Why does protein have 4 calories per gram?

Ultimately, the 4 kcal/g numbers come from calorimetry. That is, scientists take a small amount of glucose or protein, put it in a device which burns the material and figures out how much energy is released. Now, this doesn't account for certain factors which complicate matters, such as the fact that humans excrete waste nitrogen as urea and not fully oxidized nitrogen (as is produced in a bomb calorimeter). As such there's some corrections which are applied to account for those differences. When you do the math, you find that carbohydrates and proteins both have about 4 kcal/g energy. As such, most people these days don't actually bother to do the calorimetry to find the energy content, but instead take the content of carbohydrate/protein/fat/etc. and do the calories-per-gram calculation from there.

Now, you're correct that those numbers (from combustion calorimetry) don't match the number you got from the mass balance in gluconeogenesis. Part of the reason for this is that, like most processes, gluconeogenesis isn't 100% efficient. You get some loss as heat due to steps not being 100% reversible. The nutritional content is intended to be more of an estimate of the once-through energy content. (That is, the amount of energy you'll extract if you go directly from the input into a totally metabolized state.)

But perhaps a more important difference is that the mass/energy balance equations for gluconeogenesis from protein can be more complicated than your simple 3:1 analysis suggests -- there's various offshoots of ATP, NADH, etc. generated going from the raw amino acids to glucose. Each of these carries away some energy, and to get a true energy balance. You also need to account for these alternative offshoots of energy.

Which amino acids you're talking about also makes a difference. Alanine is probably the simplest amino acid to feed into gluconeogenesis. It's transformed at a 2:1 molar ratio, which works out to an approximately 1:1 mass ratio (as expected from the calorimetric ratios). Other amino acids like leucine are ketogenic, meaning that they cannot be converted in gluconeogenesis at all (at least in humans). The differences in how different amino acids metabolize can account for the discrepancy. The 3:1 ratio may refer to a "typical" amino acid distribution, which includes a mix of some 1:1 converted amino acids, some which are only partially converted, and some which aren't converted at all.


How RNA primer on leading strand is removed during DNA replication and how the gap is filled?

The group of cellular enzymes that remove RNA primers include the proteins FEN1 (flap endonuclease 1) and RNase H. The enzymes FEN1 and RNase H remove RNA primers at the start of each leading strand and at the start of each Okazaki fragment, leaving gaps of unreplicated template DNA. Once the primers are removed, a free-floating DNA polymerase lands at the 3' end of the preceding DNA fragment and extends the DNA over the gap. However, this creates new nicks (unconnected sugar-phosphate backbone).
In the final stage of DNA replication, the enyzme ligase joins the sugar-phosphate backbones at each nick site. After ligase has connected all nicks, the new strand is one long continuous DNA strand, and the daughter DNA molecule is complete.

Source: Boundless. “DNA Replication in Eukaryotes.” Boundless Biology. Boundless, 08 Jan. 2016. Retrieved 14 Mar. 2016 from https://www.boundless.com/biology/textbooks/boundless-biology-textbook/dna-structure-and-function-14/dna-replication-101/dna-replication-in-eukaryotes-437-12941/


Why prefer $MgSO_4$ over $MgCl_2$ in recipies

My guess is its the solubility properties of the anions.

Chloride ions can precipitate with some metals that might appear in a complicated buffer or medium. And yes they could even compete with enzyme binding.  Sulfate will remain in solution with just about anything.

There are exceptions, but if you're making a buffer you're probably going to do better if you use the general solubility rules.


What is this (seed/berry)-like object and where is it coming from?

Barring further details or photos, your fruits remind me of the drupe  from a hackberry (Celtis spp.)  tree.

Hackberry drupes are relatively small, often being only about 6-10mm in diameter.

Examples:
1,
2.

Do you have any warty looking trees nearby?
(like this).

Do you ever see the fruits in a different color? (purple, black, red, orange)?


a biochemical pathway for evaluating the effect of 3' to 5' exonuclease on the proofreading activity of DNA synthesis

well I tried to implement this pathway in MATLAB and it seems to me that it makes some sense. Here are two versions of the reaction progress simulation, one with low and the other with high affinity of the 3' to 5' exonuclease domain for the mismatches. The violet curve of the simulation corresponds the amount of synthesized dsDNA and the green curve corresponds to the error-free amount of that dsDNA.
The next figure shows that with low affinity of the exonuclease for the mismatches, the error rate is high (12%).

The figure below shows that the dsDNA synthesis error rate decreased with the increase of the affinity of the exonuclease for the mismatches.

The MATLAB code of this simulation is provided
https://matlab.mathworks.com/users/mwa0000016879211/Published/x551/x551.html
Your comments and suggestions are most appreciated.
Thanks,


How do I offer a generous gift to sweet-seeking wasps, bees, hornets, bumble-bees?

There are many scientific methods for that which are widely used in animal behavior studies, specifically in honey bees. Read this this. If you search you can find similar for mice and rats also :P


What chemicals/substances exist in green capsicum (peppers) that do not exist in red capsicum?

Your limited understanding is indeed correct - the different colours indicate different stages of maturation, even though different colour cultivars exist (e.g. some that remain green even if fully ripe).

It is known that the different maturation states have different vitamin and/or mineral concentrations (see here or here). This indicates that different biochemical pathways are active and that therefore the enzymatic set-up is variable during pepper maturation (which could have an effect on tolerability as it might also affect other plant components).

Moreover, you are right that the green colour is - at least partially - caused by chlorophyll but also non-green bell peppers often have chlorophyll (Lancaster et al., 1997) but that probably is not the cause of your friend's responses.

More likely the cause is 3-isobutyl-2-methoxypyrazine (IBMP) which gives the characteristic (green) pepper smell and has highest concentrations in green peppers (that's why it is called green pepper smell). It has one of the most intense odours that can be detected at very low concentrations, even within the complex odours of wine (Pickering et al., 2007), according to Roth, 2014 perhaps even below PPT concentrations.

So how does this fit together? Pickering et al., 2007 also suggest that one should determine 'consumer rejection thresholds' for methoxypyrazines, indicating that it might be repellent to some people even in low concentrations of 1-2 ng per litre. This could explain your friend's aversion but evidence for the allergy component is dubious.

I did find one paper (Jensen-Jarolim et al., 1998)  about allergen expression in peppers (birch allergy like). However, no green-specific allergens are reported, and it even seems like green peppers would be a better choice to avoid these allergens.


The carnivora can be seen in this phylogeny tree which comprises most of today's mammals. They suggest that rodents, elephants, monkeys, dogs and sea mammals all diverged from about 30 million years before the asteroid, until 5 million years after. The placentals and marsupials had a common ancestor previous to 100 million years ago.
Image from genomic study:

Previous to the Felix clade we have Feliforma, which includes mongooses and hyenas.
Image from wiki Feliformia:

There's a tree here
The last common ancestor of cats and dogs was about 40-55 million years ago. Feliforma family tree.
If you want to see previous to that, there are some basal carnivora, where the Feliforma are at the end of the tree.


How does the partial pressure of oxygen affect mental focus?

Long term exposure to hyperoxia actually does more harm than good. Though short term hyperoxia is recommended after brain injuries (http://www.medscape.com/viewarticle/741751_3) as a valid clinical strategy.

For lower concentrations of oxygen, there seems to be evidence that cognitive function is improved:

You can read more about that here: Chung, Soon-Cheol, et al. "Effect of 30% oxygen administration on verbal cognitive performance, blood oxygen saturation and heart rate." Applied psychophysiology and biofeedback 31.4 (2006): 281-293.

And also this:

  This study aimed to investigate whether inhalation
  of the air with 30% oxygen compared with normal air
  enhances cognitive functioning through increased activation in
  the brain. The verbal and visuospatial tasks were performed
  while brain images were scanned. The results showed that
  there were improvements in performance and also increased
  activation in several brain areas under the condition of 30%
  oxygen. These results suggest that a higher concentration of
  the inhaled oxygen increases the saturation of the blood
  oxygen in the brain, and facilitates cognitive performance.

Taken from: Sohn, Jin-Hun, Soon-Cheol Chung, and Eun-Hye Jang. "30% oxygen inhalation enhances cognitive performance through robust activation in the brain." Journal of physiological anthropology and applied human science 24.1 (2005): 51-53.

Though you have to be a bit careful about oxygen poisoning.

  While oxygen is an essential component for living organisms, the
  formation of reactive O2 intermediates is commonplace in aerobically
  metabolizing cells. The stability of a variety of reactive O2
  intermediates varies, but in some instances their interaction with the
  intracellular environment sets the basis for the pathophysiology of
  several disease states.

Adapted from: Cadenas, Enrique. "Biochemistry of oxygen toxicity." Annual review of biochemistry 58.1 (1989): 79-110.

  Pathophysiological processes are associated with increased levels of
  hyperoxia-induced reactive O2 species (ROS) which may readily react
  with surrounding biological tissues, damaging lipids, proteins, and
  nucleic acids. Protective antioxidant defenses can become overwhelmed
  with ROS leading to oxidative stress.

  The continuous exposure of newborn rats to 70–80 per cent oxygen at atmospheric pressure throughout the first 9 days of life significantly inhibited the growth of the brain which normally occurs during this period of life. The accumulations of DNA, RNA, total protein, and proteolipid protein which accompany brain growth during this period were all approximately proportionately depressed by the oxygen-enriched atmosphere. RNA/DNA and protein/DNA ratios were unaffected. The increase in brain mass in the first week of life reflects mainly cell proliferation, and since the decreased DNA accumulation occurred with no changes in RNA/DNA and protein/DNA ratios, we conclude that the effect of oxygen was to inhibit cellular division. We estimate that the oxygen exposure caused an approximately 7 per cent deficit in the cell population of the brain. These results indicate that the use of elevated concentrations of oxygen may have serious deleterious effects on the growth and development of the brain.

Taken from:* Grave, G. D., C. Kennedy, and L. Sokoloff. "Impairment of growth and development of the rat brain by hyperoxia at atmospheric pressure." Journal of neurochemistry 19.1 (1972): 187-194.*

Also hydrogen peroxide is  produced:

  Thus the H2O2 concentration in brains of rats exposed to room air is calculated to be about 7.7 pM, rises 60% when O2 tension is increased to 100% O2, and increases 300% at 3 ATA 100% O2, where symptoms of central nervous system toxicity first become apparent. These studies support the concept that H2O2 is an important mediator of O2-induced injury to the central nervous system.

Taken from: Yusa, T. O. S. H. I. K. O., et al. "Hyperoxia increases H2O2 production by brain in vivo." Journal of Applied Physiology 63.1 (1987): 353-358.

You can also always read the wiki page for oxygen poisoning: http://en.wikipedia.org/wiki/Oxygen_toxicity and also hyperoxia itself: http://en.wikipedia.org/wiki/Hyperoxia


How does the human body metabolize gasoline?

Gasoline toxicity through ingestions seems to be a topic where there's not a great deal of in-depth information available. I don't know how this works for chronic use, as most literature refers to acute scenarios. Either way, orally ingested, 30-50g is said to be toxic to humans while 350g can be fatal.[3].

So...

Gasoline's Constituents

A lot of components that make up gasoline are toxic to humans. This includes for example, benzene, toluene, xylene and butadiene. It's a mixture of more than 500 hydrocarbons and additives made up of:

60–70% alkanes (paraffins)
25–30% aromatics
6–9% alkenes (olefins).[2].

If you really want to know specifics about metabolism of gasoline, you can probably check out how some of the constituents are metabolised (processed) and their effects. This is because different components have varying metabolic pathways.

If you want to check this out, see Reese, et al at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1520023/pdf/envhper00383-0118.pdf.[3].

Ingestion and Toxicity

Apparently, most reported cases of toxicity from gasoline occur from inhalation or absorption through the skin (intravenous use has also been reported). Even though ingestion is a frequent occurrence, there's not much data on outcomes after oral ingestion.[1],[2]. Gasoline can however be well absorbed through the gastrointestinal tract[2].

The main target organ of gasoline toxicity is the nervous system and at high doses, this effect can cause death within minutes.[3]. However, generally, the primary cause of mortality seems to be related to gasoline's toxicity to the lungs. There are severe effects on the pulmonary system. Other effects of ingestion hasn't been as well documented.[1],[2].

It's suggested that these compounds have a direct effect on lung tissue and  disrupts gas exchange and causes fluid buildup in the lungs (pulmonary edema). This in turn causes the oxygen levels in the body to drop (hypoxemia).[2]. There are many other toxic effects on the lungs as well.

Additionally, liver damage, kidney damage, damage to blood cells, gastric ulcers and toxicity in the heart can occur.[2],[3]. Again, this is discussed in Reese, et al.

Hope that helps!

Rahman I. Gasoline ingestion: a rare cause of pancytopenia. Am J Med Sci. 2009. 338(5):433-4.
Domej W. Successful outcome after intravenous gasoline injection. J Med Toxicol. 2007. 3(4):173-7.
Reese, et al. Acute Toxicity of Gasoline and Some Additives. Environmental Health Perspectives. 1993. 115-131.


This article from Live Science provides some insight (no pun intended) into box jellyfish eyes.
“Whereas we have one set of multi-purpose eyes that sense color, size, shape and light intensity, box jellyfish have four different types of special-purpose eyes. The most primitive set detects only light levels, but one set of eyes is more sophisticated and can detect the color and size of objects.”
This article from Science Daily may also help.
“The researchers examined the function of one of two types of "upper lens eyes," already known to form images, to work out just what those eyes can see and how well. It turns out that those four eyes cover precisely the visual field needed to see through the water's surface up into the world above.”


pI and pH relationship in context of ion exchange protein purification

Have a look at this table, it really depends on the buffers you use:

The table is from this website, which is definitely worth reading when you are interested (or work) with ion exchange chromatography.


Why is the rough ER necessary to make extracellular proteins?

Extracellular proteins are proteins that function outside the cell, meaning they are made in cells (transcribed from ribosomes) and then are transported to the plasma membrane to be delivered to the extracellular space. The proteins that need to be secreted aren't secreted as free proteins, rather they are packaged into vesicles. Vesicles are membrane-enclosed structures. When ribosomes are translating mRNA and come across a specific sequence called a signal peptide (wiki), the ribosome goes to the ER and delivers the peptide into the ER. From here, the peptide gets packaged into a vesicle-- first a membrane budding off from the ER.
 source(NCBI)

This is also how secretory proteins get into the Golgi, by vesicle trafficking. From the golgi, proteins are packaged into vesicles. It is a hotly debated topic whether proteins are sorted into specific vesicles or proteins within vesicles (that do not belong in that vesicle) are sorted away (and degraded by the lysosome).


Why aren't there any competing biologies on Earth?

There are indeed almost certainly other potential alternatives to DNA-based biology and the RNA-based biology that may have predated it, which could be used to form viable organisms.
Many of them likely have some energetic disadvantage relative to DNA and RNA (e.g., requiring a higher bond formation energy, having a less flexible backbone) and those would naturally be expected to be outcompeted. But some probably aren't so different from DNA and could indeed have formed a viable alternative---if nothing else, the opposite chirality molecules are certainly candidates. Why aren't alternatives still around?
Surprisingly, it turns out that when time scales are long enough, we should expect a natural loss in the number of different independent lineages. Another more recent example of this is the fact that all modern humans are descended from Mitochondrial Eve and Y-chromosome Adam, despite the fact that these two individuals were members of thriving human populations at entirely unrelated times. Biodiversity is constantly being gained through divergence of existing lines and lost through lines that fail to reproduce. Over many generations of reproduction, this produces a random walk pattern that converges toward elimination of all but a single lineage in a given population even if all lineages are equally fit.
Now back to the origin of DNA-based life.  If abiogenesis is a rare and difficult event, then we would expect only one or a small number of life models to have emerged billions of years ago. Random fluctuations over all that time will tend to drive all but one toward extinction. With evolution at play as well, any lineage that randomly gains an advantage will be even more likely to outcompete the others.
And once there is life of any sort around? Well, potential alternatives to DNA are still nutrients, and therefore will simply be eaten by existing life forms before they have the chance to evolve into something new and interesting.


Species Identification: Coniferous tree, Italy

To me, it looks like a species of Taxus (Yew), for instance Taxus baccata. This is based on the flat needles, "flat" apparence/growth of the branches and the red berries. It's a bit hard to see what the red things are in your 3rd picture though (berries, shoots, flowers??). It should also have reddish bark where you can easily peal of loose scales. They can become very old (>1000y), have been used for many human purposes (woodcarving, medical purposes, bows), and all parts except for the berries are toxic.

Abies alba might be an alternative (if the red things are flowers), but then the needle underside should be relatively white and they also look to broad, soft and shiny to me.

Some pictures:

(from wikipedia)

(from http://linnaeus.nrm.se/flora/barr/taxa/taxus/taxubac.html)

(from wikipedia, a 1200-year-old tree in Poland)


Reason behind using DNA primer in PCR techcnique while RNA primer use in replication in vivo?

The (very) basic answer to your question about in-vitro vs. in-vivo primer usage is:

In-vivo - Although either (DNA or RNA primers) can be used for in-vivo primer extension biochemistry, DNA primers are not available (not made) in living cells. Therefore all natural in-vivo primer chemistries utilize RNA primers.
In-vitro - DNA primers are easily synthesized, inexpensive, functional, and substantially more stable (less likely to be degraded). DNA primers are therefore primarily used for most in-vitro purposes (i.e. PCR and other in-vitro primer extension applications).

Beyond that, all other reasons (complex evolutionary reasons vs. human choices in-vitro); involving subtle differences between RNA and DNA chemistry, structure, and function, similarly can play a role. The links below may be helpful to address some of these differences.

https://en.wikibooks.org/wiki/Structural_Biochemistry/Nucleic_Acid/Difference_between_DNA_and_RNA

https://en.wikipedia.org/wiki/Primer_(molecular_biology)


Alcoholic beverages, ingested casually, deliver two main nutrients the body will metabolize: sugar and ethanol. The body's natural response to a rise in blood glucose will be stimulated secretion of insulin (from B cells of the pancreatic islets). Alcohol is metabolized primarily by the liver, being first converted to acetaldehyde by alohol dehydrogenase and a coezyme NAD+. Acetaldehyde metabolism quickly converts this to acetate. Acetate is then eventually metabolized elsewhere in the body to carbon dioxide and water. The interesting effects are mediated by acetaldehyde, which can accumulate to toxic levels in some people. This ties into insulin because this article suggests that alcohol consumption changes blood flow from exocrine pancreas (responsible for digestive enzymes) to endocrine pancreas (responsible for secreting homrones, such as glucagon, insulin, somatostatin). Alcohol seems to modulate the late-phase of insulin secretion, increasing secretion, which leads to exaggerated glucose disposal and at least for diabetics causes hypoglycemia.

Huang Z, Sjöholm A. Ethanol acutely stimulates islet blood flow, amplifies insulin secretion, and induces hypoglycemia via nitric oxide and vagally mediated mechanisms. Endocrinology. 2008 Jan;149(1):232-6. Epub 2007 Oct 4.


First, the glucose is reduced by anaerobic fermentation to ethanol and carbon dioxide. The yeast uses the produced energy for a fast growth and division (1). As soon as all glucose is consumed the metabolism of the yeast changes from anerobic fermentation to aerobic respiration (oxygen is required). This is called diauxic shift. During this time the yeast stops growing (2). After this shift the yeast further reduces the ethanol to carbon dioxide and water. The generated energy is used for the second growth phase (3).
Hope this answers your question.
Best
Vanessa


Ejaculation without orgasm: is this possible to do it at will without external stimulation?

Yes, it is possible. It is all in the brain. One can be sufficiently aroused to ejaculate without any contact.

The most obvious example of this is the case of nocturnal emission

  A nocturnal emission, informally known as a wet dream, is a spontaneous orgasm during sleep that includes ejaculation for a male, or vaginal wetness or an orgasm (or both) for a female. Nocturnal emissions are most common during adolescence and early young adult years, but they may happen any time after puberty. It is possible for men to wake up during a wet dream or simply to sleep through it, but for women, some researchers have added the requirement that she should also awaken during the orgasm and perceive that the orgasm happened before it counts as a wet dream. Vaginal lubrication alone does not mean that the female had an orgasm.

Depending by what you mean by "without such external stimulation", you might want to read about premature ejaculation

  Premature ejaculation (PE) occurs when a man experiences orgasm and expels semen soon after sexual activity and with minimal penile stimulation. It has also been called early ejaculation, rapid ejaculation, rapid climax, premature climax, and (historically) ejaculatio praecox. There is no uniform cut-off defining "premature", but a consensus of experts at the International Society for Sexual Medicine endorsed a definition including "ejaculation which always or nearly always occurs prior to or within about one minute".


A few words on genomic prediction
No complex trait is 100% heritable, hence no prediction based entirely on DNA would ever be perfect. With that said, predictive genomics is progressing at a quite amazing rate right now. So while predictions can be nowhere near perfect, it is getting possible to make DNA predictions that correlate substantially with observed values.
The genes that correlate with phenotypic differences are found using genome-wide association studies (GWAS). The total effects are then aggregated up to what is called a polygenic score.
A success story --  Height
Height is highly heritable, meaning that much of the phenotypic variance (although not 100%) is due to genetic differences. Height is also highly polygenic -- it's a trait influenced by many genes, each of small effect.
Many variants that correlate with height have now been found. Polygenic scores of height correlate higher than ~0.60 with observed height. DNA predictions are generally within a few centimeters of true height (Lello, Avery, Tellier, Vazquez, de los Campos, Hsu, 2018). According to an interview with Stephen Hsu, one of the authors of this paper and co-founder of the company Genomic Prediction, they can correctly predict the height ordering of siblings within the same family 80-90% of the time (source). So based purely on DNA, can we say which of two siblings are going to be taller than the other? Not perfectly, but with decent reliably, yes.
This is about as good as predictions of complex traits can be based on current methods. There are a few principal reasons that correlations are not higher (even though it is quite impressive already in its own right). First, as I said, complex traits are not 100% heritable and therefore predictions are not expected to ever be perfect. Second, current GWAS are typically based on SNPs which are common gene variants. Rarer gene variants are expected to contribute to the variance and their effects are still needed to be uncovered. Third, only additive effects are taken into account, not gene-by-gene interactions.
Genetic IQ Prediction?
IQ, like height, is a heritable trait and is highly polygenic.
There are several approaches to finding gene variants correlated with IQ, however they can broadly be categorized into two. The most obvious approach is to simply give people intelligence tests and get their DNA. The problem with this is that it is difficult to get large samples with good intelligence tests. When this approach is used, usually a very short (say, 2 min) intelligence test is used. The second approach is to use a proxy phenotype. With this approach, the variable years of educational attainment has been used to good success, and has been shown to have a high genetic correlation with intelligence ($r_g \approx 0.7$).
Many variants that are associated with intelligence or educational attainment have been found, see e.g. (Lee et al, 2018; Savage et al, 2018). While many variants are known, IQ is not as well understood as height, and current SNP predictors correlate about ~0.3 with observed IQ (See e.g. Allegrini et al, 2018). This correlation is bound to increase in the coming few years.
Further Information
If you want a simple introduction to what can be read from the genome so far, there is a TED talk on this subject, TED2016: How to read a genome and build a human being. Although, major improvements have already been made in the years since 2016. For anyone that is more interested in the mathematical techniques used for prediction and the underlying theory, I recommend this talk by Stephen Hsu if you're further interested in genomic prediction of complex traits. I also recommend reading this review by Robert Plomin and Sophie von Stumm to get an easily understandable overview of the current state of knowledge on the subject.
References
Lello, Avery, Tellier, Vazquez, de los Campus, Hsu (2018). Accurate Genomic Prediction of Human Height. DOI: https://doi.org/10.1534/genetics.118.301267
Marty Nemko (2018). The Future of In-Vitro Fertilization and Gene Editing. Psychology Today Link.
 Lee, ..., Cesarini (2018). Gene discovery and polygenic prediction from a genome-wide association study of educational attainment in 1.1 million individuals. DOI: https://doi.org/10.1038/s41588-018-0147-3
Savage, ..., Posthuma (2018). Genome-wide association meta-analysis in 269,867 individuals identifies new genetic and functional links to intelligence. DOI: https://doi.org/10.1038/s41588-018-0152-6
Allegrini, Selzam, Rimfeld, von Stumm, Pingault, Plomin (2018). Genomic prediction of cognitive traits in childhood and adolescence. DOI: https://doi.org/10.1101/418210
Sabatini (2016). How to read a genome and build a human being. TED2016 Link to Talk.
Hsu (2018). Genomic Prediction of Complex Traits. Youtube Link to Talk.
Plomin, von Stumm (2018). The new genetics of intelligence. DOI: https://doi.org/10.1038/nrg.2017.104


what is “a group of living things that can interbreed and produce full interfertile offspring”?

Based on the biological species concept, you're referring to two different species that experience ecological isolation (also called "habitat isolation") as a prezygotic reproductive isolating mechanism.

See here for a simple explanation of various concepts regarding species.

This, of course, is just one of the many reasons (see here for more) why we have multiple species concepts. Some might argue that these organisms are the same species based on their ability to produce interfertile offspring. If said researcher wanted to do so, they would define these organisms using a different concept.

Recognize that “species” is an artificial construct to allow conceptualization and organization of an incredibly complex, dynamic, and otherwise continuously variable genetic world.

We have not found a perfect way to "cut up" the world neatly/consistently into describable and functionally useful units, and --in fact -- we likely never will. Why? Because the lives of these organisms do not care about our cataloging and description systems -- these concepts are strictly for humankind to functionally relate to and react to their presence. The concept chosen almost inherently relies on the underlying motivation of the describer for naming the organism in the first place.


The ability to produce offspring has more to do with the compatibility of the chromosomes than the number. This is why hybrid species (such as mules) are able to survive (but are infertile). If you want to learn about why hybrids are infertile here is stackexchange question about.

Although, this would all be dependent on weather gametogenesis could occur with the tetrasomy. But as seen here with Down syndrome, it can be successful.


Ok let me try to tackle this one - still could be off - let me know.

The book Chapter from UCDavis that is linked from your wikipedia page is a good reference I think. Overall the term 'water potential' will try to estimate an energy function that describes the behavior of water in a chemo-mechanical sense.

$\Psi_{total} = \Psi_{reference} + \Psi_{solute} + \Psi_{pressure} + \Psi_{gravitational} + \Psi_{humidity} + \Psi_{matrix}$

It looks a lot like a Hamiltonian expression of total energy that tries to see the water as a fluid.  The water potential is not the same as an energy equation for fluid dynamics which tries to understand the motion of a body of liquid and does not typically take into consideration chemical changes like solute in the behavior.

So first we are looking at a set of behaviors that the fluid experiences.  some of them treat the fluid as a body ( pressure, gravitational) others look at the potential for evaporation or diffusion (solute and humidity to some degree).  wetting of surfaces and surface tension (matrix).

The water potential is an equation broken down into a set of measurable or approximately measurable energy terms.  But like a lot of Energy equations, when  you are looking at a biological system, it is more often qualitative than a quantitated entity.  The general observation that surface tension decreases when temperature goes up, or when the solutes have higher concentration is used to make arguments of the mechanism of say physiology

Generally speaking looking at the magnitudes of the various terms you can see how influential they are and then try to focus the hypothesis into a test that can make a distinction about the mechanism with specific measurements.  The actual overall measurement of a water potential or any total energy is almost always intractable.  The difference in energy is what you might be able to measure, but in the case of the water potential, the measurement will usually be an observation, with some uncertainty that water is moving from point A to B and not elsewhere.

Take a look at this paper describing Drought Stress in Arabidopsis.  The water potential is cited as a critical element of drought response - and of course it should be.  But all this work here, with all the proteins acting to change the physiology of the cell, adjust the chemical potential (and therefore the osmotic potential) of the cell membrane, its hard to imagine how measuring a root system at all points would be possible.

  Physical properties of the cell wall play a crucial role in the response of plants to water deficit (Bacon, 1999). Transcriptome analysis of pDr showed the repression of many expansin genes (Bray, 2004), while mild osmotic stress revealed the induction of expansin genes (Skirycz et al., 2010). Cell expansion in response to drought was characterized in the maize (Zea mays) root system as an adaptation to low water potential (Wu and Cosgrove, 2000).


In short, the difference stems from different values regarding the number of ATP attributed to the electron carriers in the electron transport chain (ETC).

My guess is that your class didn't go too far in depth on the subject, and also that your class or text is using mixed sources of information.

I have overviewed (general) glucose metabolism here, but feel free to skip this section if you don't need it.

Glucose metabolism is generally composed of 4* processes:

Glycolysis: a 6-C glucose molecule is broken down to 2 pyruvate molecules producing a net gain of 2 ATP and 2 NADH (electron carrier) molecules. Note that this is a net gain.
Pyruvate Dehydrogenase Complex (PDC): Here Pyruvate is made into Acetyl CoA, which enters the Krebs Cycle (step 3). This is the Link reaction step that you mentioned. This step produces a 1 NADH molecule per pyruvate.
Krebs Cycle (TCA): The Krebs cycle is central to cell metabolism and produces a lot of electron carriers, netting 1 GTP (ATP energy "equivalent"), 3 NADH, and 1 "FADH2" (electron carrier) PER Acetyl CoA entering the TCA.
Oxidative Phosphorylation (ETC): This step converts your electron carriers into ATP. It does this by using the energy released by electron transfers (e- are transferred from your electron carriers NADH, FADH2 to intermediate compounds to oxygen. This provides the energy to actively transport protons) to pump protons (H+ atoms) across a semi-permeable membrane to create a electro-chemical gradient. These H+ atoms will flow down this gradient through the channel of the ATP synthase, creating ATP. Currently, it is pretty widely accepted that an NADH molcule provides enough energy to net 2.5 ATP, and a FADH2 molecule provides enough energy to net 1.5 ATP.

As a result, we get the following:

+2ATP, +2NADH
+1NADH x2
(+1GTP, +1FADH2, +3NADH) x2
-10 NADH, +2.5ATP x10; -2FADH2, + 1.5ATP x2

This yields 2+2+25+3=32 ATP, which is what you obtained in your calculation.

However, a previously accepted value states that the 4th step nets 3 ATP/NADH molecule and 2 ATP/FADH2 molecule. Running the same calculation, we obtain 2+2+30+4, netting 38 ATP, causing the discrepancy you notice. I wouldn't say either set of values is universally accepted, but I would say that 32 ATP is generally recognized as the "right" answer.

  In other words, 32 ATP is the result of the more recently accepted equivalences of 2.5ATP/NADH and 1.5ATP/FADH2 in oxidative phosphorylation, whereas 38 ATP is the result of the older pair accepted equivalences of 3ATP/NADH and 2ATP/FADH2.

Some notes and caveats:

Please note that in (most) Eukaryotes, the NADH produced in the cytosol (Glycolysis) is "reduced to FADH2" via the mitochondrial shuttle as the high energy electrions enter the ETC. This means that each NADH produced by glycolysis only nets 1.5 ATP, resulting in 30 ATP/glucose in majority of eukaryotes.

It is also important to note that the numbers that I have provided are mostly used in classroom calculations for general systems. Real organisms will often deviate for a multitude of reasons. Further, some organisms may not follow this rule at all.

*A few sources might classify the PDC as part of glycolysis or as part of the TCA.


what is meta-sympathetic nervous system?

As @mgkrebbs says, metasympathetic nervous system is still a matter of debate and is not fully accepted in the scientific world due to lack of research and evidence.

Metasympathetic nervous system, just like sympathetic and parasympathetic nervous system, is a part of Autonomic Nervous System.

  On the basis of a number of structural and functional indices, application of pharmacological analysis as well as recording of neuronal activity, the autonomic nervous system is subdivided into the sympathetic, parasympathetic and metasympathetic parts. The metasympathetic system includes the complex of microganglia situated in the walls of visceral organs and having marked motility activity (the heart, ureters, intestine, stomach). According to the localization, separate areas of this system can be defined by its site (for example, the cardiometasympathetic area in the heart). The metasympathetic system attains the features of true autonomy. Its cells have no direct connection with the high centers: this connection is established through mono- and polysynaptic sensory and afferent units of sympathetic and parasympathetic nature.

Source

Full article here

How is it different from sympathetic & parasympathetic systems?

One major difference is in the location.

The Metasympathetic system

  includes the complex of microganglia situated in the walls of visceral organs and having marked motility activity (the heart, ureters, intestine, stomach).

while Sympathetic system

  consists of cells with bodies in the lateral grey column from T1 to L2/3. These cell bodies are "GVE" (general visceral efferent) neurons and are the preganglionic neurons. There are several locations upon which preganglionic neurons can synapse for their postganglionic neurons:

and Parasympathetic system

  consists of cells with bodies in one of two locations: the brainstem (Cranial Nerves III, VII, IX, X) or the sacral spinal cord (S2, S3, S4). These are the preganglionic neurons, which synapse with postganglionic neurons in these locations:

For detailed location, see this image:


What nocturnal animal sound am I hearing in the trees in Maine?

My initial guess (knowing almost no information) is that it's a Northern saw-whet owl (Aegolius acadicus). These owls live year round in Maine but also increase in number as some migrate from Canada through Maine for winter. You can hear their advertising song here.

Northern Saw-whet Owls have a distinctive too-too-too call -- an insistent series of whistled notes on roughly the same pitch, given at a rate of about 2 notes per second. Males calling to advertise their territory can be heard up to half a mile away. Other males respond with a softer, faster, lower version of the call.


Calculation of final magnification when using a CCD camera

Assuming that the FOV that is captured by the CCD on the screen is 100µm wide as determined by the micrometer, and you are viewing the 920 pixel wide image on a standard 96 ppi monitor, the zoom would be approximately 2434 times.

$$\frac{920p}{96p/in}/100µm \approx 2434$$

Additionally, you should ensure that the minimum resolution on the micrometer is at least twice as large as each pixel on your microscope CCD.

The reason that the pixel size must be at least 2 times smaller than the minimum resolution present in the image is due to the Nyquist-Shannon sampling theorem.

This being said, all microscopes (and arguably all measurement devices) should be calibrated against a standard. This paper explains the usage of a standard to calibrate confocal microscopes.

A similar technique used to calibrate normal optical microscopes using a stage micrometer standard can be used if you do not possess such a standard. First calibrate the normal microscope, then image an identical sample using both microscopes in order to obtain the size of the field of view.


There are four hypotheses with varying levels of supporting evidence for why humpback whales sing.

Yes, only males have been shown to sing. It used to be thought that the songs only occurred on breeding grounds and therefore served a reproductive purpose. However, songs have since been recorded on migration routes and feeding grounds, though not as prolifically.

The hypotheses are:

"Mate Attraction" whereby males sing and females approach them to mate. No evidence has ever shown a female humpback whale approach a singing male. Rather, a group of males will swim after a female, vying for position, until she is receptive to mating. Then the closest whale (the primary escort) will be best poised for success. In my opinion, this is the least plausible hypothesis.
"Lekking" whereby a group of males sing to stimulate the females to begin estrus and advertise their body size and health for female mate choice. https://en.wikipedia.org/wiki/Lek_mating This may allow for female selection of choosing a mate later while being pursued as part of competitive group. I am unaware of which articles support this hypothesis and provide evidence. Birds and land mammals are much easier to observe in a lekking behavior than any underwater animal is.
"Territory establishment" whereby males sing to mark their territorial bubble of water. If a male has a larger territory, then it is more likely a female will pass through that larger territory so that the male can respond by pursing her. This could be supported by proving that male humpback whales respect each other's territories and space themselves consistently across their watery world. Refer to http://dx.doi.org/10.1121/1.4962217
"Orientation by echolocation" has recently been put forward by Edward Mercado that song reflects on a broad scale around the whale's environment to provide feedback for navigating the general area. Many researchers argue the plausibility of such low frequencies echoing effectively.

New studies into cultural transmission of parts of songs across ocean basins may suggest the song is not just for reproduction but to fulfill wider communication needs or generate a form of social creativity. See work by Ellen Garland.


Why don't phosphatases both add and remove phosphate groups if enzymes catalyze reactions in both directions?

I think the description of enzymatic reactions as 'reversible' is potentially a bit misleading. It might be better to think of enzymes as agnostic to reaction direction.

The big missing piece is the difference in free energy of the reaction itself. Reactions that remove a phosphate group are energetically favorable in biological conditions. A phosphatase will effectively never add a phosphate group back because one would have to supply additional energy to make the reaction proceed in that direction.

Phosphatases catalyze a reaction that results in a free phosphate ion. However, kinases that add phosphate groups are catalyzing quite a different reaction, where a phosphate group is lost from a molecule of ATP which becomes ADP. This reaction is also energetically favorable, and the reverse reaction does not occur.


How do I look for pathogen in water with a microscope? Is it possible?

Yes your teacher is right. In a microscope you can see microorganisms. Now the question is to identify them as pathogens.

I guess what your teacher has in mind is to use specific culture mediums for different pathogens and see if anything is growing there, then you have a positive.

You could also do a PCR. This is extracting the DNA and amplify specific genes that you know belongs to pathogens.

But the most currently trendy analysis is metagenomics. Basically, you exctract the genetic material from the sample, then sequence and compare against public databases. This methodology allows the identification of everything that is there pathogens and non-pathogens.


A limit to birds affinity for high vantage points

Birds find their niches based on many reasons. Their choice is based on primarily resource availability, predation risk, and competition. Keep in mind there are variations among species, most birds like to forage for food at a hight safe enough to avoid ground predation, at the same time to be able to see and find food without much competition. Therefore very high altitudes do not seem beneficial for food resources and its a cost in energy, thus reasonable altitudes are preferred. But again many variations depending on species and location.


It hard to figure out what sort of data you have. qPCR? Let me give you an example with tools involved on how I get differential genes for RNAseq data, that is whole transcriptom and for mouse that transcriptom that's about 23000 genes.

Step 1. Map raw reads to the reference genome.
Step 2. Count number of reads within the feature. Feature can be several things, but lets just take protein coding feature (feature == gene).
Step 3. Do differential expressions analysis

From step 2 you get a matrix of counts.

      sampleA_rep1 sampleA_rep2 sampleB_rep1 sampleB_rep2
gene1      2             5        20             23
gene2      10            12       50             50
gene3      20            23       4              6
..
geneN

The packages that I use are limma and/or edgeR. You can find them on bioconductor Both packages take raw counts and give you topTable of DEG, default is top 100 genes.

I recommend reading edgeR or limma manuals, there come with great explanations as well as examples. Also A scaling normalization method for differential expression analysis of RNA-seq data is original paper that explains TMM normalisation (mention a bit more in depth below)

Two things; one you need to filter genes with low counts, convert to cpm() counts per million before filtering as this takes library size (depth of sequencing) into consideration. two calcNormFactors() will do TMM

The hardest thing (I understand) in RNAseq is to get total RNA output for each sample. Because a treatment will effect the number of transcripts expressed in that sample, increasing or decreasing amount of transcript, which give you unbalanced counts. You won't know just by looking at raw counts if geneA has less counts because it's been down regulated OR because that sample after treatment has more transcripts present in the cell and geneA simply has less coverage, due to other transcripts also getting reads now. I can't really explain that too technically because I don't understand this myself, but TMM normalisation takes care of this and  gives you an estimate of degree of variability.

I know that I'm not giving that much info on actual differential testing, which was your question. edgeR has exactTest() which is Exact Tests for Differences between Two Groups of Negative-Binomial Counts , which might help you, but you might have normalise your counts differently as mentioned above. The general idea (I understand) is you need to fit a model (lmFit()) and then do the test eBayes()

Other

Degust this is very nice tool that uses limma and edgeR in the backend, but simplifies a lot of things as well as gives you nice interface to work with your data. You upload raw counts! in the format shown above
DESeq one of the other rather popular R packages that can also do differential gene testing


Can vaccines move from person to person?

Most immunizations are not transmissible. A few are. To be transmissible, an immunization would have to be a live attenuated vaccine (i.e., a vaccine that can reproduce in the host, but doesn't cause disease), AND have the necessary reproduction rate and virulence factors that would allow for person to person transmission. There are many live attenuated vaccines in use today, but only one that is transmissible, Oral Poliovirus Vaccine, or OPV. OPV is currently not in use in the US, but is used in the developing world, and can circulate in communities. Some would argue that this is a good thing, as it further disseminates immune protection to the population, but it is a little problematic, because it is not without risk, including reversion to a virulent type that can cause Vaccine associated Paralytic Poliomyelitis.

On editing your question, I'm reminded that your example was of TB. I would note that BCG, the vaccination against Tuberculosis, may be a particular case, and I'm not as familiar with it except as a complicating factor in interpreting the results of a TB test in U.S. immigrants. BCG is a live attenuated strain of Mycobacterium bovis, can (rarely) produce disseminated disease itself, and the mycobacterium itself can be isolated in the blood of individuals some time after vaccination. There is also a possible report of vertical transmission of the mycobacterium (from mother to child), but these results use novel methods, and I'm unfamiliar with this group's work. Whether this would lead to immunity of the child is definitely an open question. BCG even when administered in the standard way (as in intradermal inoculation) isn't particularly good at producing immunity, though it is good at preventing meningitis and miliary TB in young children. I'm not aware of any documented case of horizontal person-to-person transmission, but wouldn't declare it impossible.


Where are the ATP synthases synthesised?

The interesting thing is that the mitochondrial ATP synthase consists of many subunit proteins, both encoded by nuclear DNA and mitochondrial DNA. It has long been unclear exactly how these synthases are assembled, and what differences exist between bacteria, yeast, and humans - where ATP synthase formation is normally studied. Regardless, each of these proteins is translated on ribosomes from mRNA transcripts of genes, just like regular proteins. However, these must come together correctly (in the right order) and end up in the correct location.
There are recent publications that answers your question rather directly.
Assembly of the membrane domain of ATP synthase in human mitochondria
In short:

We have shown that the assembly of human ATP synthase in the inner [mitochondrial] membrane involves the formation of a monomeric intermediate made from 25 nuclear-encoded proteins into which the two mitochondrially encoded subunits are inserted and then sealed by association of another nuclear-encoded protein, thereby dimerizing the complex. Association of a final nuclear protein oligomerizes the dimers back-to-face along the cristae [inner membrane of the mitochondrion] edges.

A commentary on the paper is also available, which provides insight into the historical and biological context and difficulties which the paper addresses and overcomes. It may be worth reading their synopsis first. You can find it here:
Assembling the mitochondrial ATP synthase


When should endocytosis inhibitors be used in cell binding assays?

As with so many things, it depends. Also, I'm a bit unclear when you say antibody-receptor interaction, do you mean that you have an antibody that's specific for a receptor, or that you're studying Fc receptors binding to antibodies? (for the following, I assume the former)

For most cell types and most cell surface molecules, simple antibody binding isn't going to induce endocytosis, and keeping the cells on ice is sufficient to prevent most background endocytosis (i'd do the assays in a cold room as well so that even when you take tubes out of the ice bucket they stay cold).

On the other hand, if you're using highly phagocytic cells (like macrophages), and/or you're triggering a receptor through cross-linking or some other mechanism, you might get some endocytosis that affects your results.

The mechanism (clathrin vs non) can also vary, again depending on what's being bound.

You should do some optimization - ie: do the same assay on a set of samples, with or without  inhibition and see if your antibody binding is affected. But be aware that a lot of drugs for inhibiting endocytosis can do other stuff too, so watch out for artifacts. Maybe read this: http://www.ncbi.nlm.nih.gov/pubmed/18369934


There are two types of MHC molecules:

All nucleated cells express MHC class 1 proteins.  A sample of all proteins produced within the cell are 'sliced' into their constituents which are then presented by MHC-I receptors.  This means that if a virus infects a cell, the foreign proteins the cell is induced to make are expressed on the cell membrane by MHC-I.  This is important as antibodies can not cross cell membranes, therefore this is the method by which a cell signals that it is infected by a virus.

MHC II are the special molecules that are only expressed in antigen-presenting cells, which I think is what you are referring to.  As neither CD4 or CD8 T-cells present antigens, they do not express MHC-II themselves.  Instead CD4 have receptors for MHCII  (while CD8 have receptors for MHCI), allowing them to interact with antigens presented by other immune cells.

If a virus infects T-cells, the viral proteins are sampled by the MHC-I pathway and presented via MHC-I on the surface of the infected T-Cell.  The immune response then progresses as for any other virally infected cell, destruction by CD8 T-Killers that destroy the cell by non-phagocytic means.


Recommended applications for commercial antibodies

Maybe WB is easier for them to test?

In general, however, my recommendation is to check if they provide refs to paper using those antibodies and look at the images on the paper.

Be careful putting your trust in the supplier's pictures, I have seen obviously photoshopped images on commercial websites.
Also always double-check the referenced papers, as sometimes they don't really use the same product that is sold...

Other than that, in my experience, the recommended application is just that: recommended. The antibody may as well work for other application.
That said, note that there is a rationale for an antibody working for WB and not IHC, for instance: perfusion with fixators such as PFA will change the 3D structure of the target protein and may mask (or reveal) certain epitops, so the antibody may be more or less efficient depending what form of the protein you're dealing with (native, fixed in PFA, fixed in glutaraldehyde, SDS-denaturated etc.)


Intro course to evolutionary biology
I doubt you can get much from the below answer. At the end of the day, the only thing that would really allow you to increase your knowledge is probably an intro course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.
Question

Is it possible to artificially select for flight in pigs?

If by 'artificially select' you refer to selection on available genetic variance, then No, it is not! You'll need plenty of new mutations and it would take a very long time.
Selection
You cannot select for something that does not exist. Selection requires pre-existing phenotypic and genetic variation for the trait of interest. No pigs are flying today, so you cannot increase the frequency of individuals flying by selection.
You will need to wait for mutations that confer such flying ability. Of course, there won't be a single mutation that turns a pig into a flying pig. Simply because flight is really not a simple adaptation for a pig! There are few species you could have chosen for which flight would be harder to think of! You are going to go on a long step-by-step procedure, fixing mutations one at a time by selecting every one of them and that will probably take hundreds of thousands of years or maybe millions of years.
Step-by-step procedure
I suspect you would consider using their front limb for flying. Here is a potential and extremely simplified step-by-step procedure. Of course, if you were thinking of pigs flying using their ears, the procedure wold be drastically different!
You should probably start by attempting to modify their limbs then. You can maybe try to start by selecting for individuals that are better able to manipulate objects with the front limb. Also start selecting for lighter bodies. Also, remove any selection for the ability of fast displacement or moving in the mud as that would select for their current front limbs. Start with some very very simplistic manipulation and increase up to eventually ending up with individuals that have pretty flexible front limb. Make sure to select for front limb that can move perpendicular to the body axis.
Then I don't know if you should aim to make wings out of skin or out of hair-feather like structure. If you're aiming with feather-like structure, you can try play it out with sexual selection just like it evolved in birds. Let's say you're choosing skin wings. Then, maybe selecting for those having broad and thing front limbs might be a good way to go. In the meantime, you've reached anything like that, you probably managed to reduce the body size of your pigs to the size of a mouse with a very elongated body.
Select for jumping abilities and then slowly for flying abilities. You've got flying organisms who's ancestors were pigs! Be aware nobody is going to fund such a useless and incredibly long experiment.


How do nasal and aural passages connect?

The eustachian tube connects the nasopharynx to the middle ear, on each side. The (naso)pharynx is basically the back of the mouth, and the middle ear is a cavity behing the eardum.

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

It is normally closed when there is no pressure difference between the middle ear and the nasopharynx, by extension between the middle ear and the air around one. Its function is to avoid a ruptured eardrum that could be caused by such difference in pressure. (This could be the case when ascending a mountain, or diving underwater, where the ambient pressure drops or increase, but not the pressure inside the middle ear)

What you are doing is closing all passages for the air to flow out (mouth and nose closed), yet trying to blow it out : this artificially increase the pressure and opens the tubes. While it is usually a passage for air, if there is a fluid buildup it could flow through it too.

Whether it is safe is a more of a medical question, which would be better suited for your physician.


Why does beta-2-Thienylalanine inhibit bacterial growth?

β-2-thienylalanine is an analogue of phenylalanine. It is incorporated into proteins in place of phenylalanine, and the resulting proteins are inactive because of the substitution. Consequently growth medium supplemented with β-2-thienylalanine will not support bacterial growth.

Addition of phenylalanine to a medium containing β-2-thienylalanine will result in a competition between the two compounds - if there is an excess of phenylalanine then this will out-compete the analogue and incorporation of the analogue will be minimised, allowing growth. Blood from a patient with PKU contains phenylalanine, so the addition of this to the growth medium will relieve inhibition of growth.

Here is a link to a patent application in which a screen for E. coli strains overproducing phenylalanine was based upon the same principle.


Do humans emit more carbon through respiration or defecation?

The short answer
In a comparison between exhaled and faecal carbon, exhaled carbon wins.

The long answer
Warning: Assumptions, approximations and averages ahead.
Calculating faecal carbon excretion
The average human being produces about $29 \text{ g}$ faeces (dry weight) per day, the major component of which is bacteria [1]. For now, neglect variations with fibre and other dietary components. Also, assume that all of it is bacteria.
Now, carbon makes up about $50 \%$ of bacterial dry weight [2]. Thus daily carbon excretion in faeces is about $15 \text{ g}$.
Calculating carbon exhalation
An adult human being breathes about $20$ times a minute [3]. Each breath has a volume of about $500 \text{ mL}$ [4]. Thus the exhaled volume per day is $20 \times 60 \times 24 \times 500 \text{ mL} = 1.44 \times 10^7 \text{ mL}$.
Exhaled air is about $4 \%$ carbon dioxide [5]. The density of carbon dioxide at $37 \  ^{\circ} \text{C}$ and $1  \text{ bar}$ is $1.713 \text{ kg m}^{-3} = 1.713 \times 10 ^{-3} \text { g mL}^{-1}$ [6].
Hence, the mass of carbon dioxide exhaled per day is $0.04 \times \left(1.44 \times 10^7 \right) \times \left(1.713 \times 10^{-3} \right) \text{ g} \approx 987 \text{ g}$.
And since $\text{CO}_2$ is $\frac{12}{44}$ carbon, the mass of carbon exhaled per day comes out to be $\frac{12}{44} \times 987 \text{ g} = 269 \text{ g}$, which is at least an order of magnitude greater than the figure we got for faecal carbon.
References

Rose C, Parker A, Jefferson B, Cartmell E. The characterization of feces and urine: a review of the literature to inform advanced treatment technology. Crit Rev Environ Sci Technol. 2015 Sep 2;45(17):1827-1879. https://doi.org/10.1080/10643389.2014.1000761.

Lawford H, Rousseau J. Studies on nutrient requirements and cost-effective supplements for ethanol production by recombinant E. coli. Appl. Biochem. Biotechnol. 1996 Mar 1;57-58(1):307-326. https://doi.org/10.1007/BF02941710.

Hooker EA, O'Brien DJ, Danzl DF, Barefoot JA, Brown JE. Respiratory rates in emergency department patients. J Emerg Med. 1989;7(2):129‐132. https://doi.org/10.1016/0736-4679(89)90257-6.

https://en.m.wikipedia.org/wiki/Tidal_volume

https://www.bbc.co.uk/bitesize/guides/z9hycdm/revision/3

https://www.engineeringtoolbox.com/carbon-dioxide-density-specific-weight-temperature-pressure-d_2018.html


I would consider physical filtering properties of the corpuscle sheath as well as adaptation of the neuron or downstream targets.


The difference between "Hunger" and "Appetite"

According to the website "Appetite vs. hunger", the difference is very similar to what you were saying:

  Hunger is the need to eat.

Hunger is instinctive, it is the body's way of letting you know it needs sustenance.

and

  Appetite is the desire to eat.

It is a coordination between the brain and the stomach, this is learned behaviour.

Some further information can be found in the article preview "The Biological Nature of Appetite" (Stellar, 1992)


Cells created using differently aligned proteins

The problem with this is something called the structure-function relationship. The function of a protein or enzyme is completely dependent on its structure. For example, take a look at this representation of the active site of chymotrypsin:

The side chains of D102, H57, and S195 all need to be in a perfect conformation in order for the enzyme to function properly, with the hydrogen bonds being essential. If any one of those amino acids was in the D-form, the enzyme would lose its activity completely. Having every single amino acid in the D-form wouldn't help either, as the entire protein's structure (and hence its function) would be altered.


Indian tropical fruit trees and fruit bearing

Trees fruit before the monsoon season to maximize seed germination and seedling recruitment. previous studies have shown that in many species, fruiting occurs just before the wet season such that seeds germinate and establish during the wet season when conditions are most favourable.

Smythe N. 1970 Relationships between fruiting seasons and seed dispersal methods in a Neotropical forest. Am. Nat. 104, 25–35. (doi:10.1086/282638)

So the answer is 4.


Is a wet-mount needed to use Immersion Oil?

When I prepare my slide to use immersion oil, do I really need to wet-mount the specimen? Can I do it with just the coverslip?

Ideally you shouldn't use either with immersion oil. You should match the mounting media index as closely as possible to the immersion oil index, otherwise you'll reduce the resolution and contrast of your image. See:

http://www.microbehunter.com/the-importance-of-mounting-medium-refractive-index/

  Using water for the wet-mount gives you a sort-of time limit. You have to do your work before the water evaporates else you get little rivers at x100.

There are lots of options for higher index mounting media that will also preserve your specimen at least as well as air.


Mitochondrial DNA is circular, like bacterial DNA, and around 16.6 Kb long. It codes for 37 genes in total but the majority of these are simply the machinery for gene expression (curiously, mitochondria have a slightly different codon->amino acid translation 'table' to nuclear DNA) and so just 13 code for proteins. Single mitochondria usually have multiple copies of the DNA.

Mitochondria are thought to be most closely related to the bacteria Rickettsia, an obligate intracellular parasite that causes typhus. Mitochondria are so degenerate, however, that they've lost nearly all the genes that normal bacteria have.

While there is some small level of heterogeneity in mitochondria in a single person because mitochondria are exclusively transmitted down the female line most people typically only start with a single clonal population of mitochondria. Because of this, there is no other mitochondrial population present that the mitochondrial DNA could undergo recombination with.

Mitochondrial DNA does undergo recombination with nuclear DNA, however, in that genes can be transfered from the mitochondria to the nuclear DNA and because of this the majority of genes necessary for mitochondrial function are now coded not on the mitochondrial DNA but on the nuclear DNA and their protein products transported into the mitochondria after translation.


Design primers for PCR from given DNA sequence

As alluded to in the comments above, remember that you are amplifying double-stranded DNA, so two new reverse-complementary strands should be generated from each cycle (so that they can hybridize with eachother). As written in your answer, both of your primers would hybridize with your given strand, and the amplicons would not overlap (one binds at each end, but both would amplify in the same direction).

To fix this, you need one primer that binds to the target sequence, and one that binds to the reverse complement strand, which you have already generated. The new amplicons extend 5' -> 3' (from the 3' end of the primer not the template), so your primers need to bind at the 3' end of their respective strand. This link has a good visualization of that.

The 3' end of the primer needs to hybridize tightly with the template, since this is where extension happens (discussed in this guide). So your flanking restriction site sequences will always be on the 5' end of either primer (notice that the question actually hints at this by indicating the 5' end of each flank).

The primer given as your "reverse" primer will actually bind to the 3' end of your given sequence in the appropriate orientation, but you may want to put your 3' flank onto the 5' end of that primer sequence, as this will be theoretically be the 3' end of your amplicon. Your other primer will need to bind the 3' end of your reverse complement (which is the 5' end of your target), so it will have the 5' restriction site flank.

By convention, primer sequences are always given in 5'---3' format. So make sure your answer follows that convention. (i.e. 5'-Flank-primer-3').

If all of this sounds really confusing, that's because it is. I do this for a living, and I still always double check my primers in a program like Primer3


How many Watson-Crick + Hoogsteen triple base pair combinations are there?

You are correct in assuming that the image labeled TAA should be labeled TAT and the second one labeled TAT should be labeled AAT. The image should be removed from the Wiki page until it has been corrected (even so I find it unclear).
Only some of these images show Watson-Crick/Hoogsteen combinations. To answer your question of how many such combinations there are, let us first recall what a Hoogsteen base-pair is. As stated in the first diagram on the Wiki page, this is a non-standard AT or GC base-pair formed by purine rotation about the glycosidic bond and base-flipping. In the diagram I have produced by canabilizing the above I show W-C and Hoogsteen base-pairs with the difference in the glycosidic link shown in yellow overlay. Because the pyrimidines A and C in a W-C base-pair have no groups left to hydrogen-bond, the only way you can theoretically make a W-C/H combination is by ATA and CGC as shown in my diagram. Therefore there are only two such possibilities.

I am not quite sure why you want to know about WC/H combinations, other than to understand the diagram in the article, because they are not particularly important. The author of the diagram shows such combinations because they apparently occur in triple-helices of artificial copolymers, however his diagram also shows some non-Watson-Crick base-pairs, e.g. CGG and CGA (which are not examples of WC/H combinations). The molecule where most Hoogsteen base-pairs are found naturally is RNA, not DNA: e.g. tRNA and ribozymes, in regions which do not have a standard double-helical structure. In these case they can occur in combination with both WC base-pairs and non-WC base-pairs (e.g. the GG illustrated above), so there is nothing special about Hoogsteen base-pairs being combined with WC base-pairs.

What I would consider important to realize is that in the context of the DNA double-helix WC base-pairs give the most thermodynamically stable structure, but outside this context, especially in RNAs that have protein-like structures, a variety of alternative base-pairs and base-triples are structurally and thermodynamically possible, including but not restricted to Hoogsten base-pairs.


Insects and vertebrates are extremely distantly related: they're on opposite sides of the oldest split among bilaterally symmetric animals.  Their most recent common ancestor lived in the pre-cambrian and was almost certainly worm-shaped with no limbs at all.  There's no way that insect wings are homologous to any body parts of vertebrates.

The evolution of insect wings is a somewhat difficult topic, because it happened 350 million years ago in animals that do not fossilize well.  Wikipedia discusses several possible theories for what parts of non-winged insects are homologs of insect wings.  Currently the situation does not seem to be resolved.


What kind of fish did I see in waters off a tropical island in the Philippines?

This is a Blackspotted puffer, Arothron nigropunctatus a commonly found fish on coral reefs in the Philippines. Although this species has a large color variation, the photos provided show common coloration (white body with black spots, a large black area around the dorsal ray). The white strip above the mouth is also a commonly found characteristic of this species, along with a face and snout that resembles a dog.

CC- Attribution - Photo by John E. Randall


How essential is vitamin B3 to the diet?

According to one study:

  It was calculated that if the excretory percentage of niacin metabolites in the urine were 60%, of the tryptophan ingested, the conversion factor would be a value of 67, meaning that is 67 mg of tryptophan is equal to 1 mg of niacin.

However, the study has a pretty low power with only 10 participants and an indirect measure of niacin.

Is it possible that a person could get all of their niacin from tryptophan? Probably - you just need to eat enough tryptophan, which is also an Essential Amino Acid. The body may preferentially keep Tryptophan (which it does not store) until Niacin runs out (which also cannot be stored).


What is the Definition of Homologous Chromosomes? length, gene position are the same or similar?

Unfortunately despite the impression given by the many poor explanations available (including the one you quoted), homologous is not a synonym for similar.

Homology is defined as the existence of shared ancestry1,2.  Thus, structures being homologous simply means they had a common ancestor — i.e. homology is a relationship not a property of an individual structure.

The "definition" you quote is actually a description of what you typically see when comparing two homologous chromosomes within a species. High levels of sequence similarity suggest homology, but are not sufficient to prove it.  (To test that requires building phylogenetic trees.)

(One classic example of this is the superficial similarity between dolphins and sharks, which is an example of convergence not homology.  Another is the homology between bird and bat wings — they are not homologous as wings, though they are homologous as tetrapod forelimbs.)

Consequently, for two chromosomes to be homologous they must have descended from a (potentially much earlier) chromosome that has been duplicated possibly for many generations (the ancestral chromosome might even have existed in a now extinct ancestral species).

So, if an inversion happens within a chromosome (and changes the ordering of the genetic loci) that chromosome is still homologous to the parental type chromosome that didn't undergo inversion.

ETA: Note that chromosomes don't need to be in the same cell (or even the same species) to be homologous and chromosomes can be homologous even if the cell they are in is not diploid.  For example, the human chromosome 1 is homologous to the chimpanzee chromosome 1.

Similarity is a measurement of "distance" between sequences, but while very similar sequences are likely to be homologous there is no magical value of similarity that proves (or disproves) homology.

Individual humans are about 99.9% identical (depends on how you measure this) at the nucleotide level, so that will also be true for chromosome 1.

Finally, the UC Berkeley Museum of Paleontology also has useful resources for understanding evolution including some material on homology — e.g.:
https://evolution.berkeley.edu/evolibrary/article/lines_04

References:
1: Brigandt, Ingo, "Essay: Homology". Embryo Project Encyclopedia (2011-11-23). ISSN: 1940-5030 http://embryo.asu.edu/handle/10776/1754.

2: Mindell, D. P., & Meyer, A. (2001). Homology evolving. Trends in Ecology & Evolution, 16(8), 434-440.


Why Is Action Potential Propagation Not Described by Telegrapher's But Cable Equation?

I am the individual who answered your earlier question.  The answer remains much the same.  The Cable Equation is inappropriate.  It was developed originally as the Heat Equation of Thomson,  While Thomson disowned its application to the axon as a cable, Herman continued to promote the solution within the Biology community.  The problem is the Cable Equation requires as an initial condition that the stimulation of the cable continues until the signal reaches the terminus of the axon by conduction (diffusion).
When exploring the myelinated axon, the Telegrapher's equation must be used.  The formal name for this equation is the General Wave Equation, GWE, of Maxwell. It involves an initial condition that is much more lenient.  The stimulus must only be applied to the axon for long enough to ensure the desired full waveform is represented. Thus the GWE involves propagation and not conduction (or diffusion).  See section 7.4 of Chapter 7 of "Processes in Biological Hearing," PBH, on my website.
Cole & Baker, "Longitudinal Impedance of the Squid Giant Axon", Journal of General Physiology, (1941) vol 24(6) pp 771-783 present their initial measurements of inductance within the large axon of a small squid.  This axon generated "swim waveforms" and not "Action Potentials" as currently defined.  The inductance is much smaller in a non-myelinated axon than in a myelinated axon.  It remains calculable in either case.
I have reviewed the two papers by Lieberstein & Mahrous you cited for my benefit.  The authors are apparently two very good mathematicians without much knowledge of biophysics or the biophysics literature.  They quote a diffusion velocity from Hodgkin & Huxley (1952) that is several orders of magnitude slower than the phase velocity along an axon that is very well documented by Cole and more recently by Smith et al.  I have uploaded a more complete analysis in Section 9.1.1.4.3 of the above citation to chapter 9 of my work, 9SignalTransmission.pdf.
These two papers should not be relied upon until reviewing Section 9.1.1.4.3


Need for proper air filter for bioreactor?

Well then you need to get a filter specific for air filtering.  I recommend Polytetrafluorethylene PTFE membrane filter.  Now the only issues are size and "how sterile."

There are a lot of vendors out there that supply these.  If your institution has an agreement with VWR, they certainly have them.  If not, I have used Sartorius in the past, but I don't have any particular brand loyalty to them.

Let me know if you need any more help.


Why do membrane proteins at lower temperatures contain more alpha helices than beta sheets?

The reason could be the greater motility of the alpha helix, compared with the more rigid beta sheet.
This allows the enzyme to remain functional at low temperature.
The proteins of such organisms tend also to have less hydrophobic regions and covalent bonds.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1692995/pdf/12171655.pdf
Molecular basis of cold adaptation
Salvino D’Amico, Paule Claverie, Tony Collins, Daphne´ Georlette,
Emmanuelle Gratia, Anne Hoyoux, Marie-Alice Meuwis, Georges Feller
and Charles Gerday*

This doesn't refer to alpha helix explicitly, however alpha helix are known to allow more flexibility than beta sheets, so it's reasonable to argue that the increase in alpha helix could be one of several strategies used to obtain more flexible enzymes, as well as other means cited in the paper.

This point is also made by Brock-Biology of microorganisms(2015) pag.161

  Several cold-active enzymes whose structure is known show a
  greater content of α-helix and lesser content of β-sheet secondary
  structure ( Section 4.14) than do enzymes that show little
  or no activity in the cold. Because β-sheet secondary structures
  tend to be more rigid than α-helices, the greater α-helix content of cold-active enzymes allows these proteins greater flexibility
  for catalyzing their reactions at cold temperatures.

However unfortunately no reference is provided about this claim.


The sporophtye is the diploid stage in the life cycle. In comparison, with humans, you and I would be sporophytes.

The Gametophyte is the haploid stage in the life cycle. In comparison, with humans, spermatozoids and ovules are gametophytes.

Independence

Note for what follows: "independent" can be understood in terms of "ability to survive". Being independent according to its ability to survive. One might use the word "independent" for other concerns though! For example: "Independent" in the sense "no nutrient exchange between the two"

Therefore, one could say that in humans, the gametophyte is not independent (in it's ability to survive) of the sporophyte. Similarly, in moss (bryophyta), the gametophyte is not independent of the sporophyte because the gametophyte grows on the sporophyte using its nutrients (one could say that the gametophyte parasitize the sporophyte but that would be a bit misleading!). If the sporophyte is independent of the gametophyte (or vice-versa), it means that there is alternation of generations. In other words, sporophyte and gametophyte live separately (like two different individuals).

Life-cycle

You can find tons of examples of weird life cycles, in particular in plants, fungi and parasites but not only. And you may find many examples for which the type of sexual reproduction or the type of life-cycle are hard to defined with these relatively simple concepts.

Identity

The question of identiy (how separate or genetically different should two individuals be so that we consider them to be two different individuals) is rather a question of philosophy. Such discussions about identity occur when we talk about clones (ramet and genet), about life cycle or about level of organisation/level of selection. The book Major Transition in Evolution (Revisited) provides many of the philosophical discussion on the subject of identity in population genetics.


This question is a bit hard to answer for me without more context.
However, it is clear that the n refers to the tyrosine which is highlighted in the figure as well (especially the interaction of its phenol). The other positions (n+1, n-1) are shown relative to the tyrosine.
I'm unsure about the role of tyrosine in the primary structure of proteins, but maybe this is more clearly explained where you found the figure. I'm also unsure if the glutamic acid is terminal.


How does a cell regulate what leaves its vacuole?

Your question is not entirely clear, even after the edit. However, I believe it's worth mentioning that the vacuole, just like any other membranar organelle1, is surrounded by a biomembrane.

Such biomembranes have transport proteins, which can be channels, carriers or pumps, and those transport proteins can determine which substances will get in/out of the vacuole, either down the electrochemical gradient (channels and carriers) or independent2 of it (pumps).

Here is a diagram showing the membrane of the vacuole with some transport proteins:

Therefore, since the cell can open or close a give gate or activate/deactivate a given pump (just like the transport proteins in the plasma membrane), that helps to explain how the cell decides what gets in or goes out the vacuolar lumen.

1: Unfortunately, there is not a consensus around the definition of organelle. The definition I use states that all organelles have a surrounding membrane (therefore, a ribosome is not an organelle), which renders the expression membranar organelle pleonastic.

2: It's very common reading that pumps will transport the substance against the electrochemical gradient. That's not correct. They will transport the substance independent of the gradient, that is, they can pump a substance against the gradient or down the gradient.


The pdb file that you mention is entitled:

  V-Amylose at atomic resolution: X-ray structure of a cycloamylose with 26 glucose residues (cyclomaltohexaicosaose).

So, it isn't a protein at all, it is a circular oligosaccharide consisting of 26 glucose (GLC) residues. I imagine that the usual fields in the pdb file have been fudged to accommodate this.


Why half of the protein is saturated when [L] =Kd

The Hill equation in that link uses the simplifying assumption that all ligands bind simultaneously and that the binding sites are identical. The reaction is then P + nL = PL,
and Kd = ( [P][L]^n )/[PL]
Then by rearranging you get the expression in the link.

The equation "fraction occupied binding sites = [L] / [L] + Kd" Is not the Hill equation. It is called the binding isotherm. You can see that if Kd = [L] then the fraction of occupied binding sites (let's call it theta) = 1/2. Thus half of the binding sites are occupied.


How does the body really react to exposure to the vacuum of space?

With regard to the vacuum - Apparently nothing happens as long as you don't hold your breath, just like you shouldn't hold your breath when ascending after scuba diving and the pressure drops. See NASA's answer to the same question. Of course there's the radiation that does other funny things in space, see the NASA link.


Are there examples of now-living species where one is descended from the other?

First, you probably want to have a look at this answer who offers an introduction to phylogeny.

There are few subjects that yield to as many semantic issues than the definition of species and the definition of life. Your question is at the border of the species definition. Therefore the question is not so much about Biology than about Philosophy, so let me advertise: The following answer is nothing else than a semantic discussion (philosophy) and has no relevance of our understanding of evolutionary processes. Note however that semantic discussions might be very helpful to evolutionary biologists as well.

Sexual organisms

Dogs and wolves

Commonly, in sexual organisms, species are defined by the concept of reproductive isolation. To address @WYSIWYG's comment, wolves can breed with dog. The offspring is called a wolfdog and it suffers from little inbreeding depression.

Is the MRCA contained in the species of one descendent

But I'll use the wolf example anyway and make some fake assumptions. There are probably better examples I could pick though. Let's assume that wolves and dogs can't interbreed, that they are therefore separate species. Let's assume as well that somehow we manage to recreate the Most Recent Common Ancestor (MRCA) of wolves and dogs (which has some issue due to parental effect incl. culture and epigenetic) and this MRCA can breed with wolves and but not with dogs, then we could eventually say that the MRCA and the current wolf (there are actually 3 species of wolves that are probably not real species) are the same species. One could then say that dogs descend from the wolf.

Feeling that we talk about improvement over another species

I think that much of the issue in saying that the dog descend from the wolf is that some people would understand things like "dog is more evolved than the wolf", which makes no sense. Both the current wolf and the current dog has evolved for exactly the same amount of time. Any living species on earth has evolved for exactly the same amount of time (almost 4 billion years).

Temporal constraint in the definition of species

Therefore, it is eventually possible to say that one node on a phylogenetic tree is of the same species that the previous and the next node. I think that in reaction to the misleading feeling that early evolutionary biologists and current non-biologists people have in hearing that one species descent from another one, we tend to make a temporal constraint to the species. A species is what it is only at the exact moment we talk about it. This prevents us to consider a MRCA as being of the same species of any descendent.

Note that the definition of species yield to various issues such as the case of ring species.

Asexual organisms

Same issue as above

Now, if we talk about asexual species. There is no clear definition of what is a species there. Of course if we were to use the definition based on reproductive isolation, then any asexual individual would be a new species. We therefore define a species when we see a group of phylogenetically related individuals that all share some feature that we find "interesting enough" (very arbitrary) to describe this group as a different species from the some other group of individuals. In asexuals, you may see one lineage that accumulate 10 mutations, while the other lineage accumulates 1000 mutations (this other lineage may eventually live in a different environment than the MRCA of the two lineages). Therefore, you get to the same issue when thinking about asexuals than about sexual organisms. If one lineage ressemble more their MRCA than the other lineage, then is their MRCA part of the species of one lineage?

Is a species a thing?

Well... the concept of species is useful in the sense that it is often not ambiguous to classify one individual into one species or into another. The concept of species allows us to better communicate.. so yes I guess it is useful.

The concept of species existed way before we had any understanding of natural selection, mutations, genetic drift and other basic concepts in evolutionary biology. Aristotle used the concept of species (he also thought without having any good evidence that life evolves). This concept of species has been very well conserved because of the static view we had on what a species is before Darwin. Now that we have a better understanding of evolutionary biology, ecology and reproductive biology we discover that the concept of species is not a natural category but is a man-made unclear category.

Other discussion on the subject

In this post I made an overview of the issue related to the concept of species. I did not go into the details but tried to list important concepts.

You will find many websites that address the concept of species in philosophy. I particularly like discussion in the concern of how current bad semantic may yield to bias in the way we think nature and may yield to bad decision in applied science. Here is a podcast (in french) on the origin and consequences of the concept of species.


I am completely shooting in the dark here, but do you mean the ones between 1:06 - 1:13 minutes in the video? (After Hammerhead and before Baby and Mama white Shark :) )

SPECIES IDENTIFIED: Pseudorca crassidens (False Killer Whale)

Matching image from the internet (used for identification):

Courtsey: UAE Dolphin Project

PS: Images are screenshot from the video Documentary film “Un Jardin d’Eden sous les mers” (“A garden of Eden under the seas”) are completly owned by the owner of the video and "arte HD" channel.

PPS: Anyone reading this, if you haven't already, then please watch the video. Though it is completely in french, the videography is amazing.

References:

Pacific Islands Cetaceans
Other Whales


What would happen if you slowly crushed a live brain?

It seems there's way too many variables here.  Crushing can occur in a number of ways, leading to different primary damage in different regions first and different people have a different level of system failure thresholds.

Technically, there are no pain sensors on the brain, so you wouldn't feel any pain in the classical sense.  However, it's hard to determine how you would affect the pain interpretation circuits (again, "crushing" can occur a number of different ways); you could inadvertently cause pain signals.

Losing consciousness would also depend on when what region of brian is crushed.  And how it's crushed.  Most of our higher processing regions associated with consciousness are on the very outer surface of our brain.  In one scenario, if it just gets compressed, and damage tend to accumulate in the center of the brain first, it would be a different outcome than if it was some kind of shear crushing force that damaged outer brian first.


Why aren't all strongly self-recognizing T cells made into regulatory T cells?

The selection is based upon the strength of the binding. A strong bond causes a signal in the T-cell to self destruct (apoptosis).

Wikipedia has a post on T cells. Perhaps the moderate bonding become regulatory cells, because these cells have to recognize those T cells that survive negative selection, which are most likely to cause autoimmune responses over a long period of time.

Strong affinity to self means the immune response will become a danger to the host.


Is there any relationship between heartbeat rate and life span of an animal?

Interestingly there is a inverse negative correlation between heart rate and life span, meaning the faster your heart rate is, the shorter is your lifespan. See this figure (from the paper 2 cited below):

When the authors plotted the approximately total heartbeats vs. the lifespan, the amount of total heartbeats was in a pretty narrow corridor:

So it seems that at least the hearts in mammals have a maximum number of strokes they could do. The obvious question what causes this phenomenon is not really answered.
Since the metabolism of small animals is (compared to their weight) higher and also their oxygen consumption is higher because of that, it is hypothesized that this causes more reactive oxygen species and related damage which subsequently leads to an earlier death.

See the references for more details:

Rest heart rate and life expectancy.
Heart rate, lifespan, and mortality risk
Oxidative damage to DNA: relation to species metabolic rate and life
span


Lot of classic books available, most famous (at least in India) are

Molecular Biology of the Cell by Alberts et al [ Free Online | Amazon ] -- Simple language, good figures and my personal favorite
Molecular Cell Biology by Lodish et al [ Free Online | Amazon ] -- Very detailed with good examples
Gene IX by B Lewin [ Amazon ] -- Nice examples and figures. Lessons are in different order than most cell biology books.

If you want to just learn quick concepts, use online resources like Scitable by Nature. Pretty nice information with references and recommended reading.


Is an athlete's heart rate after exercise greater than a non-athlete

Whilst exercising, the heartbeat of a non-athletic individual is faster than that of an athletic individual. The untrained heart beats faster, but less efficiently than that of an athlete. Both the maximum, and the resting heart rate of an athletic individual are lower than the average heartbeat. In a non-athletic individual, the heart rate when resting is about 60 to 90 beats per minute, whilst in athletes it can drop below 40 beats per minute.

When you exercise, the heart works harder when other muscles in the body pump more blood back to the heart. The major muscles of the legs have large veins that will fill during the relaxation stage of the movement, and the muscle contraction in the active movement pushes the blood back into the circulatory system. Increasing blood flow triggers a faster heartbeat. Because the heart muscle of conditioned athletes enlarges and strengthens, the hearts of athletes pump more blood per beat. 1


The problem is that for most sequencing operations you nowadays still need more than one cell - even though this will change soon.

Accordingly, you have to sample cells from a tissue which often, if not usually, contains more than one cell type, see e.g. this picture from a lung tissue from the Wikipedia article on tissues linked above:

It is not always easy to pick cells of one type only (think of trying it with blood, which is a tissue as well). So what you then get is a mixture of different cell types which probably differ in methylation patterns.

  Does it refer to the composition of a specific cell-type in terms of its methylation pattern (or can it refer to something more general outside this context)?

No, it means that you have cells of different types within your sample.

  It makes sense to me that different cell-types should have different methylation patterns, that's why there are different cell-types in the first place.

At least one of the reasons, there are more, e.g. other modifications and mutations.

  But is it that even within one specific cell-type, the composition of methylation pattern is different across different individuals?

That is a different problem and may also be true. But this is not what your quotation, as I understand it, refers to. They refer to the problem that you might sample the same tissue across patients but still get a different composition of cells from different types due to sampling error.


Yes, In most cases, osmosis is the diffusion of water. To my understanding, what I think Wikipedia is trying to do is to assert the fact that osmosis is also be the movement of water from a region of lower water potential to a region of higher water potential. These kinds of contradictions, as much as scientists try to avoid them, still come to play because science is very complicated. Just when we start accepting a theory, it gets discarded by another theory.


Differentiation of norepinephrine and epinephrine in indications

The differences in the action/indication is because of differential affinity of the two molecules to different adrenergic receptors. The wikipedia page on Ardenergic receptor has a table which summarizes this.

Wikipedia doesn't cite references for it. You may have a look at some of the following old articles.

α- and β-Adrenergic Receptor Subtypes

  In the periphery, α1-receptors are located postsynaptically, mediating the excitatory effects of catecholamines at α-receptors. α2-Adrenoceptors, on the other hand, are autoreceptors involved in the regulation of noradrenaline (norepinephrine) release. In the central nervous system, both α1- and α2-receptors exist on postsynaptic cells; there are also 2 principal subtypes of β-adrenoceptors. β1-Receptors have a high affinity for both noradrenaline and adrenaline (epinephrine) and are found in the heart, brain, and adipose tissue. β2-Receptors have a low affinity for noradrenaline and are involved in mediation of relaxation of vascular and other smooth muscles and in many of the metabolic effects of catecholamines.

β-Adrenergic Receptor Subtypes: Properties, Distribution, and Regulation

                  NE=Norepinephrine, EPI=Epinephrine, ISO=Isoprenaline


What decides whether a lysogenic cycle or a lytic cycle will take place?

It depends on a few factors, such as how many phages infected the cell, whether or not the cell is in good growth conditions, and so on. If the cell is in stress or has low amounts of nutrients, the lysogenic pathway is typically activated.

The underlying mechanism has to do with a protein cascade involving either the cro or cI protein that is encoded by the virus. The cI protein is a repressor, and it will prevent the lytic genes from being transcribed. By default the virus will transcribe the lytic genes, so they must be repressed for lysogeny to occur. Similarly, cro is also a transcriptional repressor. The two proteins work in opposition to each other. cro binds to an operator, oR3, that is involved in repressing cI, which may prevent cI from being expressed and thus preventing it from repressing lytic genes (however the importance of this is debatable because if you replace oR3, the cell can apparently still lyse).

There are numerous other proteins, such as N and Q, that are involved. The N protein has to be transcribed by the polymerase ‘anti-terminating’, or reading through a termination signal. This will happen more frequently when the protein RNase III is present at high concentrations. The N protein is a lytic regulator. Thus, when there are high amounts of RNase III there will be more N expressed which leads to the lytic cycle. RNase III is not a viral protein. It is a host protein and the host expresses more of it when nutrients are abundant. This is how the virus is able to ‘sense’ if nutrients are high enough to enter the lytic cycle.

The whole system is way more complicated but this is it in a nutshell.

http://www.annualreviews.org/doi/full/10.1146/annurev.genet.39.073003.113656