Do mitochondria use ATP in order make another ATP from glucose?

During ATP production through the citric acid cycle, some ATP is used to transport necessary molecules for the reactions.

piruvate molecules are actively transported into the mitochondrial matrix [2]
two NADH equivalents from glycolisis are transported into the mitochondrion and consume two molar equivalents ATP [1]
protons leakage across the mitochondrial membrane leads to reduced ATP from NADH and FADH2 [1]

In theory, one molar equivalent of glucose can generate 38 equivalents of ATP. The actual number is only 25 [1].

References:

Wikipedia contributors, "Citric acid cycle," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Citric_acid_cycle&oldid=610117265 (accessed June 26, 2014).
Wikipedia contributors, "Mitochondrion," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Mitochondrion&oldid=614223751 (accessed June 26, 2014).


Why is it that I can only detect smells if I breathe, and not when I hold my breath?

The olfactory epithelium is located in the highest part of the nasal cavities, overlying the cribriform plate of the ethmoid bone.  In order for you to smell something, the odoriferous molecules have to travel the length of the nostrils (which are a pair of very narrow passages which also happen to be filled with hair) and up though the full height of the nasal cavities, having to pass three sets of baffles (known as the nasal conchae) on the way.

When you take a breath, your lungs and inspiratory muscles form a suction pump which pulls air through the nostrils up into the nasal cavities; some of this air, along with any odoriferous substances contained therein, is swirled up to the top of the nasal cavities, where the olfactory epithelium is located.

In contrast, when you're holding your breath, there is no significant air movement through the nasal cavities, and even airflow contained entirely within the nasal cavities is considerably obstructed (thanx to the aforementioned hairs and baffles); therefore, for any odoriferous substance (such as the perfume you're probably sick of smelling by now) to reach the olfactory epithelium, it has to diffuse all the way from the tips of the nostrils to the top of the nasal cavities on its own.  This is a much slower process, and, therefore, it takes rather a while to notice anything smelly when you're holding your breath - even if it's, literally, right under your nose.


Correlation between muscle size and absolute strength

The short answer to your question is that the work output from a muscle is a combination of physiological cross-sectional area, length, fiber type, and recruitment (how many motor units are activated).

Read on for more details.

Force output (tension) of a muscle is proportional to its physiological cross sectional area (Fundamental of Medical Physiology), and shortening is proportional to the length of the muscle. Work output (force X length) is a function of both. Power (work / time) involves both force, length change, and the shortening velocity. Shortening velocity is related to muscle fiber types.

There is a complex relationship between force output and length. In the graph below, the x-axis is relative length (1.0 being resting). When muscles operate outside a relatively narrow range (gray box), the cross-bridges are either too close together or too far apart to optimally generate force. When the muscle gets really stretched, force goes up, but only because passive tension (the intramuscular connective tissue is getting stretched) increases.

The force-velocity curve below relates relative force output to how fast the muscle is shortening (which can be negative; i.e., lengthening contraction). The green part of the curve is muscle shortening. As velocity approaches 0, the muscle produces maximal shortening force. When the muscle goes into the red part of the curve, force is even higher. In order for a muscle to shorten very quickly, it can't produce a lot of force (far right).

Muscle fiber type generally relates to both the force output of a muscle fiber and it's shortening velocity. There are different ways to classify muscle fibers (enzyme activity, myosin isoform, or the "classical" method):

SO ("slow oxidative"; the dark meat of a chicken) fibers contract slowly, produce lower force but are fuelled by oxidative reactions and thus have good endurance. At the other end of the spectrum, FG ("fast glycolytic"; the white meat of a chicken) fibers contract quickly with high force, but fatigue easily because they get energy from glucose, which is rapidly depleted. FOG fibers are intermediate between the two.


Do lysogenic viruses only infect bacteria?

Bacteriophages are the only viruses where this phenomenon is called lytic and lysogenic cycle. There is a similiar phenomenon in humans (and other mammals as well) which is called "endogenous retrovirus" and is pretty common.
For humans, there are estimations that something between 5 and 8% of the human genome are made of endogeneous retroviruses. See these two references:

Long-term reinfection of the human genome by endogenous retroviruses.
Endogenous Retroviruses and Human Evolution

Otherwise I can recommend reading the article on "Endogeneous retroviruses" in the Wikipedia, it is pretty extensive and has a lot of references.


If you search the web or Google Scholar, you should be able to find plenty of examples of colocalization protocols.
In general, though, for each target you're going to want to have an unstained control sample (you can use one for all targets), a secondary-only sample to look for non-specific background staining, and a single-color sample (primary plus secondary). Then, you'll have a sample with both primaries and both secondaries. You always add the primaries at the same time, and the secondaries at the same time.
As you start getting into higher numbers of colors, you'll also need an FMO (fluorescence minus one) control for each color so you can test for signal bleed-over from one channel to another. This sample will combine all the colors except for one.


I think the poster wants only a simple answer, so I am going to answer in simple terms. The fates can be -

1 Used in cellular respiration as fuel and some amount can be converted to useful energy which can be used to build other substances and some energy can be lost as heat.

2.The animal can become prey for other animal.

3.The animal throws away some matter as feces.


How is C4 pathway more water efficient than C3 pathway in photosynthesis?

Actually, water is used in the light-dependent portion of photosynthesis, not the Calvin cycle.

The added water efficiency doesn't actually relate to water's involvement in chemical processes of photosynthesis at all. Water is instead lost incidentally through stomata when they're opened to allow CO2 into the leaves (see here for explanation). This CO2 IS required for the light-independent Calvin cycle.

Both C4 and CAM plants preserve water by decoupling (in space or time) C-fixation from the rest of the Calvin cycle (see here). They instead "store" carbon in 4-carbon molecules to use as a C source in the absence of CO2 (i.e., when stomata are closed). In doing so, they can perform the Calvin cycle without receiving more CO2. As a result, C4 and CAM plants can photosynthesize without having their stomata open all the time (or during the heat of days for CAM plants). The final result: less water lost through evaporation out of the stomata


Albeit used in the keywords of the paper, feather pecking is not an addiction, but normal behavior turned pathological in artificial (overcrowded) environments.

Addiction typically arises through overstimulation of reward centers in the brain, most notably the dopaminergic pathways involving the nucleus accumbens. Massive dopamine release, e.g. through cocaïne or meth intake, results in euphoria (Wise & Bozarth, 1985). When the drug's effects wear off it is followed by the 'crash', characterized by dysphoria and a longing for more drugs (CSAT, 1999). Gambling addiction works much in the same way.

Addiction develops because of an interplay of dependence and tolerance. Dependence is caused by downregulation of dopaminergic responses in the reward centers. Notably, dopamine receptors are downregulated when dopamine agonists like stimulant drugs of abuse are chronically administered. Downregulation of dopaminergic responses causes the physiology of the reward pathway to adapt to the presence of dopamine agonists. While the drug is in the system, everything is OK. However, once the levels of the dopamine agonist wears off, the body enters a state of lack of dopaminergic responses, causing dysphoria and depression. Tolerance develops as the liver and other tissues start breaking down the drug more efficiently due to upregulation of the necessary catabolic enzymes. Hence, more of the drug is needed, and the user becomes more and more tolerant. The interplay of dependence and tolerance form the dreaded vicious, downward spiral of addiction.

The reward centers have been crucial in evolution, as they provide motivation to vital acts of life, including eating and sex (University of Colorado, Boulder). Without a proper reward system, why eat or reproduce? However, drugs and other addictive acts such as gambling also activate the reward system.

Highly purified drugs such as crystal meth and cocaïne result in massive dopamine release that is unparalleled by normal physiologic processes such as eating. Before the occurrence of stimulants and things like gambling, the reward system was nothing but essential to life and evolution. Now, things are different and man needs to adapt to these novel, artificial pleasures in life.

References
- Treatment Improvement Protocol (TIP) Series, No. 33. Center for Substance Abuse Treatment. Rockville (MD); 1999
- Wise & Bozarth, Psychiatr Med (1985); 3(4): 445-60


Identification of brown butterfly with orange/black/white spots

I think this is the "Dark Evening Brown" or Melanitis phedima possibly Melanitis phedima bela:

Some further information can be found here (image 1) and here (image 2). If you look close at the second image, you can see the spot on the wing.

Why they are coming into the houses is something I can only speculate about, but probably they are either attracted by light or by warmth.


Given that skin tags are considered benign, it doesn't surprise me to find very little published research focusing on them. It's unlikely that much grant money exists to answer questions about them.

That said, though, I found a handful of groups that have done some work on them. It seems that they all noticed a statistical relationship between the occurrence of skin tags, obesity and metabolic syndrome. These are the papers describing their research efforts so far:

http://onlinelibrary.wiley.com/doi/10.1111/j.1468-3083.2011.04401.x/epdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740583/

http://www.ncbi.nlm.nih.gov/pubmed/21860156

None of the groups suggest a mechanistic explanation for the occurrence of skin tags, which makes me think that this remains a very open question. However, they all notice a correlation between skin tags and elevated leptin levels.

Leptin is best known as a hunger/satiety regulating hormone. However, it functions through the activation of the JAK/STAT pathway, which in turn activates a number of genes involved in cell survival and in turning off apoptosis, or programmed cell death.

This image comes from this paper in Nature, which, unfortunately, is behind a paywall.

So, my guess based on these data is that increased levels of leptin activate proliferative pathways in cells, leading to the occurrence of skin tags. That this proliferation results in benign cell growth probably has to do with competing tumor-suppressor and related pathways, which I can reasonably assume to be active and functioning, where outright cancer is not present.

What I wonder now, but can't find any information on, is whether skin tags are the only visible evidence of differential cell proliferation, or whether there are other instances within the body. That is, if the leptin-to-skin-tag hypothesis holds, is there something special about skin cells in that response, or are they just the only visible signs of it?


Pros and cons of amino acid structure vs DNA sequences for evolutionary comparison

Amino acid (protein) structure has its advantages over raw DNA.

Protein structure already has introns (noncoding regions) trimmed out which aren't obvious from a plain DNA string.

A protein can have different shapes (such as unbound/bound) or even folded/misfolded (as in the case of prions). DNA doesn't have a way of encoding these changes as they are dependent on substrates, environmental factors and available energy.

Visualizing the 3D structure of a protein can give insight into its functionality that you can't read off a DNA string.


Can elephants trumpet when they have water in their trunks?

I think no. Because the elephant uses its trunk to make noise and if the trunk is filled with water then there is no chance the voice would come out.


What's the smallest animal with hemoglobin running in its veins?

It depends how different from human hemoglobin it can be and still count as hemoglobin.  Here is a cool evolutionary tree of globins.

http://www.mhhe.com/biosci/genbio/enger/student/olc/art_quizzes/genbiomedia/0329.jpg

Here is the worlds smallest fish.  Fish have hemoglobin similar to that of humans.
from Wikipedia:  The world's smallest fish is Paedocypris progenetica1 from Indonesia, with mature females measuring 7.9 mm (0.31 in).

But I think bloodworms are even smaller. They have hemoglobin too.  It is evolutionarily more distant from us but they use it for the same reason we do.

from https://www.prestoninnovations.com/img/media/Seq-7.jpg

http://www.allaboutworms.com/the-basics-of-blood-worms

  Blood worms are red because their blood plasma contains haemoglobin,
  like human blood. Also spelled “hemoglobin,” haemoglobin increases its
  ability to take up oxygen. The larvae commonly burrow in the
  oxygen-poor mud bottom of pools and rivers, so haemoglobin is of great
  value to the larvae.

If you are going to allow very distant relatives,  I think this snail is even smaller than the smallest bloodworm.  Less than 1 mm.  Molluscs have hemoglobin too.

from https://www.slideshare.net/fmoretzsohn/texas-seashellsmore-than-you


Disuse and lack of exercise are actually exceedingly new problems when considered on an evolutionary scale.  The bigger evolutionary pressure for the last few million years has been not starving to death, therefore not maintaining expensive muscle fibers unless they were absolutely necessary.

I haven't found any evidence of previous musculature effecting growth, but I'm going to look into it more (only some quick pubmed searches), and edit this answer.  If someone else knows more immediately, please feel free to answer.


Is it ok if I define Genes this way in Biology?

The term gene has been defined (by Wilhelm Johannsen) much before we even knew about the structure of DNA (by Watson and Crick). As such, a gene is typically a vaguely defined functional unit in the genome that codes for a gene product (typically a protein). Have a look at the wikipedia entry for more info.
For a given gene, you might have different variants. Such variant is called an allele. Let's consider a given phenotype such as eye color for example. There would be a gene that we could call "EyeColor" and there could have different alleles at this gene that we could call "BlueEyes", "BrownEyes", "GreenEyes", ...
Of course, in reality it is rarely that easy. A given phenotype is often the result of the interaction of alleles at several genes. Also, the environment (type of food, temperature and many other things) affect a lot the phenotype of an individual.
From your comments, it is made clear that you do not understand the interplay of the different factors that affect variance for a phenotype in a population, you have to understand the concept of heritability. You might want to read Why is a heritability coefficient not an index of how “genetic” something is?.

Genes are found in chromosomes

This sounds like a chromosome is a box containing genes which is misleading. In this regard, I like the folded shirt analogy by @terdon below in the comments.

and their job

In science, always avoid the concept of purpose, of goal, of intention. Things just happen.

is to show us

As if genes wanted to please humans. Sounds very wrong.

the traits of someone (height/hair color)

Genetic variance in population does affect phenotypic variance in the population indeed.
Answer to comment

just want a clarification on why genes are found in chromosomes isn't clear?

No, it was not clear and it still is a bit unclear (but I'll give some info below that will hopefully help). The easier for you is probably to have a look at an intro course to molecular genetics such as this one by Khan Academy for example

DNA is found in chromosomes, and large strings of DNA are genes so why?

DNA is a big molecule which contain the genetic information. It looks like that

To be more accurate the genetic information is held in the sequence of base pairs (base pairs shown on the figure). In eukaryotes (animals, plants, fungi and others but not bacteria, archea or viruses) there are several big molecules of DNA and each one is organized into a chromosome. Here is a drawing to help you visualize that

If you screen through a human genome, you will realize that the vast majority of the sequences of base pairs are not within genes. There are many other sequences such as regulatory sequences, repetitive sequences and other things. Note, also that within a gene (but again the term gene is typically poorly defined) not everything will end up coding for a protein. Only about 1.5% of the human genome directly code for a protein.
Giving you a complete answer would require writing way too much. It is much simpler to seek for further information on such introductory questions in a introductory course to molecular genetics (as the khan academy course I recommended earlier).


Three different types of cones in the eye are sensitive to three different, contiguous and slightly overlapping, sections of the visible spectrum. The nerve signals from these three different types of cones are interpreted by different sections of the brain as cyan, magenta, and yellow, from which all the discernible colours are composed. This forms the familiar Colour Triangle.

The sides of the Colour Triangle bulge slightly (I believe) because of the slight overlap in the sensitivity ranges of the three cone types.

Colour blindness occurs when someone is born with only two (or rarely one or none) different types of cones, instead of the usual three. This causes an inability to detect one of the thee sub-spectra.


For some classes of antiseptics the effect is more simple chemistry or even physics than biochemical toxicity. Ethanol will just denature proteins and dissolve the membrane, and the used concentration of ethanol is so high that no amount of efflux pumps is going to save the bacterium. Some other compounds work in a similar brute force way: QACs will break the membranes, hydrogen peroxide will just oxidize everything. For iodine (like in PVP-1) the mechanism is not really known, but probably it also just reacts with all kinds of things in/on the bacterial cell and kill them.

Antiseptic resistance could happen for some other antiseptics (or low concentrations of the compounds mentioned above). For some antibiotics, resistance is caused by the expression of efflux pumps that just pump out enough antibiotics so the cell survives. Bacteria could do the same for these antiseptics. The reason why it's not that much of an issue is that the application is rather different. Antibiotics are for inside use, antiseptics for topical use, you cannot just flood your whole body with 70% ethanol to kill all bacteria, but for a wound / something dirty this is just fine. This makes it much easier to avoid creating resistance.


What is the evolutionary advantage of red-green color blindness?

Short answer
Color-blind subjects are better at detecting color-camouflaged objects. This may give color blinds an advantage in terms of spotting hidden dangers (predators) or finding camouflaged foods.

Background
There are two types of red-green blindness: protanopia (red-blind) and deuteranopia (green-blind), i.e., these people miss one type of cone, namely the (red L cone or the green M cone).

These conditions should be set apart from the condition where there are mutations in the L cones shifting their sensitivity to the green cone spectrum (deuteranomaly) or vice versa (protanomaly).

Since you are talking color-"blindness", as opposed to reduced sensitivity to red or green, I reckon you are asking about true dichromats, i.e., protanopes and deuteranopes. It's an excellent question as to why 2% of the men have either one condition, given that:

Protanopes are more likely to confuse:-

Black with many shades of red
Dark brown with dark green, dark orange and dark red
Some blues with some reds, purples and dark pinks
Mid-greens with some oranges

Deuteranopes are more likely to confuse:-

Mid-reds with mid-greens
Blue-greens with grey and mid-pinks
Bright greens with yellows
Pale pinks with light grey
Mid-reds with mid-brown
Light blues with lilac

There are reports on the benefits of being red-green color blind under certain specific conditions. For example, Morgan et al. (1992) report that the identification of a target area with a different texture or orientation pattern was performed better by dichromats when the surfaces were painted with irrelevant colors. In other words, when color is simply a distractor and confuses the subject to focus on the task (i.e., texture or orientation discrimination), the lack of red-green color vision can actually be beneficial. This in turn could be interpreted as dichromatic vision being beneficial over trichromatic vision to detect color-camouflaged objects.

Reports on improved foraging of dichromats under low-lighting are debated, but cannot be excluded. The better camouflage-breaking performance of dichromats is, however, an established phenomenon (Cain et al., 2010).

During the Second World War it was suggested that color-deficient observers could often penetrate camouflage that deceived the normal observer. The idea has been a recurrent one, both with respect to military camouflage and with respect to the camouflage of the natural world (reviewed in Morgan et al. (1992)

Outlines, rather than colors, are responsible for pattern recognition. In the military, colorblind snipers and spotters are highly valued for these reasons (source: De Paul University). If you sit back far from your screen, look at the normal full-color picture on the left and compare it to the dichromatic picture on the right; the picture on the right appears at higher contrast in trichromats, but dichromats may not see any difference between the two:

Left: full-color image, right: dichromatic image. source: De Paul University

However, I think the dichromat trait is simply not selected against strongly and this would explain its existence more easily than finding reasons it would be selected for (Morgan et al., 1992).

References
- Cain et al., Biol Lett (2010); 6, 3–38
- Morgan et al., Proc R Soc B (1992); 248: 291-5


Which information can be obtained from a list of gene names?

I would suggest searching the name in any trusted genetics database such as NCBI's GenBank (http://www.ncbi.nlm.nih.gov/genbank/). You can just Google search it, but it may take a little longer to find useful information that way.

I hope this helps and good luck with your research,

CDB


What exactly is this small puffer fish doing and how did it manage to accomplish such a feat?

A tiny Japanese puffer fish creates a grand sand sculpture on the featureless seabed by using his fins to dig furrows. He uses this to attract the attention of passing females.

  Why do puffer fish build sandcastles? (BBC)

  Further observation revealed that this “mysterious circle” was not just there to make the ocean floor look pretty. Attracted by the grooves and ridges, female puffer fish would find their way along the dark seabed to the male puffer fish where they would mate and lay eggs in the center of the circle. In fact, the scientists observed that the more ridges the circle contained, the more likely it was that the female would mate with the male. The little sea shells weren’t just in vain either. The observers believe that they serve as vital nutrients to the eggs as they hatch, and to the newborns.

  http://www.spoon-tamago.com/2012/09/18/deep-sea-mystery-circle-love-story/

Here is the source of the video:

Puffer Fish Constructs A Masterpiece of Love - BBC Earth (YouTube)

The following papers analyse said structures and the ethology in more depth:

  We report that male pufferfishes (Torquigener sp., Tetraodontidae) constructed large geometric circular structures on the seabed that played an important role in female mate choice. Males dug valleys at various angles in a radial direction, constructing nests surrounded by radially aligned peaks and valleys. Furthermore, they created irregular patterns in the nest comprising fine sand particles. The circular structure not only influences female mate choice but also functions to gather fine sand particles in nests, which are important in female mate choice. Strangely enough, the males never reuse the nest, always constructing a new circular structure at the huge cost of construction. This is because the valleys may not contain sufficient fine sand particles for multiple reproductive cycles.

  Role of Huge Geometric Circular Structures in the Reproduction of a Marine Pufferfish (2013)

  Here, we examined the process of the outer ring construction, and extracted the ‘rules’ followed by the pufferfish. During construction, the pufferfish repeatedly excavates ditches from the outside in. Generally, excavation starts at lower positions, and occurs in straight lines... A simulation program based on these data successfully reproduced the circle pattern, suggesting that the complex circle structure can be created by the repetition of simple actions by the pufferfish.

  Simple rules for construction of a geometric nest structure by pufferfish (2018)


Application of molecular dynamics simulation (or alternatives) for the full pathways of protein interactions?

MD is used for studying structural changes. Simulation of biochemical pathways involves the kinetics (you are not really looking at how enzyme structure changes when it binds to substrate). You can certainly pool all the modelling strategies together to make a hybrid multiscale model.

There are many people who work on such kind of modelling approaches. You can search multiscale modelling and check out recent reviews. This is a somewhat recent (2016) review on multiscale modelling of pharmacokinetics-pharmacodynamics.


The cones and rods would not contain the images from our dreams. Visual scenes get transferred from the eye to the thalamus (which serves as a relay to the cortex) by optical fibers that are overwhelmingly uni-directional (information is carried from the eyes to the thalamus and not vice-versa).

Dreams do, however, activate the thalamus, the visual cortex, and the visual regions that control eye movements (see refs 1,2). I don't believe there has been successful attempts to decode the activation, mainly, I think, because fMRI would be the best that we could use for humans and it does not have good temporal or spatial resolution.

Hong, Charles Chong‐Hwa, et al. "fMRI evidence for multisensory recruitment associated with rapid eye movements during sleep." Human brain mapping 30.5 (2009): 1705-1722.
Dresler, Martin, et al. "Neural correlates of dream lucidity obtained from contrasting lucid versus non-lucid REM sleep: a combined EEG/fMRI case study." Sleep 35.7 (2012): 1017.


Where are newly discovered medicines tested

This is a very broad question, so I won't attempt to answer it fully. Instead, I'd recommend starting out by reading the Drug Development and Drug Discovery articles on Wikipedia, and if you have more specific questions after that then feel free to ask them here.

Basically, new drugs (either small-molecule "chemicals" or large-molecule "biologicals") are discovered in myriad ways, from pure accidents (see Penicillin) to specifically-targeted research. Once a lead compound is identified, it is put through a series of biochemical assays to determine, for example, if it inhibits certain enzymes of interest. From there, it moves into testing by cell-based assays using both normal cells and disease-specific models. All the while, investigators are looking for high specific activity (potency), low toxicity, and minimal off-target effects.

If a compound or group of them looks promising in these in vitro assays, experiments then move into animal models. The goals are similar here - high activity, low toxicity, and few (if any) side effects. The experiments get progressively more complex, with different endpoints depending on the exact aspect being studied.

It is only after extensive animal testing that a compound will be tested in humans. There are different phases of testing, each with different criteria, dosing patterns, number of patients, and reporting rules. The link I just gave explains each phase briefly.

Hopefully this is enough to get you started. Like I said earlier, if you have more specific questions after reading through all the references, please let us know.


Is there a way to examine amount of red/white muscle fibers without biopsy?

Indeed, a paper was published in 2011 regarding the same for humans by using a magnetic resonance spectroscopy to measure carnosine content.

A significant positive correlation was found between muscle carnosine, measured by 1H-MRS, and percentage area occupied by type II fibers. Explosive athletes had ∼30% higher carnosine levels compared to a reference population, whereas it was ∼20% lower than normal in typical endurance athletes.
Muscle carnosine content shows a good reflection of the disciplines of elite track-and-field athletes and is able to distinguish between individual track running distances. The differences between endurance and sprint muscle types is also observed in young talents and former athletes, suggesting this characteristic is genetically determined and can be applied in early talent identification. This quick method provides a valid alternative for the muscle biopsy method. In addition, this technique may also contribute to the diagnosis and monitoring of many conditions and diseases that are characterized by an altered muscle fiber type composition.

Baguet, Audrey, et al. "A new method for non-invasive estimation of human muscle fiber type composition." PLoS One 6.7 (2011): e21956.


Telomerases are tightly controlled on all level: Expression, post-translational modifications and by external factors. I think for this the external factors, a protein class called telomeric proteins. They bind to the end of the telomere and regulate the telomerase.

The figure is from this paper, which looks into the topic quite extensively:

Regulation of telomerase by telomeric proteins.


If you suspended your DNA like a rope in its 6ft full length, could you feel it if you waved your hand through it?

Research on tactile detection has found humans can detect wrinkles in a surface on a nanoscale. One could argue that we may be able to feel a strand of DNA.

However, this research found only wrinkles of 10 nm were detectable. Therefore it is unlikely we would detect a DNA strand by simply touching it, considering DNA has a radius of one nanometer radius (10 ångströms).

We still may feel a pull of the strand depending on the tensile strength and bond strength but I'm not sure how those values relate to human perception.


Cattles actually hate shrubs which are very tough to break and tasteless(for a cow). Some plants they won't touch are:

Lantana urticoides (West Indian shrub verbena),
Malvaviscus arboreus var.drummondii (wax mallow)
Rhus copallinum (winged sumac)
Viburnum acerifolium (mapleleaf viburnum).
Morella cerifera (wax myrtle)
Ilex vomitoria (yaupon).

Source:

https://www.wildflower.org/expert/show.php?id=2108

Lantana urticoides

http://www.wellgrowhorti.com/Pictures/Landscape%20Plants/Shrubs/Web%20Pictures1/M/Malvaviscus%20Arboreus.jpg

Malvaviscus Arboreus

http://www.floridata.com/wallpaper/jpg/Rhus_copallinum_frt800.jpg

Rhus copallinum

(source: naturallandscapesnursery.com)

Viburnum acerifolium

Morella cerifera

Ilex vomitoria


What is the difference between disruptive, divergent and diversifying selection?

I think you are conflating selection and evolution. Diversifying selection is when the variance of a trait in the population increases and even potentially becomes bimodal. This may lead to divergent evolution, i.e. a speciation event. Whereas directional selection still leads to evolution but not necessarily a the formation of a new species.


What is the difference between naive and adjusted p-values in a GWAS study?

There’s an XKCD comic which explains the problem. Unfortunately, that comic is too big to post here. Briefly, a p-value of 0.1 says (roughly) that there’s a 10% chance (0.1) of the observed result being as extreme1 as it is simply due to chance (sampling variation from a population), assuming the null hypothesis is true.

Often, 5% is more or less arbitrarily chosen as “cut-off”: results with p-values below that (which occur by chance 1 time out of 20) are called significant – results above are insignificant.

However, this directly implies that when doing multiple studies, say 20, there’s a very high chance of getting a “significant” result by pure chance, without there being a real effect.

GWAS studies essentially perform experiments on many (hundreds or thousands) of factors simultaneously. Therefore, reporting the pure p-values would be very misleading since there would be a lot of spurious results with “significant” p-values. The probability of getting one or more spurious hits is called the familywise error rate (FWER).

The FWER can be reduced by adjusting the p values, for instance by performing the Bonferroni correction. The resulting p-values are quite a bit higher, which reflects the reduced certainty that the result is due to chance, i.e. the reduced significance.

It doesn’t generally make sense to report the unadjusted p-value. It was probably reported here because correcting for FWER is quite conservative (i.e. it trades a low false-positive rate for an increased false-negative rate) and the authors feared that the adjusted p-value looked less impressive than it should. This involves a fair bit of interpretation.

1 extreme = different from the expected result under the null hypothesis


The holotype specimen originally discovered in 1993 is described as being 26m in length:

  An articulated neck of a large, mature sauropod, with enormously elongated cervical ribs, was discovered in strata of Late Jurassic age in the eastern Junggar Basin, Xinjiang, People's Republic of China. The animal is estimated to have originally measured 26 m in length, but was lightly proportioned relative to Brachiosaurus and Apatosaurus.

  ...

  In the present specimen, one rib from the midregion of the neck was seen to be at least 3540 mm long in the field, and after preparation measures 4100 mm in length.

  "A large mamenchisaurid from the Junggar Basin, Xinjiang, People Republic of China", Russell, D.A., Zheng, Z. (1993) Canadian Journal of Earth Sciences

The larger measurements come from additional remains attributed to this species, but not yet formally described. Here is the relevant section from Paul's book:

The Princeton Field Guide to Dinosaurs, Paul, G.S. (2010), Princeton University Press.

Paul's figures are echoed in the following papers:

  2006 年，中科院古脊椎所在新疆昌吉奇台（原中加马门溪龙标本发现地附近）发
  掘出一具巨型蜥脚类恐龙，经初步鉴定应归入马门溪龙。从发现的部分颈椎长度推测，
  这具马门溪龙长度可达 35 m 以上，成为了中国乃至亚洲目前发现的个体最大的恐龙。

    [Google Translate]

    In the year, the ancient spine of the Chinese Academy of Sciences was located in Changjiqitai, Xinjiang (near the original site of the discovery of the Jiamamen brook specimen).

    A giant sauropod dinosaur was excavated and the initial identification should be attributed to Mamenchisaurus. From the length of the cervical spine found,
    This [Mamenchisaurid] can reach a length of more than 35 m, becoming the largest individual dinosaur ever discovered in China and Asia.

  马门溪龙化石研究综述, (2008)

  Mamenchisaurus sinocanadorum (体长26~35 m)

  Advances in research on dinosaur gigantism, X XU, Q ZHAO (2016)

Though the first paper does not cite a source, and the second paper cites only Russel and Zheng's original paper describing the 26m specimen.


What is the expected amount of DNA shared by first cousins and the people between them in a family tree?

To simplify your problem, let's just consider autosomal DNA. In this case,  your expected amount of shared DNA should be synonymous with genetic consanguinity, which can be conveniently checked from this image.
Thus, you share approximately 1/8 of DNA(I know saying so is not scientifically strict as there are recombinations and mutations that prevent the DNA to be exactly the same.) with your first cousins. Same is true between first cousins.
Source: Wikipedia image gallery.


How can I get the yield of my purified immunoglobulins?

You can use western blotting with a anti IgY secondary antibody conjungated to  a HRP (or other reporter), this method will primarily help with troubleshooting your purification and locating IgY in the different fractions and flowthroughs.

If you want to quantify, consider using an ELISA kit. Here is one such kit (https://www.antibodies-online.com/kit/1563240/IgY+ELISA+Kit/)


Can restriction sites be used as PCR primers?

If you aren't digesting prior to amplification, sure.  Nothing in PCR cares about whether or not some other protein interacts with the site.  There are thousands of restriction enzymes in nature.  No one would ever be able to do PCR if you had to avoid every single potential restriction site.


Is it true that bees and wasps don't sting if struck by hand while they are in flight?

I can confirm that I have often enough slapped a wasp or bee in flight without being stung. The reason is probably pure chance.

It is kind of like asking if a human can bite when slapped. If I come up to you and slap you, fast and hard, you will probably not be able to bite my hand because of surprise and the blinding speed with which I hit you. If, however, you happen to be talking to me and have your mouth open at the time, you might be able to pull off a quick bite.

In a similar vein, if I happen to swap a wasp (no anagram intended) and hit it on the sting, I will probably be stung. If I hit it on the side and move fast enough, I doubt it will have the time to reorient itself and sting me before my hand is gone.


What are the structural factors affect enzyme's Km?

Computationally, using molecular dynamics (MD) simulations, it is difficult but not impossible, to quantitatively reproduce the effect of mutations on ligand-binding free energies, and activation and reaction free energies of enzymatic reactions. The most useful MD simulation methods for such a purpose are: free energy perturbation (FEP), linear interaction energy (LIE), linear response approximation (LRA), empirical valence bond EVB), and their combinations---developed by Arieh Warshel (The Nobel Prize in Chemistry 2013).

Mechanistically, mutations affect short- (van der Waals and electrostatic) and long-range (electrostatic) interactions with the surrounding environment, which comprises the rest of the protein and the solvent. Note that free energy is an attribute of an ensemble, not of a single 3D structure---which is why exploring a single structure of the mutated protein is unlikely to reveal the effect of the mutation qualitatively, not to mention quantitatively. One has to sample the conformational space of the protein---and MD simulation is the most efficient computational technique for such a sampling.

In summary, the effects are simple, but the system is extremely complex . . .

Klvana et al. (2012) Biochemistry 51: 8829-8843.

Klvana et al. (2016) J. Phys. Chem. B 120: 13017-13030.


Carrier females= 2pq= 2 x .08 x 0.92

Because carriers say with genotype  Aa (A=dominant, a=recessive)  can arise due to two types of inheritances;one when A is from father and a is from mother and the other when it is just opposite.


Are "sympathetic nerves" the same as "cardiopulmonary splanchnic" nerves?

You might consider cross-posting to SE Medical sciences who know more about this stuff.

I think that they are simply using a more general term than other authors. In the same way, most people call crabs crabs, but some people might occasionally refer to them as crustaceans.

Based on wikipedia, it seems that cardiopulmonary splanchnic nerves are a subset of sympathetic nerves. The sympathetic nervous system innervates a large number of organ systems of the body (see image), such that the cardiopulmonary splanchnic nerves are simply the sympathetic nerves that innervate the heart and lungs.

Looking further at the wikipedia for splanchnic nerves, it seems that this is a technical term relating to the fashion in which organs are innervated by the sympathetic nervous system; e.g. in my crude understanding they are organ hookups to the sympathetic nervous system.

In other words, all cardiopulmonary splanchnic nerves are sympathetic nerves, but most sympathetic nerves are not cardiopulmonary splanchnic nerves.


Is it wrong to consider an allosteric inhibitor a non-competitive inhibitor?

No, you cannot assume that an allosteric inhibitor is non-competitive. "Allosteric" refers to the location of binding, whereas terms like competitive, non-competitive, uncompetitive, or mixed inhibition refer to how (or if) the binding of the inhibitor affects binding with the substrate.

The Wikipedia page on competitive inhibition is a reasonable source for this question.

A competitive inhibitor is one that prevents binding of the normal substrate(s) at the active site. It is possible to achieve this either by literally getting in the way by binding in the active site or by binding elsewhere, causing a conformational change that prevents binding the active site. Both cases are considered competitive inhibition because of how they influence substrate binding.


Can botulinum toxin be grown or kept from denaturing in an UNWRAPPED 50 pound hay bale?

Clostridium botulinum toxin is present ubiquitously in soil. As such it is more than plausible that hay bails, which come into contact with soil can and I should expect almost probably will be infected with these bacteria. However it is not the mere presence of the bacteria itself which causes poisoning, it is the toxins they produce when the appropriate conditions are met. These toxins are produced as a consequence of spore formation.

Traditionally in human cases, the presence of toxins has been linked to home canned foods, where there is an anaerobic environment with a ph < 4.5 (http://cid.oxfordjournals.org/content/41/8/1167.full). It is conceivable that such an anaerobic environment exists within a hay bail (even if not wrapped). The following site from the ontario minestry agriculture and food (http://www.omafra.gov.on.ca/english/livestock/horses/facts/info_haylage.htm) suggest that the pH certain methods of hay bailing have pH < 5. This would seemingly confirm hay as potential source for botulinum toxins.

With regards to testing the hay for C. botulinum I would expect there to be a very high chance of finding this, due to soil contamination, however this does not imply this was a definite source for poisoning. A more conclusive test would be for the toxin. So in summary it is logical to suggest that hay could be the toxin source, but this does not mean it was the source.


What is a good review article source for Physiology?

The Journal of Physiology

Annual Reviews Physiology

Journals from American Physiological Society

Frontiers in Physiology

Experimental Physiology

Often, notable research papers are published in journals with high impact factors, although being published in a journal with high impact factor does not mean the research is better over research in smaller journals. But it can be a rough indication.


C765 is a transgenic Drosophila strain that has a specific Gal4 expression pattern ("embryonic salivary glands and larval wing and leg discs").

Gal4 is a transcription factor from yeast which binds an upstream activating sequence (UAS) and also happens to function in other species (like flies). In the Gal4/UAS system, a strain expressing Gal4, under the control of a tissue specific promoter or a minimal promoter in an enhancer trap, is crossed with a strain expressing a gene of interest flanked at the 5' end by the UAS. The F1 generation will thus express the gene of interest tissue specifically (ie only in the tissue(s) expressing Gal4).

[source]

Further reading:

Phelps CB, Brand, AH. 1998. Ectopic Gene Expression in Drosophila Using Gal4 System. Methods 14(4):367-379.


-Bacteria 1 is least related to Eukaryote 4 (the furthest branch is always the least related as there common node is furthest away, correct?)

In terms of relative relationships, eukaryote 4's least-related relative is Bacteria 1. Bacteria 1's least-related relative is the entire rest of the tree

  -The most related organisms are Bacteria 2 and 3, and Eukaryote 2 and 3

You cannot actually answer this question because a cladogram only shows relative relationships. To know which species pair is the most related (has the least total distance between them), you would need to know the branch lengths.

  -Is Eukaryote 2 the least related to Bacteria 1 as its branch is the furthest away?

To determine relationships, you want to look at the total branch length between two species. Therefore, this is correct

  Or is it Eukaryote 4 as it is the furthest away (bottom of list)?

Avoid this way of thinking. A phylogeny is not a 'list'. Pay no attention to the order the species labels appear: you only want to pay attention to how the species are connected. The same phylogenetic tree could be drawn differently, placing Eukaryote 3 at the bottom, for example.

  -Is Eukaryote 1 most closely related to Eukaryote 3?

Eukaryote 1's closest relative is Eukaryote 4: the distance from Eukaryote 1 to Eukaryote 4 is the shortest out of all possible pairs with Eukaryote 1.


short-day facultative plant, abrupt change to photo period

There is nothing you can do to alleviate the effects of (presumably) gro lights being left on for a 24 hour period. It's not likely to have a particularly dramatic effect on a short day facultative plant, other than to possibly delay flowering - it may mean the plant has to go through an extra period of darkness at nights for a longer time, in other words, the process of flower induction may need to start all over again. Or, as it was just one night, you might get away with it and they'll flower when you expected them to. The biggest interruption in the flowering process of a short day plant is a few minutes light in the middle of a period of darkness over successive nights, but either way, it's not possible to offset that 24 hour period of light in any way. I'm afraid you'll just have to wait and see, but in the meantime, maintain the growing routine with regard to lighting.


How can I learn about how cloning works in nature (twins)?

To learn about the process of how cloning works, you need to appreciate the underlying principles. A general bio textbook should suffice (most popular one is Alberts, where you should focus on chapter 21, but maybe read other chapters for background)

Nature Scitable is also a good source.

I'd discourage reading research papers at this stage, primary research paper are often very specialized, and reviews are aimed at other researchers in the field, that is unless you find one that is focused on communicating science to the public.


Which extinct creatures were most genetically distant from everything alive today?

The very first ones to go extinct would be the most genetically distant; at that distance, the issue becomes more "how do you define life?" or "how do you define a species?" to get the actual most distant. Overall, it sounds like an interesting question, but it really isn't: extinction isn't special, it's the norm. There are most certainly extinct organisms or pre-organisms of some level of development that never contributed to the existing life on earth and have no descendants or relatives.


Do non-green flower colors have any functional interactions with the sun?

Some functions of non-green flower colors:

#1: plant-animal interaction. Flower colors act as signals received by animals with eyes (e.g., pollinators, which many plants need to attract in order to reproduce).

However, it sounds from your question as if you're looking for other physiological effects. Two that come to mind are:

#2: heat. Flower color and opacity have a great effect on flower temperature.

This can be especially important for arctic and alpine flowers. Many of these are not only shaped like satellite dishes, but even pivot to follow the sun. This creates a warmer micro-environment which can be important to attracting pollinators and to increasing/speeding seed production. (See, e.g. Mølgaard 1989)

#3: UV protection. Certain pigments can be more effective at filtering UV.

I work in the alpine and occasionally encounter "glasshouse" plants, which have translucent floral parts that act to create warmer microenvironments, with the same effects as above. In addition, these floral parts have been shown to be more effective at UV filtering than green floral parts (Tsukaya 2002)

*edit: as these papers are behind paywalls, I'll also point out that the Wikipedia pages on Heliotropism and Rheum nobile contain similar information.

 Mølgaard P. 1989. Temperature Relations of Yellow and White Flowered Papaver radicatum in North Greenland. Arctic and Alpine Research 21: 83–90.
 Tsukaya H. 2002. Optical and anatomical characteristics of bracts from the Chinese “glasshouse” plant, Rheum alexandrae Batalin (Polygonaceae), in Yunnan, China. J Plant Res 115: 59–63.


Do any birds have established "poke a predator's eyes out" behavior?

From this paper about black-headed gulls responding to a hedgehog:

  The gull might peck the intruder, or strike it with its feet. Pecks were
  mostly directed at the hedgehog's head and might be delivered after a
  horizontal approach with the wings partly lifted.

Although not directed at the eyes specifically, they observed the birds directing attacks to the predator's head.

There's another paper (Ratner 1975) that also looks promising, but I'm on my home computer and can't access it right now


Chaperone proteins are still proteins and they can certainly misfold just like any other. If that happens, it will either be assisted by another chaperone and given time to fold successfully or it will be destroyed. If this is happening too often and the amount of chaperones drops too low or the number of unfolded or incorrectly folded proteins becomes excessive*, the unfolded protein response may be triggered and, if it does not resolve the issue and the cell remains stressed, the cell will undergo apoptosis and die.

Some chaperones, especially heat-shock proteins, may be more resistant to misfolding. This is true because they need to be able to withstand noxious conditions that denature other proteins. Not all chaperones are resistant to heat though and many are no more intrinsically resistant to denaturing.

*  It's not uncommon for a "bad" batch of proteins to be created. This can happen with a transcription error during mRNA synthesis since each mRNA molecule is read by many ribosomes. This can naturally happen with chaperones as well.


Primer Design with Primer-BLAST over specific site

I think various ways can be apply, but the easiest way could be to indicate the range to set a forward primer.

Decide the length of primer you are going to get.

Let's say you would like 25 mer.

You can set the range from chr12:25398261 to chr12:25398309.

When you identify where chr12:25398285 is in NG_007524.1, you are ready to design your primers.


What is the benefit of oxygen tanks to persons trappped in an enclosed space?

There are a couple of ways to answer your question. If we assume the cave is an air-tight chamber, we've entered the domain of a very specialized field in medicine, so I can't speak as authoritatively as I'd like there, but lets start, with the fact that the cave is not air tight.
It's a cave
A cave is not a submarine or a lunar module. It is not air-tight, but in a large environment with various types of gas exchange. The cave may already have it's own $CO_2$ scrubber of a sort, since common minerals reversibly bind $CO_2$. I expect there is a whole science around $CO_2$ cycles in, e.g., limestone caves, but the point here is there is likely a sink of some sort for the $CO_2$ produced by the boys. For example, I think we could reasonably speculate that the following equilibrium in a limestone cave would be driven to the right with additional $CO_2$:
$CaCO_3 + H_2O + CO_2 \rightleftharpoons Ca(HCO_3)_2$
Why would you give oxygen?
Here I can speak authoritatively. I'd refer you to both of West's excellent texts (Respiratory Physiology and Pulmonary Pathophysiology) for further reference.
Lets clear up a misconception in the comments. It is correct that we're concerned about the concentration (typically expressed as partial pressure) of gas, not the amount. It is not correct that $O_2$ eliminates $CO_2$ from the body. This can be confusing, but it is a misapplication of Dalton's law to human physiology, based on a misunderstanding about where and how the gas is exchanged. By Dalton's law, you can reduce the concentration of $CO_2$ in a container by increasing the concentration of some other gas (e.g., $O_2$). If $CO_2$ is accumulating in the cave (rather than being taken up by the environment), then delivering compressed gas with no $CO_2$ would decrease the concentration of $CO_2$ in inspired air. Inspired air, however, is not the same as alveolar air or arterial or venous gas, and the human body is not well modeled as a container full of various gases.
While it is true that when $CO_2$ is retained in respiratory acidosis, arterial $P_{O2}$ must go down by whatever amount arterial $P_{CO2}$ goes up, it doesn't work the other way around. Delivering a higher $F_{iO2}$, or fraction of inspired $O_2$ does not cause an inverse change in arterial $CO_2$. This ends up being fairly complicated, and a full discussion is beyond the scope of this question. Let me just emphasize that supplemental $O_2$ specifically treats low $O_2$ (or, in a very specific case, $CO$, carbonmonoxide, poisoning). High $CO_2$ is treated by increasing ventilation. In fact, there are a few special cases where supplemental $O_2$ actually increases a patient's $CO_2$ levels, two of which involve hypercapnic respiratory failure. We do give $O_2$ for hypercapnic respiratory failure, but it is given to treat the associated hypoxia, not the hypercapnea. The only way to decrease $CO_2$ is to increase ventilation. This is a very important concept in critical care and respiratory medicine. I'd refer you to West Pulmonary Pathophysiology, Chapter 10, or any critical care textbook.
So, back to the reason you might want to give oxygen...
CNN reports that oxygen levels in the cave have reached 15%. If the atmospheric pressure of the cave is 760mm Hg, then the $P_{O2}$ in inspired air is about 107mm Hg, ((760 - 47 for water vapor) * 0.15, see West Respiratory Physiology, or any physiology text). At 600mm Hg (equivalent to an elevation of ~2000 meters) $P_{O2}$ in inspired air is 83mm Hg. This is low, and could start to be a problem (leading to hypoxemia and hypoxia), depending on the ability of the boys to compensate (again, see West, either respiratory physiology or pulmonary pathophysiology). If the $O_2$ levels in the cave continued to drop, or if the boys weren't compensating well, then it would be reasonable to give supplemental oxygen to treat their hypoxia, regardless of what the $CO_2$ levels were.
But if $O_2$ was low, wouldn't they also have to have high $CO_2$?
I'm not an expert in cave ecology, but it doesn't seem that strange to me that the rate of $O_2$ consumption by the boys could exceed the environment's capacity to produce or release $O_2$ from organic sources, dissolved sources, or ventilation, without their rate of $CO_2$ production overwhelming the environment's $CO_2$ sink. I have no good evidence one way or the other for this speculation.
What if it is an air-tight container?
Atmospheric $CO_2$ is on the order of 400ppm, or 0.04%. Normal levels in the body are 5% (40mm Hg / 760). We rely on this gradient to dump the $CO_2$ produced by cellular respiration using ventilation, but can still operate, with difficulty, with 5% $F_{iCO2}$. Serious problems (same reference) occur at higher levels. Again, in this particular case we're beyond my personal expertise (Dammit, Jim, I'm a doctor, not an aerospace or submarine doctor!), but in an air-tight container without a $CO_2$ sink, if $CO_2$ levels were higher than 5% and rising, I'd expect you would need to directly address $CO_2$. If it's a small container, adding other gases from pressurized canisters, or pumping gases in would decrease the $F_{iCO2}$ by Dalton's law, provided you could overcome the rate of $CO_2$ production by the boys. If $CO_2$ had accumulated in the boys blood (hypercapnea), they would (need to) increase their ventilation as well, adding more $CO_2$ to the chamber.


How do humans detect temperature differentials on the skin?

Sensory neurons in the skin express TRP channels such as TRPV1 channels, TRPM8, and others (see Voets et al 2004 for more information on how these channels work). Different sensory neurons express different combinations of TRP channels .
Changes in temperature shift the probability of whether these channels are open or closed. Opening or closing of ion channels changes the membrane potential of the sensory neuron, which changes the rate of action potentials which informs the rest of the nervous system about the temperature.
The TRP channels can have other ligands, as well, such as capsaicin or menthol. The activity of these ligands at temperature-sensitive receptors is why we perceive chilis or mustard to taste "hot" and menthol to feel "cold".
More generally, the nervous system typically responds to changes better than constant stimuli through adaptation. Therefore, if your hand is fairly cold and you touch something warm or hot, you will perceive a hotter stimulus than if your hand started out already warm.
There isn't really a thermocouple or temperature difference detector in the skin, just these two mechanisms: channels whose open probability is a function of temperature, and sensory adaptation which heightens perceptual sensitivity to changes in temperature.

Voets, T., Droogmans, G., Wissenbach, U., Janssens, A., Flockerzi, V., & Nilius, B. (2004). The principle of temperature-dependent gating in cold-and heat-sensitive TRP channels. Nature, 430(7001), 748-754.


How fast does the rotor in ATP synthase spin?

According to "Resolution of distinct rotational substeps by submillisecond kinetic analysis of F1-ATPase" (Yasuda et al., Nature, 2001), ATPase rotates at 130 revolutions per second when saturated with ATP.


Heritability of heritability

Heritability is a property of a population (see here for more info), not of an individual. One can only calculate heritability for a trait if this trait can take a value for every given individual because you need variance among those individuals (as it is made clear from your equations). In other words, the trait you want to calculate the heritability from has to vary from individual to individual.

As we are looking for the heritability of heritability, then heritability would need to be defined at the individual level in order to calculate its heritability. But heritability is not defined at the individual level.

It makes no sense to talk about the heritability of heritability. Just like it makes no sense to talk about the heritability of the fitness variance or heritability of the species geographic range.

Phylogenetic signal for heritability

You might be interested of whether related lineages tend to share similar heritability (for a specific chosen trait). I do not know of any study on the subject, but it seems likely that related species are more likely to experience similar population size and structure and similar selective pressure on a given trait than more distantly related lineages. Per consequence, I would expect that heritability shows a phylogenetic signal. It would be wrong to say that heritability is heritable though.


I know how to solve these equations, but I'm not sure what t' represents?

I figured it out, t' is just a dummy variable used to represent time over the refractory period since the integral is from t-r to t.


What is a typical value of the selection coefficient s?

This is a very fundamental and important question! But first, be cautious not to confound the Fitness effect of segregating alleles with the mutational effects.
Fitness effect of segregating alleles vs mutational effects
One must not confond the distribution of fitness effect of segregating alleles in a population with the distribution of mutational effects. The distribution of mutational effects will always be narrower in comparison to the distribution of fitness effects of segregating alleles as very deleterious mutations won't stay long in the population and very beneficial mutation will sweep to high frequency very quickly so that it is unlikely to see them.
I am assuming you are interested in the distribution of mutational effects. Below are some papers and generalities that will be of interest to you. Some data come from the quantitative genetics literature and some from classical empirical population genetics. I also talk about mutation rate as these two subjects are highly related typically at determining mutation load.
Short answer
A typical deleterious mutation has a mutational effect of $s=0.1$ or $s=0.05$. In theoretical studies, authors often used a constant value of $s$ as being equal to one of these two numbers.
Longer answer
Distribution of mutational effect
Generally speaking distribution of mutational effects (on both the deleterious and the beneficial side) are thought to approximatively follow a gamma distribution with an extra bump of probability density around lethal mutations. shape might take values around 0.5 or 0.05 while the scale parameters might be of the order 0.1 to 0.001, with typically an average around 0.05. See Halligan and Keightley 2009. I have seen (see Nemo's documentation for example) that the dominance coefficent $h$ is modelled as $h=-log(2 Exp[h])/Exp[s]$.
Mutation rate
Concerning the mutation rate, a reasonable approximation is to consider a deleterious mutation rate per diploid genome of 1. This is known as Drake's law (see this post). Drake's law appears to be an underestimate for humans (Keightley 2012), about right for Drosophila, (Haag-Liautard et al. 2007), C. elegans (Denver et al. 2004) and possibly non-human endothermic vertebrates (Baer et al. 2007), and probably an overestimate for many other organisms (Baer et al. 2007, Halligan and Keightley 2009).
Quantitative traits
If you are uneasy with basic quantitative genetics and the below notation, you should have a look at this post.
For quantitative trait, there is evidence that $\frac{Vs}{Vp}≈5$ on average (Kingsolver et al. 2001, Johnson and Barton 2005). If heritability is $\frac{1}{3}$ (as it rarely significantly different from), then $Vs=7.5$. Empirical estimates of the mutational heritability $Vm$ suggests that $\frac{Vm}{Ve} = 0.001$ (Houle et al. 1996)


What is the surface area of the human heart?

The number you are looking for might be quite large depending on the level of detail you demand for the measurement.  There is no single number for the area of most objects in fact.

The importance of fractals is much related to the question of what is the perimeter or surface area of something.  The classic example is trying to determine the length of Britain's coastline.  If you took a surveyors sight and set a point every 500 ft you would get a certain number, if you paced it out in strides you would end up taking more curves and turns and you would get a longer number.  If you took out a ruler and measured down to the inch you would get a still larger number.  In these two wikipedia pictures you would get a perimeter of 2400 km and 3400 km for points set every 200 and 50 km respectively:

As you can see that makes a big difference.  So in the same thought organs also need to be measured using fractal sorts of measurements- depending on the level of detail desired. For a heart, if you were to cover the organ with a tight stretch of Saran wrap, you'd have maybe 1-2 square feet, but if you estimate the surface area for not only the inner chambers, but the blood vessels and capillaries, it would be much larger.  The latter is probably relevant if you are a physiologist and want to know how much oxygen the heart is taking in as it beats.

I can't find a reference for a human heart, but fractal calculations for the human lungs tell me that 1000 sq ft seems reasonable.  If you take the oxygen accessible area of lungs, including every bronchial passage and aveoli, the answer is 50-100 m^2. This is about 538- 1,076 sq feet.

The heart does not need to have as much surface area as the lung, but the capillaries and arteries that feed the heart need to be spaced a few millimeters apart to keep the tissue oxygen saturated.  1000 sq feet seems a possible range for the heart compared to the lung's surface area, maybe on the high end...


Sitting in a closed room filled with regular air - for how long will the air last?

Since you are considering to meditate in the room, without any excess of activity, you can consider the average resting O2 consumption, which is C = 3.5 mL/(min.kg) [1].

If we ignore the volume of your body, initially the room is filled with VO2(t0) = 0.21 * 5 = 1.05 m3 of O2.

With you breathing in the room, you can consider the volume of O2 in the room as a function of the time:
VO2(t) = VO2(t0) - C * M * t
where M is your weight in kg, and where C is converted to m3/(min.kg).

An oxygen defficient atmosphere is an atmosphere for which oxigen content is below 19.5 % of the volume [2]. An oxygen defficient atmosphere can be dangerous for your health. So in your case you need to find the value of t for which VO2(t) becomes inferior to the threshold Th = 0.195 * 5 = 0.975 m3.

So the maximum time you can spend in your room would be:
tmax = (VO2(t0) - Th)/(C * M) = 335 min = 5 h 36 min

Of course, this value is a bit surestimated, and you should leave the room before that time.

[1]  M. Kwan, J. Woo & T. Kwok (2004) The standard oxygen consumption
value equivalent to one metabolic equivalent (3.5 ml/min/kg) is not appropriate for elderly people, International Journal of Food Sciences and Nutrition, 55:3, 179-182, DOI:10.1080/09637480410001725201

[2] https://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_id=12716


The basic reaction is ATP + H2O --> ADP + Pi + energy

It is the common hydrolysis of ATP, in which the nucleophilic oxygen of water attacks the electrophilic central phosphorus of the last phosphate group, resulting on its separation from the rest of the molecule (which becomes ADP).

In this image: LINK you can see more clearly the steps of the reaction. Keep in mind that the arrow 3 should be pointing to the P and not the O.

To know more about the energy and thermodynamics check this page: http://www.life.illinois.edu/crofts/bioph354/atp_hydrolysis.html

The trick here is the cells being able to utilize that freed energy to their benefit, instead of letting it disperse. This can be done, for example, by adding a phosphate group to a protein, altering its shape and consequentially its function, or by the nucleophilic attack of the first or second phosphate in the ATP molecule of a susceptible electrophilic centre, starting a reaction that could otherwise be energetically unfavourable. If the hydrolysis happens spontaneously in water without coupling it with another reaction, the freed energy will be "wasted" as heat.


What kind of beetle is this? (Black and yellow)

This shield bug belongs to the species Perillus bioculatus, and has the nickname "two-spotted stink bug". They're native to the United States, and come in a variety of colors.

You mention that its colors are yellow & black, however, from the image you provide, it seems more of a pale yellow/off white. Because of that, I think it your found insect more closely resembles the first of the following images, whereas you may think it's closer to the second.

And then, a few other colors:


Evolution theory - roses spikes - being more bulgy doesn't give you advantage

I think that the most important point has been given by CactusWoman, when (s)he says "Just because you cannot forsee a use for more "bulgy" spikes doesn't mean there isn't a use for them."

In addition to that, I would like to say that several plants evolved traits that were beneficial at a time where other herbivores existed and that are now useless. Those lineages did not lose their traits (yet?) just because there is a relatively low cost to making the trait in question.

Your post shows several of the very common misconception about evolutionary processes. Evolution is not all about Natural Selection. It is more interesting than that.

  "small improvement"

The conception that evolution proceed through "small improvements" is either partially wrong or totally wrong.

First, because of the loaded term "improvement". Evolution can yield a population to have a lower mean reproductive success or a lower complexity, things that you could eventually see as deterioration.

Second, because changes not need to necessarily be small. Some mutations have a very big effect.

Third, because even small deleterious mutations can spread in the population and reach fixation (=and all individuals carry this mutation), just because of the joint effect of other evolutionary processes such as genetic drift. This post may help you to get a quick grasp of what genetic drift is. There are already multiple posts that emphasize the importance of other processes than natural selection in evolution to layman. Here is one of them.

  believe in Darwin competence

Evolutionary biology is not anymore Darwin's evolution theory. It is way more than that. We've been working on the subject a lot since Darwin and today we have a much much better understanding of evolutionary processes than Darwin at its time. Everything is not fully understood yet and therefore there are still many people researching to better understand evolution. Of course, not to better test if evolution is true as this has been known for a long time now.


To what extent is immature eggs in insects (beetles) a good approximation for maximum fecundity?

There are a number of things to clarify here; Fecundity is the number of offspring that is produced by an individual, and this can be separated into potential fecundity (maximum reproductive capacity) and realized fecundity (number of offspring actually produced). Realized fecundity is very similar to fertility, which is defined as the number of viable offspring that are produced.

Potential fecundity can sometimes be a good proxy for future fertility, and this is especially true for species where all eggs are present after metamorphosis of the adult insect (Awmack & Leather, 2002). However, in some species the formation of eggs is a continuous process in adult individuals, and this is relatively common in beetles. Therefore, the number of immature eggs might be a poor proxy of both potential and realized fecundity in these species (Awmack & Leather, 2002), and this is more likely in relatively long-lived species that feed extensively as adults. In beetle species that do not feed as adults (often lacking functional mouthparts), immature eggs is probably a better approximation of potential fecundity.

It should also be mentioned that the quality of host plants will often affect the maturation of eggs (Sterns & Smith, 1960; Hopkins & Ekbom, 1999), and will therefore also determine to what extent the number of immature eggs is a good indication of potential fecundity. When feeding on poor quality hosts eggs may e.g. be reabsorbed by females to use for other purposes (see references in Awmack & Leather, 2002 & Hopkins & Ekbom, 1999 for further information).

The review paper by Awmack & Leather, 2002 is very comprehensive, and contains a wealth of useful references on this topic.


Differences on biological classification?

Phylum and division are both listed under the same taxonomic ranks. The wikipedia page for phylum states that

  Traditionally, in botany the term division was used instead of
  "phylum", although from 1993 the International Code of Nomenclature
  for algae, fungi, and plants accepted the designation "phylum".

What you have to keep in mind is that the scientists categorizing plants and animals worked in isolation for a long time and only recently have they come together to build a tree of life for all organisms (rather than just working separately on plants / animals / bacteria)


Since Drosophila have the same system of sex chromosomes as human beings, (XY males and XX females).  Its clear that the sex determination is important - no females have yellow bodies. This is the key observation.

Amongst the males you have about 50%/50% Y/y phenotype.  This appears to be a classic sex chromosome related trait.  Does this help?  I can go further, but this should get you there.


What are the consequences of drinking water with food?

A moderate amount of water while eating will not dilute digestion
...according to Michael F. Picco, M.D. and the Mayo Clinic:

There's no concern that water will dilute the digestive juices or interfere with digestion. In fact, drinking water during or after a
meal actually aids digestion.
Water and other liquids help break down food so that your body can
absorb the nutrients. Water also softens stool, which helps prevent
constipation.

Water, after all, is the "universal solvent" which should help break food and organic materials down further.
Effect of Stomach Acid Dilution
This is a total myth, especially if you consider it from totally a chemical perspective.  Stomachs secrete about 400 to 700 mL of gastric acids per meal. Just to be conservative, let's say 500 mL.  Also, the average stomach has a pH of about 2.  Now let's look at the formula for pH and what the effects of adding water might be:
pH = log(1/(mols/volume))
2 = log(1/(mols/0.5L))

Now solve for mols, and we get mols = 0.005
Now let's assume our meal contains about a quarter of a liter of water in it.  We'll also assume that our food is completely pH neutral.  This is probably a little high on water concentration, but let's see its effect on our stomach's pH.
Since it has a neutral pH, the mols does not change, but our volume does (0.5L [previous contents] + 0.25L [from the food] = 0.75L).
pH = log(1/(0.005 mols/(0.5L + 0.25L)))

Now solve for pH and we get pH = 2.18.  No problem here, since normal digestion occurs between a pH of 1.5 to 3.5.
Finally, let's say we drink a lot of neutral pH water with our meal now.
pH = log(1/(0.005 mols/(0.75L + 4.25L)))
pH = 3

So we are still within a normal pH of digestion, even though we just drank over 4.25 liters (~1.12 gallons) of water with our fairly liquid meal of 0.25L!  We would need to drink about another 45 L of water to knock our gastic pH above 4.  But don't worry, we would die of water intoxication well before that ever happens.
Furthermore, our stomachs (and digestive tract) are incredibly good at adapting their secretions to the consistency of a meal.
Water and Speed of Digestion
Perhaps another way that water may change caloric intake is to increase the speed at which solid foods exit the stomach.
This is thought to reduce the meal’s contact time with stomach acid and digestive enzymes, resulting in poorer digestion.
As logical as this statement may sound, no scientific research supports it.
A study that analyzed the stomach’s emptying speed observed that, although liquids do pass through the digestive system more quickly than solids, they have no effect on the overall solids’ digestion speed.
Bottom Line
Water during meals should not decrease the amount of calories absorbed.  With all that being said, digestion is a very complex system, and there are still many unknowns as well as individual responses.  Before making drastic changes concerning your health and digestion, you should consult a medical professional.  This answer should in no means necessary replace any medical advice or treatments, but rather aid in your understanding of how digestion works.
A Final Word of Caution
I feel obligated to include that however you found this question/answer, staying hydrated to aid in digestion is a very healthy function, especially in considering weight loss and 'feeling full for longer.'  However, obsessive water consumption aimed at decreasing food consumption/appetite ("fluid loading" or "water loading") is a common symptom of eating disorders.  If this is a concern for you or someone you know, please, seek professional support and help.

Sources:

NCBI - Adaptive Secretions

NCBI - Digestion Speeds

www.mayoclinic.org

water.usgs.gov


Are there examples of selection on males influencing female phenotypes?

Selection in one sex can produce a correlated response in the other when there is pleiotropy (or linkage disequilibrium) (see Lynch & Walsh 1998, and Lande 1979 & 1980).

Genes can be considered pleiotropic when they affect more than one trait, for example; the male and female forms of equivalent traits, and this can be seen as covariance between the sexes. Cross-sex covariance is common (see Bonduriansky & Rowe 2005, Poissant et al. 2010, Lewis et al. 2011, Griffin et al. 2013, and Blows et al. 2015 for good examples). This means that selection in one sex will often lead to a response in the other.

The correlated response to selection is captured within Lande's multivariate breeders equation, where the change in a vector of traits ($\Delta \bar{z}$) is a result of the genetic variance-covariance matrix ("G-matrix", $G$) multiplied by a vector of selection on the traits ($\beta$).

$\Delta \bar{z} = G \times \beta$

If covariance is zero (i.e. genes have independent male and female effects) then selection does not produce a correlated response in the unselected sex. However, cross-sex covariance is generally present, so correlated responses to selection should impose constraint on the evolution of sexual dimorphism under sexually antagonistic selection. Note that the within-trait cross-sex covariance is in the diagonal elements of the B-submatrix.

One good example of selection on one sex producing a response in the other is this paper. The authors selected on male mandible size in replicate populations of broad horned flour beetles. The mandible is a male limited secondary sexual trait, but selection on the mandible in males produced changes in female fitness and female traits. Selection for larger (smaller) male mandibles resulted in significantly decreased (increased) female abdomen size, and reduced lifetime reproductive success.

  "We find that females from populations selected for larger male
  mandibles have lower fitness, whereas females in small-mandible
  populations have highest fitness, even though females never develop
  exaggerated mandibles."

One thing that is really quite cool about that experiment is that the response came in a non-equivalent trait, i.e. it was not female mandibles but other traits that evolved. There is generally less prior probability that there will be a cross-sex cross-trait covariance unless the traits have clear links.


What are the effects of the common cold in an immunodeficient person?

In one small study, rhinovirus in the immunocompromised led to significant mortality from lower respiratory infection:

  Among high-risk patients with cancer, rhinovirus infections are often fatal. In a study of 22 immunocompromised blood and marrow transplant recipients who were hospitalized with rhinovirus infections, 7 (32%) developed fatal pneumonia. The remaining patients had infections confined to the upper respiratory tract. In 6 of the 7 fatal cases, rhinovirus had been isolated in bronchoalveolar lavage fluid or an endotracheal aspirate before death.

Note that this is in hospitalized patients; it says nothing of non-hospitalized patients.

This conclusion has been disputed.

In a slightly larger study among people with hematological cancers (presumed immunosuppressed because of same):

  Respiratory viral pathogens are a common cause of morbidity in patients with hematologic malignancies. ...Both a rapid viral culture with direct fluorescence antibody (DFA) staining and a PCR-based assay (MultiCode-PLx Respiratory Virus Panel) were performed on patients with hematologic malignancies, who underwent collection of a nasopharyngeal swab or bronchoalveolar lavage from October 2006 to April 2007. Eighty-two samples from 70 patients were obtained; all patients had upper respiratory tract symptoms. Respiratory viruses were detected in 10 samples (12%) by conventional virological methods and in 31 samples (38%) by the MultiCode-PLx assay. ...40% of these patients had pneumonia in addition to the upper respiratory tract symptoms. [emphasis mine; note, there is no mention of mortality.]

So long story short, they have stuffy, runny noses, sore throat, cough, etc. Clearly the virus itself causes damage to the mucosa; that is integral to viral replication After entering a mucosal cell, the virus replicates, then the progeny virus is released by lysis of the cell. This damage itself causes inflammation (not the same as an immune reaction), pain, etc. The major difference seems to be a more severe and prolonged experience.

Respiratory Consequences of Rhinovirus Infection
Detection of respiratory viruses with a multiplex polymerase chain reaction assay (MultiCode-PLx Respiratory Virus Panel) in patients with hematologic malignancies


Does creatine-phosphate (CP) supplementation regenerate NADH?

Creatine itself is never converted into ATP. Creatine-phosphate on the other hand can donate its phosphate group to ADP, phosphorylating to form ATP and creatine. This is a buffer system for high-energy phosphates, and is very important in organs with rapid ATP turnover, notably muscle.

The mechanism of the findings described in the papers is not fully understood yet I think. But it is not via ATP, because the supplementation is not creatine-phosphate, but creatine itself, which does not yield ATP.

Regarding NADH: ATP is very different from NAD/NADH in terms of molecular structure, and the two are not interconverted by any pathway that I know of. (Probably this is not what you meant, but just to be clear.) But it is certainly true that reducing power in the form of NADH can be used to phosphorylate ADP into ATP; this is the task of the mitochondrial respiratory chain, where NADH is oxidized to NAD by complex I. On the other hand, I am not aware of a physiologically relevant process that uses ATP to reduce NAD into NADH.

The liver is a main site of synthesis of creatine itself, and this syntesis consumes methyl groups donated by the S-adenosylmethionine system. The authors of your ref1 seem to suggest that reduced synthesis of creatine following supplementation is a possible mechanism. Similar effects have been observed with choline supplementation, but again this effect is not well understood and a current research topic. A recent review is found here.


Michaelis-Menten equation; how to find the constants from enzyme activity experimental results?

Have you got data for different concentrations of hydrogen peroxode?

If so you should choose a time point that falls on the linear part of your time graph. And plot the rate at that time point for each substrate concentration.

That will give you a MM curve where you can calculate the values you desire. You cannot calculate them with just your time data that you have provided.


Help understanding the word 'glycosaminoglycan'?

Glycosamines (or amino-sugars) are monosaccharide derivatives with an amino group substituting the hydroxyl group at second carbon. Glycosaminoglycans (GAG) usually contain repeats of a disaccharide unit one of the component of which is an amino sugar. GAGs are not strictly polymers of amino sugar monomers as the name might misleadingly suggest.


Is it feasible to grow edible crops for lawns?

There are lots of things that you can eat that you could grow as a lawn.  That probably are growing in your lawn now.  My yard is about half violets and they are edible.  Purslane is a delicious succulent lawn weed.  Grab some, rinse it off and eat it.  It is crunchy!  I am telling you from experience you can eat a lot of it and you will not get sick.

Purslane image from here.
http://www.livescience.com/15322-healthiest-backyard-weeds.html

This backyard weeds link says lambs quarters are edible and I did not know that.  They are also volunteers but I did not know they were good for anything and so I was pulling them up.

We are surrounded by things we could eat and which our ancestors ate all the time but which we do not eat.  If you are in school, Johnathan, and this sort of thing interests you it would be a stellar project.  You have all summer to grow weeds in pots and then at the science fair you could have people taste them.


Why is competitive inhibition reversible?

A competitive inhibitor typically competes for the active site with the substrate. In this textbook case, binding of a competitive inhibitor is reversible, because it binds to the active site of the enzyme, but is also released, making way for the substrate to bind. The affinity of the substrate, as well as its concentration determine the amount of inhibition (Berg et al., 2002).

An irreversible inhibitor may covalently bind to the active site, permanently disabling the enzyme (McDonald et al., 2012).

References
- McDonald et al., Enzymes: Irreversible Inhibition. In: eLS. John Wiley & Sons Ltd, Chichester (2012)
- Berg et al., Biochemistry. 5th ed. New York: W H Freeman; (2002)


Why is the manchineel tree so poisonous?

According to http://www.atlasobscura.com/articles/whatever-you-do-do-not-eat-touch-or-even-inhale-the-air-around-the-manchineel-tree, it evolved to be poisonous to discourage animals from digging into it. Here's one possible way that could have happened. It was once only a tiny speck more poisonous than other trees by random fluctuations in toxicity. By natural selection, animals evolved to prefer it less. They were more likely to dislike the taste of the more poisonous manchineel trees, which in turn caused it to evolve to be more poisonous. Maybe it was such an advantage to get more energy by eating some of it that some species evolved to be more resistant to the poison so that they could eat some of it. That caused the manchineel tree to evolve to be even more poisonous to discourage animals from eating it. It was an evolutionary disadvantage for the apples to be poisonous. That was just an accidental result of the rest of the tree being so poisonous. Indeed, they did evolve to be much less poisonous than the sap for that reason. Animals evolved to dislike the taste of the apples because they're poisonous. The less poisonous ones were more likely to get eaten and have their seeds spread. Since they couldn't evolve to be nonpoisonous, they instead evolved to taste like there's nothing wrong with them so that they could get eaten. Since iguanas did evolve to be immune to the poison apples, there wasn't much of an advantage in them evolving to be even less poisonous.


What is the name of this plant with orange fruit clusters in india?

The easiest way to find out the name of this tree is to realize that the flowers (and therefore the fruit) are in the form of a raceme.

Googling India bright orange fruit raceme in Images quickly brings up your specimen among others.

The name of that image leads to other sites discussing the plant.

  Duranta erecta
  Scientific classification
  Kingdom:    Plantae
  (unranked):     Angiosperms
  (unranked):     Eudicots
  (unranked):     Asterids
  Order:  Lamiales
  Family:     Verbenaceae
  Genus:  Duranta
  Species:    D. erecta
  Binomial name
  Duranta erecta

  Duranta erecta is a species of flowering shrub in the verbena family Verbenaceae, native from Mexico to South America and the Caribbean. It is widely cultivated as an ornamental plant in tropical and subtropical gardens throughout the world, and has become naturalized in many places. It is considered an invasive species in Australia, China, South Africa and on several Pacific Islands. Common names include golden dewdrop, pigeon berry, and skyflower.


When is it better for a gene to cause a biased sex ratio?

Well first if a gene is not on a a sex chromosome there is little advantage in changing the sex ratio. This is why most of the ultra-selfish genes we know about are on sex chromosomes. A gene is not helping itself spread if makes more Male offspring unless one of two things is true, it is on the Y chromosome or there is already a bias making male offspring more successful. the latter actually helps keep populations rex ratios stable since if there are more of one sex generally having offspring of the other sex is an advantage.
The most impactful sex ratio altering genes we know about result in selfish sweeps where populations can collapse as they take over and eventually prevent mating entirely. but up until that final generations with no mates the gene in question has an advantage, evolution does not care about the survival of the species or population, if a gene can improve its own ability to spread at the cost of the population then so be it. fitness at higher levels is basically irrelevant. A gene is perfectly capable of spreading by favoring itself and driving the species/population extinct. In many ways run away sexual selection is this in a nut shell, detrimental to the individual and population but beneficial to the gene.


How does eutrophication yield lower levels of dissolved oxygen?

From Wikipedia:

  Eutrophication arises from the oversupply of nutrients, which leads to over growth of plants and algae. After such organisms die, the bacterial degradation of their biomass consumes the oxygen in the water, thereby creating the state of hypoxia.


I think you have an Indian Lily Moth (of the genus Polytela). It is considered a minor pest. Their habitat seems to only be around India and its surrounding area.

Their worm matches yours ... smooth, dark, but red patches and white spots:

If you dig in your garden, you may encounter these pupae:

And they eventually grow into these beautifully-multicoloured moths:

Here is a video showing their movements and their life cycle:
https://www.youtube.com/watch?v=2l0oxZM_6XY


Why is the frog genome so much larger than a fish's?

Genome size is a poor indicator of an organism's complexity (already an ill-defined term). We cannot assume by any means that a larger genome corresponds to a more "complex" organism. There are some plants whose genomes are larger than most mammals, and indeed the largest eukaryotic genome (at least as of 2010) is the plant Paris japonica, weighing in at 1C = 152.23 pg (compared to Homo sapiens at 1C = 3 pg). Anecdotally, in my previous research lab I discussed with a colleague a fungal species whose genome size differed by orders of magnitude between different individuals of that species.

It should never surprise you to see an organism with a larger genome size than what you may consider to be a more complex organism.


Gibbs free energy and its change for the hydrolysis of ATP

You can use tables of standard transformed Gibbs energies of formation, $\ce{\Delta _fG^{'o}}$ , such as those found in Table 1 of the following reference, to calculate apparent equilibrium constants of biochemical reactions, and to calculate standard transformed Gibbs energies of formation, $\ce{\Delta _rG^{'o}}$ (at pH 7), which I think is exactly what you require.

Calculating apparent equilibrium constants of enzyme-catalyzed
reactions at pH 7 (by R. A. Alberty)

The first thing to say it that you need to include water as a reactant.

$$\ce{ATP + H2O = ADP + P_i}\tag{1}$$

Secondly, the reaction shown in Eqn(1) is used as an example by Alberty in the paper cited above, where he calculates both $\ce{\Delta _rG^{'o}}$ (at pH 7) and the apparent equilibrium constant (at pH 7).

The following values were taken from Table 1 of the Alberty reference cited above.  They refer to pH 7, 25oC, and an ionic strength of 0.1.

              $\ce{\Delta _fG^{'o}/{kJ mol^{-1}}}$

ATP             -2276.43

ADP             -1409.95

Pi              -1059.17

H2O              -156.05

Knowing these values, it is now very easy to calculate the standard transformed Gibbs energies of formation, $\ce{\Delta _rG^{'o}}$, for the reaction shown in Eqn (1) (it is merely a case of 'pluggin in' the values).

$$\Delta _rG^{\ce{'o}} = \sum v_i^{'} \Delta_f G_i{^o} = (2276.43 + 156.05 - 1409.95 - 1059.17)\tag{2}$$

$$\ce{\Delta _rG^{'o} = -36.68 kJ mol^{-1}\tag{3}}$$

In Eqn (2), $v_i^{'}$ is the stoichiometric number (positive for reactants
and negative for products)

The criterion which determines whether a reaction will 'go' in the forward direction or the reverse direction is the transformed Gibbs energy of reaction, $\Delta_rG^{'}$, (not $\Delta_rG^{'o}$).

  If  $\Delta_rG^{'}$ is negative, the reaction goes in the forward direction.

We can say that under standard conditions, Eqn (1) goes to the right, and as $\Delta_rG^{'o}$ (not $\Delta_rG^{'}$) is directly related to the apparent equilibrium constant (Eqn 4), we can say that the equilibrium constant for the rection of Eqn (1) is very much to the right.

$$\Delta _rG^{\ce{'o}} = \ce{-RT ln K^{'}}\tag{4}$$

We can go a step further (Alberty,2000) and calculate the apparent equilibrium constant, $K^{'}$, for the reaction shown in Eqn (1).

$$K^{'} = e^{\frac{-\Delta _rG^{'o}}{RT}}=e^{36680/(8.3145 \times 298.15)}\tag{5}$$

$$K^{'}  = 2.67 \times 10^6\tag{6}$$

The great value of tables of $\ce{\Delta _fG^{'o}}$ it that they allow $\Delta _rG^{\ce{'o}}$ and $K^{'}$ to be calculated for many reactions, even those for which there is no known enzyme, or where the equilibrium constant has not been determined.

Notes

In Eqn (5) above, $R$ is the gas constant ($\ce{8.3145 J K^{-1} mol^{-1}}$
) and $T$ is the temperature (in Kelvin)

IMO, the Alberty reference cited above is a model of clarity that makes these type of calculations very easy. It is also an 'easy read' with many great examples.

Two other good refs, if you are 'into' such things, are

Biochemical thermodynamics (by R.A. Alberty)
Recommendations for nomenclature and tables in biochemical thermodynamics (by R.A. Alberty)

Other  tables of standard transformed Gibbs energies of formation, $\ce{\Delta _fG^{'o}}$, may be found in

Calculation of Standard Transformed Gibbs Energies and Standard Transformed Enthalpies of Biochemical Reactants  (by R.A. Alberty)
Calculation  of Standard Transformed Formation Properties of Biochemical Reactants and Standard Apparent Reduction Potentials of Half Reactions (by R.A. Alberty)


Excretion of monovalent and divalent ions in sharks

The main reason seems to be a mechanism to save water and allow the excretion of higher concentrations of the ions. See the image (from here):

The urine enters the glomeruli at a relatively low rate and with a low magnesium concentration. The paper cited below mentions a concentration of 1.5mM. First organic compounds as glucose are recovered actively, water follows the molecules passively. Then more ions as Ca$^{2+}$ enter in the proximal segment II. In the distal segment finally sodium and chloride are actively transported out while water passively leaves the segment. The divalent ions (magnesium, calcium) are left in high concentrations (the paper below says that the Mg concentration is now around 130mM). This helps concentrating these ions for excretion while loosing as little water as possible at the same time. Sodium and chloride are actively regulated in the gills.

For a short overview, see the link at the image above, for a detailed view, have a look at the following publication: "Kidneys sans glomeruli".


Assumption (1) is not really even true. The Nernst equation is always valid to find the reversal potential for a single ion: that is its purpose. To determine the equilibrium potential for a number of ions, you use the Goldman/GHK equation. It happens to be that the Goldman equation reduces to the Nernst in case of single-ion permeability, which of course never happens for real but is a reasonable approximation in some cases.

As far as your additional assumption, no, that assumption is not required. The Nernst equation doesn't tell you which directions ions flow, it tells you what the reversal potential is for an ion. If you add a voltage from some other source (like your example of adding a bunch of mysterious unaccounted for positive charges outside the membrane) that doesn't change the reversal potential, it changes the voltage. If you put a large positive charge on the left side somewhat like your situation (B), potassium would flow up its concentration gradient towards the Nernst potential for potassium.

Note also that your example is utterly ridiculous: if you want to know what happens when you have 10000000 M Na+ ions together on one side of a membrane you need to consult a physicist, not a biologist. I don't know where you put all the other negative charges, but you're probably about to have a) A very expensive electric bill, and b) a very big hole in your lab.

In real biology, the number of charges on each side of the membrane is similar enough that you can call it equal (see for example Why is it possible to calculate the equilibrium potential of an ion using the Nernst equation from empirical measurements in the cell at rest?). In any case where someone describes "adding sodium" to one side of the membrane, they don't mean just sodium, they mean sodium as a salt with some negative ion, it's just that the identity of that negative ion doesn't matter if it isn't membrane permeable (relative to the other ions involved).