be seen in the calculation of effective population size when the number of males and females are not equal

$N_e = \frac{4 N_m N_f}{N_m + N_f} = \frac{4 N_m N_f}{N_a}$

An example is a population of 80 males and 80 females compared to a population of 70 males and 90 females. Both populations have equal sizes but effective population size is reduced by unequal sex ratios

$N_e = \frac{4 * 80 * 80}{160} = 160 \neq \frac{4 * 70 * 90}{160} = 157.5$


Difference between the spinal cord and vertebrae column

The vertebral column is a bony, segmented structure that supports the torso/head and thorax. The spinal cord is a bundle of nerves that runs inside the structure of the vertebral column. So - they run together, but are completely separate.


How do place cells switch their response patterns when the subject moves to a different environment?

Imagine a 2x2 grid. Starting on the bottom left, how many different ways can you move to each box of the grid?

Two times: 1) up, right, down; 2) right, up, left

Now, say each of those combinations are used to store the memory of a different location. In order to activate either sequence, a different input signal would be required to tell the axon to send it's initial signal right, or up.

Your eyes will receive a signal in the form up light, and a specific electrical impulse will be sent down the optic nerve that allows your brain to perceive an image.

There are millions of nerves in your brain, and each combination of impulses serves to store a different memory.

Now, imagine a grid that has a million by a million boxes. How many combinations can you use to fill each box?

And, actually if I recall correctly, the hippocampus is one of the few areas in the brain that is consistently undergoes neurogenesis.


General time reversible model of evolution and Felsenstein model

The classic answer would be Joe Felsenstein's Inferring Phylogenies. It has substantial technical discussion of GTR and Felsenstein models, among others.
However, it does not have any index entries for "general balance" or "detailed balance". I was not familiar with these terms, so I googled them and they do not appear to be common terms in the phylogenetics field.
These terms do pop up in the MCMC literature a bit regarding transition probabilities, so it seems likely that it is somewhat related in terms of underlying math. However, I think that you are more likely to find phylogeneticists talking about "stationary" or "equilibrium" models rather than in terms of "balance". Possibly a difference in terminology between fields.
It might be helpful to know more about what you mean by these terms and why you are interested in them, in the form of links or otherwise.


For this specific question, let's divide the cells into two categories:

Cells that rarely "navigate" are the cells that are connected to give the tissue its mechanical properties. How do these avoid an "adverse stimulus"? Well, they don't avoid it. But if that stimulus "harms" cells they react in some way:

if the cell is destructed by the pathogen, it will release chemical compounds that have chemotactic properties and attract specialized cells.
if the pathogen has intracellular tropism, the cell may release some chemical compounds (see interferon) to "alert" other cells that something is wrong. Most cells can also present antigens on their surface.
there are also some stimuli which change cellular life cycle turning cells into cancerous cells. These cells can gain excretory properties and produce substances that destroy intercellular jonctions. This is how metastases occur.

Cells that "navigate" are the blood cells. White blood cells respond to different kind of stimuli (chemical) in two ways: either they are attracted (by inflammatory cytokines for example) either they are repelled. Macrophages are attracted by cytokines released when a pathogen agent triggers inflammatory response. They "ingest" that pathogen through phagocytosis and expose some parts of it (the antigens) on their surface receptors. This stimulates lymphocytes which process that antigen and decide if it is self or non-self. If it is non-self, they stimulate proliferation of specialized cells against that antigen. Another type of blood cells, the platelets, although they have no nucleus, have interesting properties: they can adhere to the broken endothelium where they change shape and start to produce different chemical mediators.

Read more on:

Wikipedia contributors, "Chemotaxis," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Chemotaxis&oldid=600637322 (accessed June 28, 2014).
Wikipedia contributors, "Interferon," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Interferon&oldid=608718450 (accessed June 28, 2014).
Wikipedia contributors, "Adaptive immune system," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Adaptive_immune_system&oldid=612379171 (accessed June 28, 2014).
Wikipedia contributors, "Platelet," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Platelet&oldid=614627651 (accessed June 28, 2014).


Technically speaking, locomotion is actually not produced by the brain in cockroaches; there are neurological controllers in the legs themselves which produce locomotion even when contact with centralized nervous system is severed.

I include this for reference, because it was not explicitly stated in your question.  However, I believe it was intended to be implied by the phrase "responsible for controlling."  In other words, from my understanding, you're more interested in what section of the brain actually controls those actions in a normal cockroach.

From Central Nervous Control of Cockroach Walking by Charles R. Froutner, you can see even just in the abstract that the movements became spontaneous when the connection with the segmental ganglion was broken, showing that this is very likely where the control is exerted.  (The segmental ganglion, for reference, is a part of the dorsal "brain" you made reference to.)


Transformation of coordinates found in PDB

The purpose of these matrices is to reconstruct the crystal lattice from the coordinates, which only contain one copy of the repeating structural unit found in the crystal. In other words, they represent the affine transformations required to convert one copy of the repeating unit to its neighbors.
To a biologist (as opposed to a crystallographer), these are not useful except if one of the crystallographic symmetry axes happens to also be a biological dimer (or other multimer) axis. However, in this case, the PDB usually gives an option to download the "biological unit", which includes the coordinates for all neighboring copies that associate in the cell with the copy specified by the original coordinates. I should point out that sometimes the biological unit is in fact smaller than the crystallographic unit, if multiple copies of a monomer or dimer or whatever occur in non-equivalent spatial contexts within the crystal. There is no substitute for biological knowledge to know what the relevant structural unit in the cell is.


Is "Pantherine" a valid vernacular name for this group in English? Sure, although "panther" is much clearer ("Pantherine" in English would mean "like a panther", not "a panther"). Also, many family names are fairly obscure: even a pretty well-known group, like Apidae, would become "Apinine" in your scheme, which is less clear to me than "a family of bees".

Is it a valid family name? No. The International Code of Zoological Nomenclature (ICZN Code), which governs all scientific names for animals, says:

  Article 29.2. Suffixes for family-group names. The suffix -OIDEA is used for a superfamily name, -IDAE for a family name, -INAE for a subfamily name, -INI for the name of a tribe, and -INA for the name of a subtribe. These suffixes must not be used at other family-group ranks. The suffixes of names for taxa at other ranks in the family-group are not regulated. [emphasis mine]

Family names that don't have an "-idae" suffix need to be corrected (ICZN Code Article 32.5.3.1).

Note that the ICZN Code doesn't cover other ranks in the family-group or above.


How can I compare the STRIDE and DSSP output files of a particular pdb file?

Here a solution that does not require you to upload the files to the servers: You can graphically visualize DSSP and Stride at the Sequence Page at RCSB PDB:

http://www.rcsb.org/pdb/explore/remediatedSequence.do?structureId=5P21&bionumber=1

"add annotation" -> Stride and look at the graphical comparison between DSSP and Stride.


How do the variable portions of antibody genes look in cells which don't produce antibodies?

Perhaps you want to ask how VDJ recombination is regulated in non lymphoid cells..

Well even in immature lymphoid cells VDJ recombination is regulated. And also Ig genes are suppressed in T-cell and TCR genes are suppressed in B-cells..
Also, the recombination of Ig is suppressed in T-cell and vice-versa.

RAG-1,2(Recombination activating gene) downregulation partly does the job, but not fully.

Earlier reports say that transcription in the locus is essential and epigenetic regulation of transcription in turn regulates recombination.
But what it exactly means is that accessibility to the RSS (Recombination signal sequences) is limited in a repressed chromatin and recent reports say that nucleosomes are appropriately positioned over the RSS to control recombination.

Have a look at these:

http://www.cell.com/abstract/S0092-8674%2802%2900675-X

http://www.sciencedirect.com/science/article/pii/S0952791506000057

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC204470/


You will find here a very good overview of the main hypotheses that explain senescence.

I am not sure I will answer your question but here are some reactions to your post..

What you say has to do with species selection. Selection selects between various objects/units that differ. These objects may be genes, individuals, populations, species, etc… In other words, there are various level of selection or different units on which selection acts. Wiki

Generally speaking, it is often assumed better to think in terms of selection acting on alleles (gene variants) or on individuals. Therefore, we tend to think that selection acting on genes or on individuals is more effective than selection acting on species. However, selection acts on species and we should not necessarily discard explanation using the concept of species selection.

What you say, if I am not mistaken, if we consider a set of species that are either mortal or immortal, we would predict that selection would benefit the mortal ones. Stating differently, mortal species have some advantage over immortal species that allow them to not get extinct or eventually to speciate more.

However, I don't quite understand the reasons why immortality would be deleterious to species. You say that it leads to overpopulation. So would you expect that a population is lead to overpopulation due to immortality and suddenly disappear because it is overcrowded. It doesn't sound like a well formulated argument to me. You could however argue that mortal species have a much greater individual turnover allowing them to adapt faster to environmental change than would immortal species.


Which texts are good for beginners to understand evolution on the genetic scope?

Books on my shelf right now (I'm an evolutionary genetics grad student)...

Entry level:

Evolution - Mark Ridley (not Matt Ridley)

A primer of ecological genetics - Connor & Hartl

Intermediate:

Elements of evolutionary genetics -  Charlesworth & Charlesworth

Advanced:

Principles of Population genetics - Hartl & Clark

Introduction to quantitative genetics - Falconer & Mackay

Further basic/popular-science books include R Dawkins' Selfish Gene/The Extended Phenotype/The Greatest Show on Earth and of course The Origin of Species by Darwin


What is it called when one human eye is seeing brighter color than the other?

here is forum discussing similar effect ,

where as similar problem which leads to double vision is single eye is called monocular Diplopia.

There are two possible causes discussed in that forum. One is a cataract or an early indication of a cataract, for which a vision specialist visit is recommended.

Another solution is much simpler one of the pupils is more dilated than the other:

  The way your eyes see colors changes throughout the day, not dependent
  only on external conditions. Try this: gently press the palm of your
  hand against one eye (closed), for about a minute; leave the other eye
  open during this time (feel free to blink, of course...). Now, look at
  the world with one eye covered (for a couple of seconds), then the
  other — the eye you help closed will see things as quite more
  saturated, partly because you've fostered its pupil to dilate in the
  time during which it was shut. I recall being confused by this when I
  first started noticing that, upon awaking, either eye would see colors
  differently from the other; simply, the eye rested on the mattress
  would be seeing colors with greater saturation.


If you look at the replication of end of chromosomes, you will see that one of the strand gets shorter every time. To prevent the genes from being disrupted, the ends of the chromosomes have repetitive sequences called telomeres which shorten with every replication but will prevent the disruption of genes.

As you can deduce from the above information, there will be a certain limit to how many times a cell can divide.So, it has been thought that any organism ages because of shortening of telomeres.

Gametes have the enzyme telomerase which will lengthen the telomeres to full length so that the zygote formed will have unshortened telomeres. But, in the case of Dolly the nucleus was taken from a somatic cell and so the telomeres did not lengthen. The age of Dolly at the time of birth was thus the age of mother from which the nucleus was taken.

See : Telomere


How are new people created from the DNA of an aged person. i.e. Why are we young?

Gametes (sperm and ovum), which fuse to form a zygote, arise from germ cells (spermatogonia and oogonia). Germ cells, like stem cells, are maintained carefully i.e the genome is preserved and transposition/recombination events are tightly controlled via different mechanisms.

So these germ cells don't have shortened telomeres. Also, during early embryonic development the future germ cells quickly migrate to an end of embryo and remain there while the rest of the body takes shape.

I'm not sure if it has been demonstrated in an article or not but once I happened to talk to Dr Wakayama (who cloned a mouse frozen for 16 years) and got to know that animals cloned by the process of Somatic Cell Nuclear Transfer have reduced lifespan. (SCNT: the nucleus of a somatic cell is transferred to an ovum and triggered to form zygote).

So, to conclude, if germ cells were not protected from mutations and deleterious recombinations, lifespan would have been reduced with every generation.


Doesn't the sarcomere contract during isometric contraction?

Yes, sarcomeres do contract during isometric contraction, they just don't change the overall length of the muscle. This is due to the tension being transferred to elastic filaments within the muscle that maintain the same muscle length but increase the muscle tension. Thus, this is how sarcomeres can contract while the muscle does not have an overall change in length. (See this link for a paper discussing these elastic elements within the muscle itself; also, this is discussed at this wikipedia link as well).

In an isometric contraction the sarcomere is increasing the tension in the muscle, but without an overall change in length. (Isometric Contraction = No change in length, but INCREASE in tension)

Once a muscle overcomes the tension needed to lift a weight/load, then the tension ceases to increase but the sarcomeres begin to shorten which moves/lifts the load. When the length of the sarcomeres change and the tension remains the same, that is called isotonic contraction. (Isotonic Contraction = No change in tension, but DECREASE in length)

The picture below is from a website discussing these muscle physiology principles and is freely available on the web.