Where can I get a file/list of the common and scientific names of species? I am searching for an un-encoded data file with common and scientific names for example of a few hundred species or tens of thousands, where I can search the common and scientific labels of organisms.

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

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

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

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

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


What step of the cloning process requires an egg cell? Have alternatives been attempted? In the famous Dolly the sheep an egg cell was required. Why was specifically an egg cell required compared to say sperm cells or any other cell types?

Given that egg cells are not trivially harvested and culturable, have clones from alternatives been attempted?

egg cells are not required for cloning, plants for instance can be cloned just fine without them. Oocytes are commonly used in animals becasue they already contain some of the chemical markers and enzymes to begin development in the mother's body and keep her immune system from attacking it. In more derived animals development is not solely controlled by the the embryo but also by the mother, so using an egg cell helps trigger those processes of the mother. If you used a standard stem cell likely the mother immune system would just destroy it as a foreign entity.


Why are interspecies hybrids so often larger than either parent species Recently doing a little reading on interspecies hybrids I noticed that it seems interspecies hybrids are most often much larger than either parent.  Notably, Ligers, Dzo and Savannah Cats, but it seems like all or at least most.

Is there a reason for this genetic expression in hybrids?

If I am incorrectly inferring this to be the case let me know that instead.

While they do not necessarily constitute the majority, it is true that there is a large number of interspecies hybrids whose members are larger in size than the parent species, and there exist explanations that account for this phenomenon.

What you are describing is an example of positive heterosis, or hybrid vigor.  While the rationale for plants is more complex, it commonly arises between related species in mammals as a sort of heterozygote advantage in which the contrast in genetic contribution during conception spawns some phenotypic benefit.  The exact implementation of this varies from species to species, but this link here is a nice, concise explanation for why ligers might be so large.


Looking to study botany, some general advice I've been doing some hydroponics lately and I've noticed I don't have much insight about how plants really work under the hood, I would like to have the full picture and understand more about it.

My primary interest is to apply botany knowledge on my hydroponics projects, not to get a job/degree. But, I do understand that studying among my peers is a rich experience, reason why I'm considering this kind of training instead of just grabbing a book.

However, I'm not sure how extensive is the study of botany, if I need a degree in X before starting it, etc.

Also a good book is welcome.

Thanks.

Have you checked out Botany classes at nearby community colleges?  You may have trouble finding an evening class, but I'm sure you'll find daytime classes opening up in the January.

If you need to study independently, can I suggest checking out the Tree Care Industry Association's store. www.tcia.org  They have various learning material to read and watch, leading towards a professional arborist certification.

Good luck in your endeavor.


Determining break/border of movement A population given inhabiting an area. I can trace every individual and I've got the hypothesis there is a break in distribution like individuals born in the upper half of the area will rarely move to the lower half and vice versa.

Tracking each individual how can I determine the line/border which divides the population in a upper and lower half. What's the math or algorithm behind to draw this imaginary line?

There are a lot of approaches to this kind of problem. Starting with the simplest approach I think you'd benefit from using a K-means classification, with K=2 (or higher numbers to address @Luigi's concerns about model bias.) Once you've defined the geometric center of each population, you can treat them as foci, and use the equidistant points between each focus to define the boundary of interest. That does import another assumption (that the boundary is equidistant to the two points).

A more sophisticated way to divide two clusters is with a support vector machine but because this is a machine learning approach, you'd need to manually annotate a number of training data sets as "group 1" or "group 2." But after training, the SVM will define the optimal boundary (hypersurface) between these groups.

The two types of approaches (clustering versus machine learning) differ in where the manually-imported assumptions lie. One can combine them fruitfully -- using K-means to define the populations and SVM to define the dividing boundary.


Why does V. cholerae produce a human specific choleragen? V. cholerae secrete choleragen to grow and escape human intestines, however choleragen does not work on other mammals, why so? Why didn't it evolve a general mammal affecting choleragen? This question is a continuation of the last comment on the only answer for my previous question, How does Vibrio cholerae benefit from infecting its host? Kindly refer to the answer and comments in that question as well.

Vibrio cholerae originated in the Sundarbans, a very large wetland at the mouth of the Bay of Bengal. Although it can exist as free living, it is much more fecund when associated with tiny crustaceans called copepods. In 1760, the East India Company settled and sprawled, hewing the mangroves and planting rice. So, that was the first opportunity of note introducing V. cholerae to a major species of land animal, humans. The frequent contact with a sizable population of humans, plus time, allowed V. cholerae to evolve the traits to become a parasite.

For example, a hair-like filament evolved which allowed the cells to clump together forming colonies that could stick to the gut. At that point, perhaps with additional traits, V. cholerae became a zoonosis. That is, a disease we acquire from animals, copepods in this case, but not directly from other humans. Further evolution over time gave it the traits to spread directly between humans making it a true human pathogen.

So, humans were the species that became available and V. cholerae evolved to take advantage.

This is a minute fraction of the whole story as related in the 2016 book Pandemic by Sonia Shah. She is a science writer, the book is extremely well referenced. Since this is your second question on this, I suspect you may well be interested in the book.


Why is it advised to avoid bubble formation during mixing? I have been told not to vortex solution containing protein. The reason I was given is bubble formation. Here I am interested in the effect of bubble formation in general.

A "bubble" per se would do no harm unless you have cells (without walls like mammalian cells) in the suspension. If you agitate the protein mixture vigourously then it may lead to denaturation of proteins by extensive intermolecular collisions. The "froth" formation is an indication of denaturation as denatured proteins stabilize these foams [1, 2].

References:

Zayas, Joseph F. "Foaming properties of proteins." Functionality of proteins in food. Springer Berlin Heidelberg, 1997. 260-309.
Schmidt, Isabelle, et al. "Foaming properties of protein/pectin electrostatic complexes and foam structure at nanoscale." Journal of colloid and interface science 345.2 (2010): 316-324.


What causes the complementary copy of an RNA molecule to separate? I have recently read an article which explains that, in the RNA World hypothesis, an RNA molecule gets 'scanned' by nucleic acid, catalysed by a different specifically-folded RNA molecule, to arrange itself complimentarily to the original molecule. However, what causes the new, complementary molecule to detach from the original molecule? I always hear people say that this complementary base pairing allows the RNA molecule to reproduce, but I never quite understood: how? If complementary bases tend to bind together, shouldn't the newly formed structure then be stable? What causes the actual reproduction?

First, I want to point out that the RNA world hypothesis is just that - an hypothesis. While it has been shown that it's possible for certain RNA molecules to make copies of itself, this is not a 'normal' function of any RNA.

Edit - to give a clearer answer to the question itself:

After replication of an RNA molecule it may form a stable structure together with its template or it may dissociate. Due to the various possibilities and complexity of RNA structures its almost impossible to predict this, since both the (exact) sequence itself and environmental conditions especially temperature are very important.

More background from the unedited answer:

Whether two complementary strands or RNA (or DNA) bind together is not something that can always be easily answered. For DNA of a given length (in a given environment / buffer) one can more or less predict the temperature at which complementary strands will separate (often called melting temperature), because DNA forms relatively stable helices.
RNA, however, often forms complicated 3-dimensional structures, often involving self-complementary and is not restricted to the typical helices seen in DNA. Trying to predict the resulting 3D structure of RNA molecules is still an ongoing field of research. Some of these structure are quite stable (e.g. in tRNA) but in other cases they can also be very dynamic and change quickly.
In the end it always depends on the RNA sequence, temperature and many other environmental factors.


Why are embryonic germ cells considered stem cells? In a class that I'm taking we were presented 3 types of stem cells.

Adult stem cells which come from bone marrow
Embryonic stem cells which come from embryos
Embryonic germ cells which come from testes

I understand that adult stem cells are a bit more specialized than embryonic stem cells, but I'm confused why embryonic germ cells are considered stem cells. From Wikipedia, the definition of stem cells is:

  Undifferentiated biological cells that can differentiate into
  specialized cells and can divide (through mitosis) to produce more
  stem cells

But from my limited understanding of biology embryonic germ cells can't specialize into any other cells unless they fuse with another gamete, so why would they be considered stem cells? What am I missing here?

The difference in designation is the timing of the foundation of the cell line and the tissue that it was sourced from.

Embryonic Stem Cells are harvested from the inner cell mass of a Blastocyst around day 5 post fertilization. This is the first or second generation of cells to have started to differentiate, but they still have Pluripotency, which means that they can differentiate into any one of the three germ line cell types. [1][2]

Those  three germ cell types are:

Endoderm
Mesoderm
Ectoderm

Embryonic Germ Cells are "cultured from primordial germ cells obtained from the gonadal ridge and mesenchyma of 5- to 9-week fetal tissue...." [1] These cells are multipotent, meaning that they will usually only be able to give rise to mesenchymal derived cell lines.[3][4]

There are also differences in replicative ability. ES cells are for the most part immortal cells able to be maintained in in-vitro culture for long periods of time, while EG cells have a life cycle of about 70 to 80 cell divisions before they reach quiescence.[1] If I had to venture a guess as to why this was the case, I would say that EG cells have likely already reached a stage of differentiation where they are repressing or down regulating the expression of Telomerase. ES cells will be expressing telomerase, so they will not experience telomere shorting due to the 3' end replication problem during DNA synthesis in S phase of mitosis.

There are other cell types of Adult Stem Cells other than Hemopoietic Stem Cells, so I am not sure why your course is making the distinction. It could be that in practice, we have only really successfully used Hemopoietic Stem Cells in treatments for diseases by doing bone marrow transplants. You would likely have to have your instructor clarify this point for you.


Do deaf people sleep better? Since deaf people can't hear, is relaxing and falling asleep easier for them? In general, do they sleep better than hearing people?

Of course some hearing people have no trouble getting to sleep, but others awaken whenever they hear a sound.

Let's firstly differentiate deafness - profoundly impaired ability to hear, and other states where the subjects can still hear at different degrees.

Secondly, differentiate the congenital deafness & infantile hearing loss and hearing loss in adults who previously had normal hearing.

The subjects with congenital and very early infantile hearing loss would have better sleep characteristics (this state will affect psychological state in a lesser degree than one acquired in more mature & "conscious" state), while persons who have lost their normal hearing would have abnormal sleep patterns at least in the period when they have just realized that they are going to lose their hearing. After this "preliminary" period, the sleep pattern should be dependent on the person's psychological status and other similar factors.

Many persons will mention that while using ear plugs they feel that their sleep is better comparing with "un-plugged" sleep.

sources

Characteristics of sleep in deafness. Rev Neurol. 1998 Jun;26(154).
Non-scientific source.

Please pay attention that scientific sources are scarce, thus take the answer as one of limited evidence.


What can pass through the intestinal membranes? As I understand it, most substances need help to pass through the walls of the intestines.

For example, in hepatic recirculation (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781307/) bile salts are grabbed and transported across the intestinal membranes by particular polypeptides.

Is there a summary of the sorts of things that can be transported across intestinal membranes? For example, hormones, stearates, lipids, etc. What general classes of molecules can pass the membrane and what cannot?

I am not looking for an exact answer, but a general characterization of major classes of organic molecules and their ability to pass through intestinal membranes into the body.

Virtually all nutrients from food can be absorbed into blood through the lining of small intestine and colon.

What can be absorbed in the small intestine:

Water
Simple sugars (monosaccharides): glucose, fructose, galactose...
Amino acids and small peptides (dipeptides, tripeptides)
Free fatty acids, monoglycerides and cholesterol
Minerals: sodium, potassium, iron, etc.
Vitamins
Nucleic acids
Alcohol
Various other substances from food (polyphenols, sulfate, oxalate, caffeine, preservatives...)
Bile acids
Steroid hormones, such as cortisol, aldosterone and sex hormones (JCEM)
Drugs
Various toxins

What can be absorbed in the colon:

Water
Short-chain fatty acids (from bacterial fermentation of dietary fiber and sugar alcohols)
Sodium, potassium and some other electrolytes

What cannot be absorbed in the intestine:

Polysaccharides (such as starch), oligosaccharides, disaccharides
Dietary fiber (soluble fiber can be fermented and the resulting substances can be absorbed in the colon)
Whole proteins and big peptides
Triglycerides, diglycerides
Peptide hormones, such as insulin, glucagon, calcitonin, prolactin, growth hormone and parathyroid hormone (Cambridge Core)

Sources:

Lumenlearning (type of transport for all main nutrients)
Best Practice & Research: Clinical Gastroenterology (detailed description with carriers involved)


Behavior of plant guard cells: open or closed stomata On an exam of mine, I had the following question:

  The interaction between the guard cells and stomata in a plant leaf can be seen in the diagram below.

  In which scenario could the guard cells and stomata be in situation 2?

  (A) High humidity

  (B) High light intensity

  (C) Low temperatures

  (D) Nighttime

The answer choices aside, I was thinking the answer should be along the lines of "a scenario in which the temperature is really hot", since an open stomata on a very hot day would cause a plant to lose a lot of water. The only answer choice that seems to fit this is "high light intensity" (although I'm not sure if high light intensity would necessarily cause high temperatures, but this seems to be the closest thing to what I predicted). However, the exam key is saying that "D", nighttime, is the correct answer. My teacher explained that since plants don't need to do the light reactions during the night, they apparently close their stomata because they don't need to intake CO2. But this doesn't make sense to me: why would a plant close its stomata during the night instead of keeping it open to stockpile CO2 for use in the day? If I'm not mistaken, this is precisely what CAM plants do (although there's no mention of whether the plant in question is a CAM plant).

I found a paper and this is the link https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258058/  it says that Stomatal opening is induced by low CO2 concentrations, high light intensity and high humidity. By contrast, closing is promoted by high CO2 concentrations, darkness, drought and the plant hormone ABA.
Another paper, Open or Close the Gate – Stomata Action Under the Control of Phytohormones in Drought Stress Conditions https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3652521/
During the night, elevated levels of CO2 in the leaves were observed due to respiration. It has been proved that CO2 has a positive effect on the stomatal closure process


Are these structures real petals? I don't know the name of the plant. It's a common house plant in Bangladesh. What interests me about its flower is the colorful leaflike structure that probably functions as a petal. What is this structure homologous to? Petal, sepal, bract or leaf?

The plant looks like something in the genus Bougainvillea. These plants are native to South America, but found as introduced ornamentals in many places.

The colored petal-like organs are bracts (see the Wikipedia link above). The entire structure is an inflorescence with the flower buds growing out from the surface of the colored bracts — you should eventually see those flowers open and you could then dissect them confirm that the usual flower structures are present.

This is a well labeled diagram:


Is eating cooked food an evolved behavior or rather an intelligent one, passed down via culture? I was just eating a rather rare steak when I started wondering whether eating foods cooked was something I would instinctively want to do if the practice hadn't been taught to me.

So, is cooking food an evolved behavior, inspired by nutritional value or health benefits, or is it a practice learned, and passed down through culture alone?

Its almost certainly instinctual, humans along with other great apes (any many other animals) show a preference for cooked foods over raw in testing, the number that prefer it increases drastically if they are have sampled cooked foods before. So it is likely as built in as your desire for sweets and salt.
Just becasue something is instinctual does not mean you don't have to learn HOW to do it. Language is instinctual in humans, but what language you learn is up to your upbringing (the same is true in some birds), and denied another human to interact with until puberty you will not develop language. that does not make language itself cultural, just the particular language you learn.
No one would argue lions do not have an instinct to hunt, but they still have to learn how to be successful at it.
https://evolutionaryanthropology.duke.edu/sites/evolutionaryanthropology.duke.edu/files/site-images/Wobber%20et%20al_%202008_%20Great%20apes%20prefer%20cooked%20food%281%29.pdf


When using a primer to replicate DNA in a plasmid, does it replicate the whole plasmid? I've been learning about PCR and plasmids. I understand that the reason for having both a forward and a reverse primer is to extract and amplify the specific piece of DNA between these two primers.

What I'm struggling to understand is that why after the first replication, a fully circular DNA strand isn't formed and hence, why isn't a fully circular DNA strand formed for each replication.

For the following diagram , let the strands be labelled strand 1, strand 2, strand 3, strand 4 from top to bottom. (Diagram from Lehninger Principle of Biochemistry, 5th Ed).

For example, in the diagram here. When cloning a plasmid I assume strand 1 is fully circular, so strand 2 (which was transcribed from strand 1) should also be fully circular and in the diagrams it should show DNA to the left of the site of interest.

Does the transcription stop somewhere along the line, preventing it from copying the whole strand? Or does the strand never join up into a circle, so that the DNA that would appear to the left of strand 2 has been copied, but doesn't join up to the site of interest so wasn't included in the diagram.

Thanks for your help.

PCR produces linear DNA, not circular. You can replicate whole plasmids using PCR, but the DNA will still be linear, as if you cut the plasmid with a blunt-end restriction enzyme.

So why doesn't the whole plasmid get copied when using PCR? Let's assume the primers are designed to bind 1000 bases apart from each other. The first round of PCR will probably produce longer pieces of DNA, because the oligos can only bind to the plasmid and the Polymerase can keep going. But the polymerase will fall off at some point, either randomly or when the temperature is pushed up for the next round of PCR. But in round 2, there should be equal numbers of circular plasmid and linear copy. The proportion of linear copy will increase every round. As the linear copies increase, the oligos are more and more likely to bind to linear copies than to circular plasmid.

Binding to linear copies is why the PCR product size is controlled. Let's assume that a linear copy is 1500 bases, because the polymerase ran an extra 500 bases past the other oligo site on the plasmid. But when the reverse oligo binds that site on the linear copy, the polymerase will run 1000 bases and fall off the end of the linear copy. This new copy will have the forward and reverse oligo sites at the ends, so it's the right size. Any copies produced from this strand will also be the right size. As the reaction proceeds, the proportion of correct-sized strands increases, and create more correct-sized strands.


How can a tongue-biting parasitic arthropod become a fully functional tongue? From wikipedia:

  The parasite Cymothoa exigua [consumes a fish's tongue and] then replaces [it] by attaching its own body to the muscles of the tongue stub. The fish is able to use the parasite just like a normal tongue.

Wikipedia says that it replaces the host's tongue and becomes fully functional. But how does the arthropodic parasite reattach the nerves of the fish, such that the fish can assume control of it? Am I misunderstanding something?

Short answer
There is no evidence whatsoever that the parasitic arthropod Cymothoa exigua develops itself into a functional tongue. Instead, it consumes the fish's tongue and occupies the freed buccal space to continue feeding onto the fish's blood or mucus.

Background
The linked wikipedia page that states that Cymothoa exigua arthropods form fully functional tongue-replacements refers to Brusca & Gilligan (1983) to back up that claim. While the journal is credible, the article itself is a theoretical work. The authors base their conclusion that the tongue replacement is functional on the relatively healthy condition of just 2 specimens of fish. They reasoned that, because the parasitic arthropods were relatively large, the fish had to be hosting them for quite a while. In turn, given the relatively healthy condition of the fish, the authors reasoned the arthropodic tongues may actually have had functionality. In the figure below taken from Brusca & Gilligan (1983) the parasite does indeed look much like the normal tongue.

Source: Brusca & Gilligan (1983).

However, there is no mention whatsoever that the parasitic tongue taps into the nervous system and I have not found any literature supporting such a claim. Further, Brusca & Gilligan (1983) specifically say that:

  [...] we propose [that] a fish with an 'isopod tongue' [is] not feeding as efficiently  as a non-parasitized fish, [but] feeds more efficiently than a fish with no tongue at all [...]

The authors' claim is much more nuanced than the blunt conclusion as drawn in the wikipedia page that it is a fully functional tongue; while the effects on its host may be relatively mild, it may not replace all, or even any, physiological functions of the normal tongue.

Reference
- Brusca and Gilligan, Copeia (1983); 3:813-6


What is the mechanism by which myelination reduces the capacitance of the axon membrane? There are two mechanisms that have been proposed to me.

1) Layering of Schwann cell membrane with conducting fluid between the layers is analogous to several capacitors in series. Since capacitance in series add by the reciprocal rule (as resistors do in parallel), this reduces the total capacitance.

2) The myelin increases the distance between the 'plates' of the capacitor. For parallel plate capacitors $ C = \epsilon A/d$ where d = distance between the plates. Thus increasing the distance reduces the capacitance.

Which of these explanations best applies to myelin, or is it in fact a mixture of both?

Circuit analogies don't 100% apply to myelin because membranes have complex electrical properties, but both of those explanations work and they are in fact essentially interchangeable: Take a membrane with distance d across the membrane and capacitance c. Then we add some myelin to get a new capacitance C at a new distance D.

If you 4X the distance between plates (D = d * 4), C=c/4 (from the formula you posted as (2) ); if you add 3 extra plates (so now you have a total of 4 plates), C=1/(1/c + 1/c + 1/c + 1/c)=c/4.

Importantly, myelin also increases the membrane resistance, and because myelin is typically very thick compared to a normal membrane (~10nm for one layer vs. 500-2500nm for myelin), you can almost consider myelination to increase resistance to infinity (compared to the axial resistance of cytoplasm) and the capacitance to zero.

See this page for some more info.

Note that the reason these explanations are interchangeable is that there is effectively no distance between the added plates in series and no difference in capacitance for each individual capacitor/piece of membrane (for example, see this page).


Why are omega-3 fatty acids so easily oxidized when they're incorporated in cellular membranes? Apparently, this has led to results with clinical significance, as we can see at http://extremelongevity.net/2011/10/03/daily-fish-oil-consumption-may-reduce-lifespan/...

  The researchers fed a special genetic variety of mice diets that
  either included 5% daily fish oil + 5% safflower oil or instead 10%
  daily safflower oil. The mice used were SAMP8 mutants that were bred
  to have accelerated aging and shortened lifespans. These mice are
  often used in longevity experiments because their average lifespans
  are only typically one year. They were fed these diets from 12 weeks
  of age on. The researchers hypothesized since fish oil is so easily
  oxidized it may lead to greater oxidative stress within cells and thus
  actually accelerate aging, a process believed in part due to
  accumulative damage from oxidative stress. Safflower oil is an omega-6
  fatty acid and is not readily oxidized – it could have beneficial
  effects without causing oxidative stress.

Let's not debate the clinical significance here - but I do wonder - why are omega-3 fatty acids so easily oxidized as compared to omega-6 fatty acids?

I think the explanation for this description of fish oils as "easily oxidised" can be found in the Introduction to the actual paper (Nutrition 27 (2011) 334–337) that is cited in the article linked to in the question.

  Fish oil contains high levels of eicosapentaenoic acid (EPA; 20:5 omega-3) and docosahexaenoic acid (DHA; 22:6 omega-3), which are omega-3 polyunsaturated fatty acids. EPA, DHA, and fish oil have been shown to have protective effects against coronary heart disease, thrombosis, inflammatory processes, carcinomatosis, and metabolic syndrome. Therefore, fish oils and components of the oils are marketed as health supplements. However, the effects of omega-3 polyunsaturated fatty acids on aging and lifespan are unclear compared with those of omega-6 polyunsaturated fatty acids contained in safflower oil and soybean oil. EPA and DHA are oxidized easily compared with linoleic acid (18:2 omega-6) and oleic acid (18:1 omega-9) in vitro .

In other words, the fish oil omega-3 fatty acids EPA and DHA have, respectively, 5 and 6 double bonds, whereas the omega-6 fatty acids in safflower oil, linoleic acid and oleic acid have, respectively, just 2 and 1 double bonds. So the fatty acids in fish oil are more prone to oxidation simply because they have so many more double bonds.

Incidentally, as you can see from the two structures below, both of the omega-3 fatty acids, EPA and DHA, also have an omega-6 double bond.

EPA:

DHA:


How does sepsis affect heart function? I have intuition that sepsis with infection can cause:

spastic functioning of heart during systole
heart working spontaneously in snatches during systole
atrial fibrillation
first contraction of ventricles ends earlier
which follows Action potential from A-V node during relative refractory period
weak second contraction
long compensatory pause

which can be recorded as spikes in the time axis.

With arrhythmic (earlier myocardial infarction) patients, sepsis seems to also cause leaking of valves, weakened compliance of vessels and structure of the heart.

So there are creaking sounds in the spectrum spaces.

How do the symptoms of sepsis affect heart function?

I am thinking if it is possible that this leakiness of valves and weakened compliance last only for short term and occurs periodically, during which also the heart pumps more frequently load during extrasystoles.

Assume that everything listed above is possible.

Can temporary acute/chronic inflammation in the heart cause such symptoms such as sudden weakening of valves and only temporary weakened compliance of coronary vessels?

I think the reason can be thromboembolism which is causing the sudden spastic function and weakened function of vessels and heart structures.

While the heart is affected during septic shock, it is the result of the chain of events that occur as a result of a systemic release of the pro-inflammatory cytokine Tumor Necrosis Factor alpha (TNF-$\alpha$) that leads to the "collapse of the circulatory and respiratory system." (Janeway's Immunobiology, 8th Edition) See also Tumor necrosis factor signaling.
When leukocytes, mainly macrophages encounter a pathogen or the antigenic product of a pathogen, pathogen-associated molecular patterns (PAMPs) such as endotoxins or exotoxins, their pattern recognition receptors (PRRs), such as the toll-like receptors, are bound and signaling occurs which stimulates the production and release of pro-inflammatory cytokines. In a localized infection, this is a beneficial response, however when the response is systemic, it will lead to a catastrophic cascade that leads to septic shock and often death.
Under "normal" conditions, TNF-$\alpha$ is an inducer of local inflammatory response. When an endotoxin such as lipopolysaccharide (LPS) is detected by TLR-4 on macrophages in the local microenvironment of an infection, the macrophages are stimulated to secrete TNF-$\alpha$. TNF-$\alpha$ produces the following physiological effects:

Activates the vascular endothelium

The endothelial cells will begin expressing a different assortment of receptors that recruit leukocytes out of the blood and into the tissue
This also allows for increased platelet adhesion to the activated endothelial vessels

Increases vascular permeability

Increased entry of Immunoglobulin G into the infected tissue
Increases entry of Complement proteins from the plasma to the tissue
Increased access to leukocytes and activated lymphocytes for extravasation into the infection microenvironment

Increased fluid drainage to lymph nodes

- Janeway's Immunobiology, 8th Edition; p 101
One of the mechanisms that is beneficial to the local inflammatory response, namely platelet adhesion will become problematic in the systemic response and will lead to multi-organ failure. In the local environment, however, it helps to prevent the spread of infection and shunts fluid flow away from the bloodstream and to the lymphatic system where it will be encountered by the components of the adaptive immune system. Locally:

Another important action of TNF-$\alpha$ is to stimulate endothelial cells to express proteins that trigger blood clotting in the local small vessels, occluding them and cutting off blood flow. This can be important in preventing the pathogen from entering the bloodstream and spreading through the blood to organs all over the body. Instead, the fluid that has leaked into the tissue in the early phases of an infection carries the pathogen, usually enclosed in dendritic cells, via the lymph to the regional lymph nodes, where an adaptive immune response can be initiated.
- Janeway's Immunobiology, 8th Edition; pp 107-108

You can begin to see where the inflammatory response triggered by TNF-$\alpha$ may become a catastrophic problem if it is secreted systemically.

Once an infection spreads to the bloodstream, however, the same mechanisms by which TNF-$\alpha$ so effectively contains local infection instead become catastrophic. Although produced as a membrane associated cytokine, TNF-$\alpha$ can be cleaved by a specific protease TACE (TNF-$\alpha$-converting enzyme, formerly called ADAM17) and released from the membrane as a soluble cytokine. The presence of infection in the bloodstream, or sepsis, is accompanied by a massive release of TNF-$\alpha$ by macrophages in the liver, spleen, and other sites throughout the body. The systemic release of TNF-$\alpha$ into the bloodstream causes vasodilation, which leads to a loss of blood pressure and increased vascular permeability, leading to a loss of plasma volume and eventually shock, known in this case as septic shock because the underlying cause is a bacterial infection. The TNF-$\alpha$ release in septic shock also triggers blood clotting in small vessels throughout the body--known as disseminated intravascular coagulation--which leads to the massive consumption of clotting proteins, so that the patient’s blood cannot clot appropriately. Disseminating intravascular coagulation frequently leads to the failure of vital organs such as the kidneys, liver, heart, and lungs, which are quickly compromised by the failure of normal perfusion; consequently, septic shock has a high mortality rate.
- Janeway's Immunobiology, 8th Edition; pp 108-109

So, as you can see, it is the effect of the depletion of clotting factor, the loss of plasma volume and blood pressure, and the alteration of the blood's ability to clot which likely is leading to the arrhythmic effects that you have observed in the heart.
The figure below summarizes both the localized and systemic effects of TNF-$\alpha$ release.
$\alpha$ can have damaging effects when released systemically" />
- Janeway's Immunobiology, 5th Edition; Figure 2.37
Effects of TNF-$\alpha$ on the heart
There is research from the 1990s and early 2000s that deals with the effects of TNF-$\alpha$ both on the heart and expression of the cytokine in failing heart tissue. Below is a brief selection of those articles. The final reference discusses the link between Toll-like receptor 4 activation and the promotion of cardiac arrhythmias:
From Cardiac-specific overexpression of tumor necrosis factor-alpha causes lethal myocarditis in transgenic mice. Kubota, et.al. J Card Fail. 1997 Jun;3(2):117-24.

Tumor necrosis factor (TNF)-alpha, a proinflammatory cytokine with negative inotropic effects, can be detected in myocardium with end-stage heart failure, after endotoxin administration, and during transplant rejection. Various studies suggest that TNF-alpha participates in the pathogenesis of cardiac dysfunction.
Overexpression of TNF-alpha in the heart leads to severe myocarditis and cardiomegaly. These results support the hypothesis that myocardial expression of TNF-alpha can contribute to the pathogenesis of cardiac dysfunction.

From Dilated Cardiomyopathy in Transgenic Mice With Cardiac-Specific Overexpression of Tumor Necrosis Factor-$\alpha$. Kubota, et.al.
Circulation Research.1997; 81: 627-635; doi: 10.1161/01.RES.81.4.627

That end-stage congestive heart failure is associated with a marked increase in circulating TNF-$\alpha$ levels has been reported by numerous investigators. Furthermore, there appears to be a direct relationship between disease severity and circulating levels of TNF-$\alpha$.
In the present study, we demonstrate that chronic overexpression of TNF-$\alpha$ results in the development of a dilated cardiomyopathy that shows (1) ventricular hypertrophy, (2) ventricular dilatation, (3) interstitial infiltrates, (4) interstitial fibrosis, (5) rare myocyte apoptosis, (6) a diminished ejection fraction, (7) attenuation of $\beta$1-adrenergic responsiveness, and (8) expression of atrial natriuretic factor in the ventricle. Additionally, mice overexpressing the TNF-α transgene had a marked increase in mortality. More than half of the mice that died spontaneously presented with exceptional dilatation of the heart, increased lung weight, and pleural effusion, suggesting that they died of congestive heart failure.

From The role of tumor necrosis factor in the pathophysiology of heart failure Feldman, et.al. Journal of the American College of Cardiology
Volume 35, Issue 3, 1 March 2000, Pages 537–544

In summary, both basic and clinical studies strongly support the hypothesis that myocardial expression of TNF alpha is an important step in the pathophysiologic pathway leading to progressive cardiac dilatation and failure.

From Toll-like receptor 4 activation promotes cardiac arrhythmias by decreasing the transient outward potassium current (Ito) through an IRF3-dependent and MyD88-independent pathway. Monnerat-Cahli, et. al. J Mol Cell Cardiol. 2014 Nov;76:116-25. doi: 10.1016/j.yjmcc.2014.08.012. Epub 2014 Aug 25.

Abstract
Cardiac arrhythmias are one of the main causes of death worldwide. Several studies have shown that inflammation plays a key role in different cardiac diseases and Toll-like receptors (TLRs) seem to be involved in cardiac complications. In the present study, we investigated whether the activation of TLR4 induces cardiac electrical remodeling and arrhythmias, and the signaling pathway involved in these effects. Membrane potential was recorded in Wistar rat ventricle. Ca(2+) transients, as well as the L-type Ca(2+) current (ICaL) and the transient outward K(+) current (Ito), were recorded in isolated myocytes after 24 h exposure to the TLR4 agonist, lipopolysaccharide (LPS, 1 μg/ml). TLR4 stimulation in vitro promoted a cardiac electrical remodeling that leads to action potential prolongation associated with arrhythmic events, such as delayed afterdepolarization and triggered activity. After 24 h LPS incubation, Ito amplitude, as well as Kv4.3 and KChIP2 mRNA levels were reduced. The Ito decrease by LPS was prevented by inhibition of interferon regulatory factor 3 (IRF3), but not by inhibition of interleukin-1 receptor-associated kinase 4 (IRAK4) or nuclear factor kappa B (NF-κB). Extrasystolic activity was present in 25% of the cells, but apart from that, Ca(2+) transients and ICaL were not affected by LPS; however, Na(+)/Ca(2+) exchanger (NCX) activity was apparently increased. We conclude that TLR4 activation decreased Ito, which increased AP duration via a MyD88-independent, IRF3-dependent pathway. The longer action potential, associated with enhanced Ca(2+) efflux via NCX, could explain the presence of arrhythmias in the LPS group.


Is the bipolar neuron of the retina considered a sensory neuron? Any neuron that participates in sending impulses from receptors to CNS are referred as sensory neurons. But I often see bipolar neurons of eye(which according to the above definition should be sensory neurons) being called interneurons. Same is the case with the amacrine cells and the horizontal cells.

So what are sensory neurons? Are all the following retinal neurons sensory?

Rods/Cones,
bipolar neurons,
amacrine cells,
horizontal cells &
neurons of the optic nerve (ganglionic neurons)

And, as soon as the neurons of optic nerve terminate in optic lobe, then are all the neurons in the optic lobe connected to the neurons of optic nerve called interneurons?

Are all the neurons of brain interneurons? Obviously, there are neurosecretory cells in the hypothalamus that  I wouldn't consider interneurons.

Still, wikipedia tells us that only 20% of neurons in the cortex are interneurons.

  Unlike the peripheral nervous system (PNS), the central nervous system, including the brain, contains many interneurons. In the neocortex (making up about 80% of the human brain), approximately 20-30% of neurons are interneurons.

Shouldn't that be about 80%?

In short, yes. Any neuron that is involved in conveying sensory information from the periphery to the CNS is a sensory neuron. So I would consider all of those neurons in the retina sensory.

Arguably amacrine and horizontal neurons do not convey information "towards" the CNS, but they are involved in the processing of sensory information, therefore I would call them sensory. However I wouldn't split hairs about it if the consensus on amacrines/horizontals was interneurons, not sensory.

I guess the confusion is that many categories of neurons are not mutually exclusive, so neurons can be both sensory and interneuron.

Once reaching the optic lobe (I assume you mean areas in the thalamus, midbrain etc.), then the CNS neurons can loosely be classed as projecting/interneurons. Interneurons will remain within a region of the brain, often inhibiting activity in other cells within the region (or exciting). Projecting neurons will carry information to a different brain region, or back out to the periphery. These are very loose, in a nutshell classifications though.

Once you start looking at a specific region, e.g. the Lateral Geniculate Nucleus, then the neurons will be further classified, either by shape, function, neurotransmitters, inputs or outputs, or a combination of the above depending on the requirements of the system.

Edit: To elaborate, the types of neurons in the brain will usually be described in an area specific fashion, e.g. the lateral Lateral Geniculate Nucleus has 3 major classes of neurons, magnocellular, parvocellular and koniocellular, as well as some interneurons and supporting cells. Whereas about a dozen types of neurons have been described in the cochlear nuclei, including pyramidal, stellate, giant, golgi etc. But at this level, you would be looking at very specific differences that are not necessarily relevant to the pathways involved.

I would argue that interneurons are small and restricted to individual brain regions, e.g. the visual/auditory cortex, many of the neurons, e.g. pyramidal neurons in layers IV and V  are generally projecting neurons that carry information around the brain. I don't have specific numbers for percentages, but about 20% interneurons sounds reasonable to me.


What is reductive deamination? This presentation on anaerobic digestion mentions (pg. 19) two major pathways for the digestion of amino acids: Stickland reaction and reductive deamination. While I find some info on the former, what is reductive deamination? What is a representative reaction and what partners are needed?

Amine is already a reduced state and therefore the reduction part is not of the amine. In chemical process of reductive deamination the arylamine is first converted to an intermediate, usually by sulphonylation of the amine nitrogen [ref], which in turn is reduced.

$ArNH_2 + CH_3SO_2Cl \ \ \  _{\overrightarrow{pyridine}}\ \ \  ArNHSO_2CH_3 \ \ \  _{\overrightarrow{NaH+NH_2Cl}}  \ \ \ ArH$

Biochemical anaerobic reductive deamination is reported but not for amino acids (I couldn't find any). It is reported for anilines which probably proceeds via a carboxyl intermediate [1, 2].

This article says that the non-classical amino acid $ornithine\ \ $ is converted to $\delta-aminovaleric acid\ \ $ via a $\ proline\ $ intermediate but no mechanism is described.

I don't think this answers your question completely; the best solution would be to ask the author of the presentation for the exact reference.


ID: Serated-leafed seedling A seedling has popped up in one of my planters (acid soil; Toronto, Ontario).
What is it?

June 4, 2020:

June 20, 2020:

An extension of com.prehensible's comment -- your sapling could be a bur oak.  It is older than the seedling pictured below, but retains a similar cotyledon.  The range of this species includes Ontario.

bur oak seedling
Photo by Todd Dwyer, via Flickr
(please ignore the image artifact -- an effect of resizing)

Your photo appears to show the tree at a stage after the seedling shown above and before the more mature sapling shown here:

bur oak sapling
Photo by John T. Fowler, Alamy Stock Photo


Is a Ginkgo tree a conifer? I know Ginkgo is a gymnosperm, but I was wondering whether Ginkgo is also technically a conifer. I did a Google search, and found several confident authoritative-sounding answers. Unfortunately, those answers were divided between "is" and "is not". So which is it? Is a Ginkgo a conifer?

The scientific answers are pretty clear: Gingkos are not closely related to the conifers, they are closer related to the cycads. See this phylogenetic tree based on the 18S RNA from paper 2:

It shows that conifers and Ginkgos are relative close related, but not on the same sub-branch of the tree. The last common ancestor between Ginkgos and Conifers is older than the one between Ginkgo and Cycadales. This classification has been made on the basis of genome comparisions and also based on an analysis of the chloroplasts.

References:

Chloroplast Phylogenomics Indicates that Ginkgo biloba Is Sister to
Cycads
Molecular Phylogeny of Ginkgo biloba: Close Relationship Between
Ginkgo biloba and Cycads
Advances in Ginkgo biloba research: Genomics and metabolomics pe
rspectives


How is cancer associated with host pathogen interaction? Does cancer by any chance fall under host pathogen interaction domain? What I mean to ask is that, is there pathogen interaction involved in cancer? I went through this article:
http://en.wikipedia.org/wiki/List_of_human_diseases_associated_with_infectious_pathogens
In the cancer category they have used the phrase "can be cause" by this and this pathogen.. Isn't cancer a disease that occurs due to abnormal growth of cells due to genetic change?

No not necessarily. Cancer can also be caused by bacteria and viruses in your body

The regulation of cancerous tumor development is converged upon by multiple pathways and factors. Besides environmental factors, gastrointestinal (GI) tract cancer can be caused by chronic inflammation, which is generally induced by bacteria, viruses, and parasites. The role of these inducers in cancer development, cell differentiation and transformation, cell cycle deregulation, and in the expression of tumor-associated genes cannot be ignored.
Although Helicobacter pylori activates many oncogenic pathways, particularly those in gastric and colorectal cancers, the role of viruses in tumor development is also significant. Viruses possess significant oncogenic potential to interfere with normal cell cycle control and genome stability, stimulating the growth of deregulated cells. An increasing amount of recent data also implies the association of GI cancers with bacterial colonization and viruses.

You can read more here: Aituov, Bauyrzhan, et al. "Pathogen-driven gastrointestinal cancers: Time for a change in treatment paradigm." Infectious agents and cancer 7.1 (2012): 18.


Why haven't modern grass based crops overrun wild grasses? Modern grass based crops are significantly superior to wild grasses, they grow faster, are stronger stemmed, have larger leaves and higher seed yields in terms of individual seed size, giving germinating seeds a significant head start vs other wild breeds.

I've heard time and again that GM crops will escape into the wild with potentially devastating consequences, out-competing wild plants for space and destroying biodiversity.

So why hasn't this happened already? Our crops are already GM (albeit through different methods and over a much longer time)

Edit:
I have seen the odd crop plant growing in the wild, amongst other grasses, but rarely more than one or two clumps of wheat or barely grass amongst a sea of wild grasses.

Modern grass crops (cereals) haven't run out in the wild is because that was the whole purpose of their development. What differs them from their wild counterparts are the domestication traits, like, seed shattering, uniform maturity, day length sensitivity etc.

  Modern grass based crops are significantly superior to wild grasses, they grow faster, are stronger stemmed, have larger leaves and higher seed yields in terms of individual seed size, giving germinating seeds a significant head start vs other wild breeds.

This is only true under well resourced conditions, such as, irrigation, fertilizer, planned planting density etc. They grow faster and stronger because that is how they are bred. They are bred to utilize these resources better and produce better.

  I've heard time and again that GM crops will escape into the wild with potentially devastating consequences, out-competing wild plants for space and destroying biodiversity.

What people generally talk about here is the genetic transfer due to pollen contamination. But this is generally hard because of species differentiation. Even if that happens it will be with very low frequency compared to wild population. As far as I know modern crops do not and probably will not out compete wild plants under natural conditions.

  So why hasn't this happened already? Our crops are already GM (albeit through different methods and over a much longer time)

Explanation above applies here too.

  Edit: I have seen the odd crop plant growing in the wild, amongst other grasses, but rarely more than one or two clumps of wheat or barely grass amongst a sea of wild grasses.

That is generally due to seed contamination due to somebody threw a seed there. Or it is due to remnant seed from previous year's crop, these plants we call volunteer plants.


Which species has the highest proportion of homosexual individuals? Are there more homosexual individuals in ducks, humans, or some other species?

Homosexual behavior have been observed more than 1500 species (according to Museum of Natural History of the University of Oslo). A full comparison between all known species is far beyond the scope of this site, but below I discuss three species of interest. Also, the details of what counts as an homosexual behavior, and also whether you compute incidence or prevalence makes the whole discussion semantically complicated.

According to Simon Levay and Aldo Polani, in domesticated sheep, 10% of the rams (males) prefer mating with other rams than with ewes (females).
About 25% of black swans are homosexuals (Braithwaite, 1981).
In lions, 8% of the mounting is in between two males (Bagemihl 2000)

In humans, around 3%-5% of the surveyed people claim being homosexual or bi-sexual (see wiki > demographics of sexual orientation#Modern_survey_results).


Phytophagous worm identification These worms appear soon after the rain lilies flower and slowly nibble on the leaves growing big and chubby. They are about 5cm long, have many small red legs underneath, have no spines or spikes, and are soft-bodied.
They leave tiny green balls of excreta. I have never seen them metamorphose.  I live in Andhra Pradesh in India. Can anyone tell what species they are? Are they dangerous?

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

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

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

And they eventually grow into these beautifully-multicoloured moths:

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


Pseudosexual reproduction Research projects with artificial life generally use creatures that are haploid. The offspring randomly inherit some genes from one parent, and some genes from the other parent.

Q1: Are there any biological species which reproduce similarly? I.e., they're haploid, but the offspring aren't clones. Perhaps hermaphroditic species like slugs or some plants?

Q2: Is there a name for this type of reproduction? If not, I guess I'll call it "pseudosexual" since it's a simplified form of true sexual reproduction.

Generally, all diploid species pass through a haploid phase in their life. This is called the alternation of generations and the cycle may be presented like this:

Commonly we see organisms that spend most of their life in the diploid phase, with greatly reduced haploid phase (e.g. humans "live" in haploid state only as gametes). However, this is not the only way possible. There are organisms, which spend similar amount of time in each phase, which change ploidy depending on the conditions of the environment and, of course, organisms which spend most of their lives as haploids, with only a short diploid stage.

As a rule, lower plants, fungi and protozoa may exibit this behaviour. Some examples:

Saccharomyces cerevisiae (yes, baker's yeast) will undergo meiosis and form haploid spores in unfavourable conditions, which then can grow as haploid colonies until they encounter a colony of opposite "sex"
Mosses commonly grow larger gametophytes (haploid) than sporophytes (diploid)
Some brown algae grow sporophytes and gametophytes that are indistinguishable form each other
Ferns often grow large sporophytes and small, but self-sufficient gametophytes.

Next question should be "why only lower plants and fungi?" And the shortest answer is that a diploid organism is usually more robust, it can survive more potentially lethal mutations than a haploid.


Understanding transplant rejection - how does the cellular, adaptive, response get underway This lay person is trying to get his head around the basic mechanisms of tissue rejection.

A lot of articles talk about T-cells being involve but I'm having difficulty following this. Human tissue is essentially similar between individuals. As I understand it the only cellular membrane protein that is (almost) unique is the major histocompatibility complex (MHC) that is expressed on all nucleated cells.

This means that killer T-cells can't recognise transplant tissue cells because of the MHC mismatch. The only cells that can identify non-self human tissue are the humoral innate immune natural killer cells (NKC) and they do this because they are built to kill anything unless it displays self MHC.

OK so NKC spew out the remains of alien tissue cells, but these residues are surely very similar to any other self cells' internals? How do I move from this view to one that involves the adaptive immune system which requires presentation of cellular fragments to lymphocytes?

There's a really good paper on this, Moreau et al., worth reading through entirely. The only caveat is it was published in 2013, so as a rapidly evolving field such as immunology we might have more insight now. However, the general concepts remain the same.

The lymphocyte compartment that we generate in our own bodies is modulated so that it isn't autoreactive. In other words, for every antigen a T cell should expect to actually encounter in vivo, the ones that attack and kill self cells are made to undergo apoptosis, the special case of course being autoimmunity, which is a set of diseases.

An organ transplant is what's known as a so-called allograft. The allo- prefix implies that the origin is the same species, but from different individuals. So how do people differ at the molecular level? Well for one, we inherit and develop slight differences to such things as protein sequences, carbohydrate chain moieties, and certain receptor combinations. So, your lymphocyte compartment may be non-autoreactive, but it could be alloreactive because those aren't your signals.

The other thing transplants do is cause damage and inflammation that result in the presence of these patterns that the innate immune system respond to called PAMPs and DAMPs, or molecular patterns associated with pathogens and tissue damage. They also bring along donor immune cells like antigen-presenting cells, resident lymphocytes, granulocytes, etc. It's also a functioning tissue, and so just like any of your own cells, a liver cell is expressing class-I HLA loaded with alloantigens. This can have two effects: graft-versus-host, so you have donor immune cells attacking the recipient, and the rejection which is where your recipient immune cells attack the transplant.

Your immune cells attack the transplant predicated on direct and indirect recognition, and the fact that all that inflammation already has the immune system up in arms. So your lymphocytes recognize an alloantigen on the donor antigen-presenting cell is an example of direct recognition. This can occur in the transplant, and also in the recipient lymph nodes as donor APCs can traffic there on signals in the lymph. Recipient APCs can also pick up on alloantigens from donor cells and active the adaptive immune response classically, which would be an indirect recognition.

The blanket treatment for this seems to be immunosuppressive therapy.


Is there any system how genes are spread across chromosomes? Every chromosome being a wrapped DNA molecule contains thousands or more genes.

Now, is there any system why a gene A goes to a chromosome K and gene B to chromosome J?

To a first approximation, it is "not too awful" to state that genes are randomly spread. In a more detailed view, it is a little more complex.

Homochromatin vs heterochromatin

Genes are not evenly spread within chromosomes. Typically, gene density is lower at the centromeres.

Supergenes

From wikipedia > Supergenes

  A supergene is a group of neighbouring genes on a chromosome which are inherited together because of close genetic linkage and are functionally related in an evolutionary sense, although they are rarely co-regulated genetically

To my understanding, such supergene may come to existence via chromosomal rearrangements or via repeated proximal gene duplication.

Supergene and synteny

From Wikipedia > synteny

  In classical genetics, synteny describes the physical co-localization of genetic loci on the same chromosome within an individual or species. Today, however, biologists usually refer to synteny as the conservation of blocks of order within two sets of chromosomes that are being compared with each other. This concept can also be referred to as shared synteny.

A classical example of supergene with highly conserved synteny among vertebrates is the case of Hox Genes (Amores et al., 1998).

Sexual chromosome

A sexual chromosome is some kind of a massive supergene! Consider, for example, the mammalian case.

Consider a locus that affects sex determination (SD) such as the SRY gene (coding for TDF) in mammals for example. Any male-beneficial, female-detrimental genes would gain at becoming closely linked to this SD gene. Over time, hence genes rearrange and recombination is reduced (mainly through chromosomal inversions if I am not mistaken). As recombination is reduced, deleterious mutations can accumulate through Muller's ratchet and eventually pieces of chromosomes are being lost to get rid of these deleterious mutations. This is how a Y chromosome (to consider the mammalian case, a W chromosome in birds) evolve to become so small compared to the X chromosome (or Z chromosome in birds).

Other Y-like chromosomes

Other massive supergenes can lead to Y-like chromosomes. For example, Wang et al. (2013) report a Y-like social chromosome in fire ants.

Additional source of information on the evolution of sexual chromosome

The post Do males of all sexual species have Y chromosomes? might be of interest to you. Charlesworth (1991) and Charlesworth et al. (2005) might also be a good reads.


Cellular Respiration/Fermentation Problem Leading to Lack of Energy A young animal has never had much energy. He is brought to a veterinarian for help and is sent to the animal hospital for some tests. There they discover his mitochondria can use only fatty acids and amino acids for respiration, and his cells produce more lactate than normal. Of the following, which is the best explanation of his condition?

A) His mitochondria lack the transport protein that moves pyruvate across the outer mitochondrial membrane.

B) His cells cannot move NADH from glycolysis into the mitochondria.

C) His cells contain something that inhibits oxygen use in his mitochondria.

D) His cells lack the enzyme in glycolysis that forms pyruvate.

E) His cells have a defective electron transport chain, so glucose goes to lactate instead of to acetyl CoA.

Answer:  A

A) So, from this assumption, pyruvate would build up in the cytosol of cell. However, I do not see why lactate would be formed. Lactate forms when there is a lack of NAD+. In this case, there is no problem with NAD+. All NADH will be recycled into NAD+ by the Electron Transport Chain in the mitochondria.

B) I do not know what will happen in this case. Too many contradicting factors. Can anyone explain?

C) This is clearly not correct. If there were no O2,then there would only be lactic acid fermentation; the protein and fatty acids would not be used.

D) If lactate is formed, pyruvate must have been formed.

E) The electron transport chain needs to work. See C). Same explanation.

So, I am debating between A and B. Can anyone explain why the textbook says A?

EDIT :
If anyone could give me a step-by-step approach to solving this problem, I would really appreciate it. This is supposed to be a challenge problem not representative of test questions, but I still want to fully get it.

Short answer
(A) is a possible answer and is indeed cause for fatigue, as pyruvate is needed for the Krebs cycle to run. The krebs cycle is an essential step in the generation of ATP in aerobic organisms. (B) is incorrect because NADH is never transported into the mitochondria in any organism (it is a nonsense answer).

Background
NADH is not transported into mitochondria. Instead, its electrons are transported into mitochondria, and I quote from Berg et al. (2002):

  NADH cannot simply pass into mitochondria for oxidation by the respiratory chain, because the inner mitochondrial membrane is impermeable to NADH and NAD+. The solution is that electrons from NADH, rather than NADH itself, are carried across the mitochondrial membrane. One of several means of introducing electrons from NADH into the electron transport chain is the glycerol 3-phosphate shuttle (Figure 18.37).

  Electrons from NADH can enter the mitochondrial electron transport chain by being used to reduce dihydroxyacetone phosphate to glycerol 3-phosphate. Glycerol 3-phosphate is reoxidized by electron transfer to an FAD prosthetic group in a membrane-bound glycerol 3-phosphate dehydrogenase. Subsequent electron transfer to Q to form QH2 allows these electrons to enter the electron-transport chain.

Hence, (B) is incorrect.

EDIT: Now why would lactate be formed in (A)? Pyruvate builds up in the cell, as it cannot be transported into the mitochondria. Since lactate dehydrogenase has pyruvate as a substrate, the equilibrium of this reaction will be pushed to the right and lactate will be formed:

Source: wikipedia page on lactate dehydrogenase

The lack of glucose oxidation takes away the main power supply of aerobic organisms, causing fatigue. Lactate buildup may also induce fatigue.

Reference
Berg et al. Biochemistry 2002, Freeman, New York


How is respiration an unbalanced equation The equation for respiration is C6H12O6+6O2→6CO2+6H2O+36ATP. The chemical formula for ATP is C10H16N5O13P3. How is this possible, since it violates the law of conservation of mass because it is unbalanced?

The ATP is not actually produced from the respiration. It comes from ADP and free phosphate ions.

The production of ATP in cellular respiration happens in all parts of a series of chain reactions, and you can read more about those here: https://en.wikipedia.org/wiki/Cellular_respiration#Aerobic_respiration


Understanding Hodgkin-Huxley's model and activation variables This question is about the Hodgkin-Huxley model as introduced in Eugene M. Izhikevich, Dynamical Systems in Neuroscience, p.33 ff.

I'm having trouble to understand and interpret the differential equation for the activation variable $m$:

$$\dot{m} = (m_\infty(V) - m)/\tau(V)$$

which enters via

$$p = m^a h^b$$

into the equation

$$I = \bar{g} p (V − E)$$

for the net current $I$ generated by a large population of identical
channels where $p$ is the average proportion of channels in the open state, $\bar{g}$ is the maximal
conductance of the population, and $E$ is the reverse potential of the current.

$m$ is the probability of one of $a$ activation gates to be open. Interchangeably: $m^a$ is the proportion of open activation channels (assuming all of its activation gates must be open simultaneously).

The differential equation might give us $m$ as an explicit function of time but it – explicitly – involves $V$ which is – implicitly – another function of time, which in turn depends on the number of open gates. Things are horribly complicated!

On the other hand — since it's about voltage-gated channels and there are "immediate" voltage-sensitive regions in the channel protein which presumably don't have memory ("the single channel has no memory about the duration of its own state"), but possibly a time lag — I expected the being-open-probability of an activation gate to be a "pure" (possibly time-lagged) function of $V$.

My question comes in two disguises

(1) Given two explicit functions $m_\infty(V)$ and $\tau(V)$ like these:

together with $m(0)$ and $V(0)$, how could we ever arrive at an explicit solution for $m(t)$, assuming that $V(t)$ depends somehow on $m(t')$ for $t'\leq t$, but possibly also on some injected currents.

(2) How can an intuitive and sensible interpretation of the terms in

$$\dot{m} = (m_\infty(V) - m)/\tau(V)$$

be given? What does the time constant $\tau(V)$ and its dependence on $V$ mean? In which respect and by which hypothesised mechanism is the gate "faster", when $\tau$ is smaller? How can the voltage-sensitive steady-state activation function $m_\infty(V)$ be intuitively explained other than by "giving the asymptotic value of $m$ when the potential $V$ is fixed (voltage-clamp)" or by some complicated description of experiments to determine it? What does $m_\infty(V) - m$ mean, i.e. "the deviation of the current activation from the steady-state activation"?

1) In practice, no one attempts to obtain explicit solutions for m(t), especially considering the presence of many other ion channel species, nor is there any need to. The standard of art is to use numerical simulations with a sampling interval dT that is sufficiently smaller than any relevant time constants.

2) I'm not sure what intuitive and sensible interpretation you are looking for; it may not make sense to come up with an intuitive explanation for each and every subset of terms. The use of time constants implies that the system is modeled as a linear time invariant system at a given voltage.

  What does the time constant τ(V) and its dependence on V mean? In which respect and by which hypothesised mechanism is the gate "faster", when τ is smaller?

The time constant is a scalar that describes the rate at which the system approaches some equilibrium. You could think of the changes in channel state as chemical reactions of the form:

Open <=> Closed

which has some equilibrium and some rate constant - both the rate constant and equilibrium conditions can be a function of voltage, as depicted in the figure you provide. The physical meaning of a rate constant being voltage dependent would be that the activation energy for the transition between states is a function of voltage; when the activation energy is lower, the reaction can progress more quickly (in either direction).

  How can the voltage-sensitive steady-state activation function m∞(V) be intuitively explained other than by "giving the asymptotic value of mm when the potential V is fixed (voltage-clamp)" or by some complicated description of experiments to determine it?

That's exactly what it means, and the descriptions are not complicated: the steady state value for a reversible reaction is the point at which the number of units moving from open to closed would be the same as the number moving from closed to open, so on average you see no more change: that's what steady-state means.

  What does m∞(V)−m mean, i.e. "the deviation of the current activation from the steady-state activation"?

Yes, "the deviation of the current activation from the steady-state activation" is accurate. The equation is an equation for the change of m, and the change of m is proportional to the "distance from equilibrium" - this is a characteristic of any process that follows linear time invariant dynamics. Note that there are other ways to write this equation that involve a "forward rate", a "backward rate", and the concentration of units in each state (the Wikipedia Hodgkin-Huxley page you linked has these equations), but you can simplify these to the equation you show here because some proportion of the "forward rate" process is cancelled by the "backward rate": your equation is sufficient to describe the net change.


Query regarding KEGG KGML pathway files With respect to the the Wnt pathway in KEGG, the KGML file of this pathway has description of each interaction between a pair of genes. These interactions are designated in the form:

  entry1="46" entry2="41" type="PPrel"
  subtype name="inhibition" value="--|"/
  subtype name="phosphorylation" value="+p"/

In some entries, the reaction "subtype" entries are 2 in number while in some, it is one, as for the above-mentioned interaction. Another entry is as follows:

   entry1="47" entry2="46" type="PPrel"
      subtype name="phosphorylation"
    value="+p"/   relation

Why do some of the entries have 2 interaction types while some have one? What does this signify biologically?

There is an interaction type called "compound". What does a compound interaction signify biologically?

  <relation entry1="17" entry2="16" type="PPrel">
    <subtype name="compound" value="4"/>
    </relation>

See the manual:

PPrel, in each of these, means protein-protein interaction, so we want to approach these by thinking about what the protein products of these genes can do with eachother.

For the first and second example, the subtype(s) give more information about the interaction. They aren't necessarily mutually exclusive. For example, phosphorylation can result in activation, inhibition, something else, or unknown. For the first one, there is phosphorylation and the effect is inhibition.  For the second one, the interaction is phosphorylation but the effect is not characterized.

When compound is under subtype for a PPrel relation, the value is the entry element ID for the compound (so go look for entry element 4), and it refers to an intermediate of two interacting proteins.


Are there any drawbacks to having immutable DNA during lifetime? Imagine that there is a way to prevent cell DNA from being changed once zygote has been formed. Would this have any negative effects on the target organism? Does DNA change during the lifetime as part of normal operation, or DNA changes are always due to mutations or malfunction?

Semantic of the post
This question could arguably be better on-topic on WorldBuilding.SE. The difficulty with the kind of question that ask What if the world was different, it is unclear how different would it exactly so to understand what consequence to draw from this scenario. The other issue is of course that the answer cannot be drawn from empirical studies but only be inspired from current knowledge and make untestable predictions.
Because definitions of epigenetic vary and some of them might be extraordinary broad, I will assume that by mutation, you are referring to any change in the DNA sequence excluding epigenetic changes.
Related post
Does our DNA change during our lives? is a related post.
What do somatic mutations do?
Adaptive Immunity
For species having some form of adaptive immunity, somatic mutations are used for producing a large diversity of antibody than can be tested on the self before being released in the body searching for antigen to bind to. In absence of somatic mutations, the adaptive immunity is pretty much inexistent. This point is probably the most important and has been raised by @Polisetty in the comments.
Cancer
Somatic mutations cause cancers. More generally speaking, somatic mutations create genetic diversity within the body yielding to opportunity for selfish cells that could proliferate to the expense of the rest of the body. In absence of somatic mutations, there would be no (or at least much fewer) cancer. This will affect selection for increased lifespan.
Somatic mutations on genetic diversity
As a fraction of the mutations that are transmitted to the offspring occur before the separation between the somatic lines and the germline, the absence of any somatic mutation would result in a lower mutation rate. This would result in lower genetic diversity overall. It would also affect selection pressure that depend upon the mutation rate and may have other consequences that are hard to predict.
Also, and more importantly, many species undergo asexual reproduction such as budding in plants. In some species, the entire genetic diversity is caused only by somatic mutations. In absence of such mutation, there would be no evolution possible.
What mutations are inherited
If a parent has a mutation in the lineage giving rise to half the gametes, then this mutation will necessarily be passed to half of the offspring. For this reason, offspring tend to share new mutations even if their parent did not have them. Absence of somatic mutations will remove this effect, which I would predict would have little impact on anything!


Is it true that oxygen has a diffusion rate in air 10,000 times greater than in water? According to the Wikipedia page on the design of gills, oxygen has a diffusion rate in air 10,000 times greater than in water. Is that true?

The WP entry refers to: M.B.V. Roberts, Michael Reiss, Grace Monger (2000). Advanced Biology. London, UK: Nelson. pp. 164–165.

Yes, according to calculations presented here and here the conclusion is that:

  The O2 diffusion coefficient in saturated air (15% oxygen) is 5,700 to 10,800 times greater than in water (60°C and 20°C respectively).

And here is a paper using this difference to investigate the transfer of O2 through the tracheal system of a click beetle.


Can you identify this animal? It was in the bathroom, 2cm in lenght (or so). It has two small antenas on the head. I live on Balkan peninsula, inland.

That is a European Millipede.

I found this picture by searching European Millipede. Obviously there are different types - and this is the one you have.
Here is a wiki link I found: https://en.wikipedia.org/wiki/Cylindroiulus

I think your specifically is a Cylindroiulus britannicus

.


Why does A pair with T and G with C? DNA is made up of pairs on AT and GC base pairs.

I know that A only pairs with T and G only with C. Does this apply just to humans, or are there animals where T will pair with G?

Also, surely there would be more possible combinations if A could pair with G or T or C, and DNA would have a better information density - less would be needed to hold the information?

There is no difference in base pairing between different kinds of organisms. Humans, animals and bacteria all share the same fundamental mechanisms as they all use DNA. Which bases can pair is determined by the chemistry of the individual bases.

The bases in DNA form the following hydrogen bonds when they are paired:

If you would try to combine other bases than the canonical Watson-Crick pairs, the hydrogen bond donors and acceptors wouldn't match. You need a donor/acceptor pair at each position.

There are different base pairs possible, but these situations don't really occur in DNA but in RNA. You can find G/U wobble base pairs and even base pairs that use different parts of the bases than the canonical base pairs, e.g. Hoogsteen base pairs.


Pictures of trigger point muscle fascia Are there any pictures of an actual trigger point looks like? All I am able to find online are animations.

You could have easily find these using a simple google search, however I will point several out:

See figure 1 of this article for an ultrasound image of a trigger point. Really interesting!
See figure 1 of this article for a schematic representation, and figure 2 for a real image. Although you did not ask for a deeper understanding of this topic, if you want to read more about it I would recommend reading this paper as it covers a lot of aspects (such as pain signals to the brain).
This article covers different imaging techniques and facilitates interpretation by using arrows to point out the trigger points.

If this is not what you are looking for please specify what you mean with "pictures"? (vibration sonoelastography, schematic, ultrasound, etc.) I cannot point you in a direction for real life images (if these even exist).


Why does the butterfly have a cocoon stage in its life cycle? Why does the butterfly have a cocoon stage in its life cycle? It could have simply grown up within the egg/cocoon, and emerged as a butterfly. Instead it is first an egg, then a worm, then a chrysalis, and finally after some time a butterfly.

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

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

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

Image file from Wikimedia Commons here

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

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

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

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

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

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

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

References

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


Could sex alone drive complexity? Imagine that complexity is measured by a positive number $f_n$.

If one has no prior knowledge about the positive number $f_n$ then from Bayesian theory one can assign $\log f_n$ an "improper" uniform prior over the range $-\infty$ to $\infty$.

A random mutation might increase or decrease the complexity of the offspring $f_{n+1}$. If we assume the offspring's complexity is likely to be close to the parent then we could simply model the random change in complexity by:

$$log f_{n+1} = log f_n + \Delta\ \ \ \ \  \hbox{with probability 0.5}$$

and

$$log f_{n+1} = log f_n - \Delta\ \ \ \ \  \hbox{with probability 0.5}$$

where $\Delta$ is some small number.

Such a random evolution will lead to the log of the complexity performing a random walk.

But now add sex.

Assume the complexity of a sexual organism is the average of the complexities of its parents.

$$f_{child} = \frac{f_{male} + f_{female}}{2}.$$

If one evolves the simple model now one finds that the complexity of the population grows exponentially.

Is this idea interesting or not? :)

Replace the word "complexity" with any other word..."height", "weight", "resting metabolic rate", etc. and the model would still be solvable in a mathematical sense and it would read the same way. So, it's hard for me to accept the model as relevant to the evolution of complexity.

I think you need to make the model have a more robust definition of complexity (as mentioned in the comments) but you also need to consider the costs and benefits of complexity in your model, which will greatly affect the dynamics and actually carry biological relevance.


Why do brain cells use shuttles that pass electrons from NADH to FAD? Brain cells are cells require one of the highest amount of energy of any cell of body. So why do they use a shuttle which will transfer electrons from NADH produced in glycolysis to FAD(and there by reduce the no of ATP that can be made ) ?

In the absence of unanimous consensus and sources regarding the actual distribution of these shuttles,(wikipedia favours G3P shuttle abundance) let me try to explain the cause if the glycerol-phosphate shuttle is assumed to be prominent in brain cells. Several possible reasons might lead to this:-

1) The existing metabolic pathways are all intertwined to form a complex metabolic net. This means that invariably, the intermediates of any pathway are the products or intermediates of several other pathways. Therefore, the G3P shuttles require Glycerol-phosphate and Glycerol-phosphate dehydrogenase (I and II) which might be naturally abundant in brain owing to its use in strict lipid metabolic control in nervous tissue. This means that tapping the already high G3P for use as a shuttle compared to synthesising and operating a distinct metabolic shuttle is more profitable. Furthermore, operating Malate aspartate shuttle migh require intermediates whose high concentrations (required to maintain the shuttle) might negatively interfere with existing metabolic pathways like protein synthesis and regulation.

2) This shuttle has much faster operation time than Malate-Aspartate shuttle and hence is very useful in shuttling reducing equivalents fast in muscles and brain. Compared to the malate aspartate shuttle, it is shorter and hence faster and less prone to cessation due to unavailable intermediates or enzymatic disruption. Due to several enzymes working in Malate-aspartate shuttle, it has a narrower pH and temperature optima than the G3P shuttle which is shorter and depends on lesser intermediates, and hence is less prone to disruption.

3)The last and the most far-fetched (but relevant)reason is that the loss of one ATP may not cause much of a problem because of already high respiratory rate, high Oxygen delivery to brain and ability of the body to quickly transfer available energy sources to brain at the cost of other parts, at times of energy stress. This means that replacing the shuttle with a more energetically conserving one may not have a strong driving force for evolution to operate on, and therefore the presence of G3P may be because of something like phylogenetic inertia, that is, the prevalence of an ancestral character just because it is neutral and does not influence the fitness in a considerable manner. Therefore, the ancestral G3P shuttle would just not have been replaced here but this is very unlikely as G3P shuttle is prominent in 2 very high energy-demanding organs, muscles and brain.

Except the last outrageously far-fetched reason, all other reasons should be enough to explain its prominent presence (if it is true) in brain tissues.


Help with the Price equation The Price equation describes mathematically the evolution of a population of units from one generation to the next.

  $\bar{w}\Delta \bar{z}$ = $Cov (w_i,z_i) $+$ E(w_i\Delta z_i)$

I would like to know how to actually employ the equation to some data. Perhaps a simple online "walk-through" type guide of the Price equation would help. It should simply show the calculation of the Price equation using numbers from an example population. For example, I'd like to see how the Price equation is applied to the following scenario:

  A population, $P$, of 5 individuals reproduces to produce population
  $P'$.

  The trait value of the $i^{th}$ individual is $z_{i}$ where $z_1$,
  $z_2$ and $z_3$ all = 1 and where $z_4$ and $z_5$ both = 2 and $\bar{z}$ = 1.4.

  Absolute fitness is $w_i$ for the $i^{th}$ individual where $w_1$,
  $w_2$ and $w_3$ all = 1, and $w_4$ and $w_5$ both = 5.

  Relative fitnesses, $\omega_i$, are $\omega_{z=1}$ = 0.077, and $\omega_{z=2}$ = 0.385.

  Thus the population $P'$ has $n$ = 13, with 3 individuals where $z$ = 1
  and 10 individuals where $z$ = 2 and $\bar{z}'$ = 1.769.

  $\Delta z $ is the transmission bias and is equal to 0 in this case
  (perfect transmission of the trait score $z$)

  The value $\Delta \bar{z}$ = $Cov (w,z)/ \bar{w}$ = ....

Here's an R script to create the above information:

# Define two trait values:
z1 = 1
z2 = 2

# Define two fitness values:
w1 = 1
w2 = 5

# Set number of units possesing each trait in P population:
n1 = 3
n2 = 2

# Create data
df = data.frame(c(rep(z1,n1),rep(z2,n2)),c(rep(w1,n1),rep(w2,n2)))
colnames(df) = c("z","w")

df$omega = df$w / sum(df$w)

n_P = length(df$z)
    n_O = sum(df$w)
z_P_bar = mean(df$z)
    z_O_bar = sum(df$w*df$z) / sum(df$w)
omega_z1 = mean(df$omega[df$z==z1])
omega_z2 = mean(df$omega[df$z==z2])

# Parental population size:
n_P
# Offspring population size:
n_O
# Parental mean trait:
z_P_bar
# Offspring mean trait:
z_O_bar
# Realtive fitnesses:
omega_z1
omega_z2

Here is a simple example using your data in which both terms of the Price equation are needed, since the value of the character for $z_2 $ changes in the second generation. I used your suggested change $z_2'=(9\cdot 2 + 1\cdot 3)/10 = 2.1$.

The Price equation or theorem is:
$$(1)\hspace{10mm}w\cdot \Delta z =  \text{cov}(z_i,w_i) + E(w_i\Delta z_i)  $$

While the idea here is just to give a credible calculation using both terms in the right side of the equation, and while the intuition behind the equation is essentially mathematical (or is it? $^1$), Steven Franks' paper, 'George Price's Contribution to Evolutionary Genetics', J. Theor. Biol. 175 (1995), 373-88, is a good introduction. His characterization of the right side may be the best one can do:

  "The two terms may be thought of as changes due to selection and transmission, respectively. The covariance between fitness and character value gives the change in the character caused by differential reproductive success. The expectation term is a fitness weighted measure of the change in character values between ancestor and descendant. The full equation describes both selective changes within a generation and the response to selection..." p. 376.

We work with reference to the following data and will define variables below.

$$\begin{array}{c | c | c | }  n_i & 3 & 2  \\ \hline
z_i &1  & 2  \\ \hline
w_i &1& 5   \\ \hline
n_i' & 3 & 10  \\ \hline
z_i' & 1 & 2.1  \\ \hline \end{array}$$

All cites WK are to the Wiki page on the Price equation:

(1) We can write $\text{cov} (w_i, z_i)$ as $E(w_iz_i) - wz.\hspace{10mm}$ WK eq. (7).

Explicitly:

$$ \text{Cov}(w_i,z_i) = E(w_iz_i)- wz = \frac{ w_1z_1n_1 + w_2z_2n_2}{n_1+n_2} - wz $$

$$ = \frac{1\cdot1\cdot3 + 5\cdot2\cdot2}{3+2} - (2.6)(1.4) =\frac{23}{5} - (2.6)(1.4)= 0.96$$

(2) We can write $E(w_i\Delta z_i) = E(w_i z_i') - E(w_i z_i).\hspace{10mm}$ WK eq. (8).

Now $E(w_i z_i') = \frac{1}{n}\sum w_iz_i'n_i\hspace{40mm} $ WK eq. (9a).

$ = \frac{1}{2 + 3}(1\cdot 1\cdot 3 + 5\cdot(2.1)\cdot 2) = 24/5.$

$E(w_iz_i) = 23/5$ from (1) above.

So  $ E(w_i z_i') - E(w_i z_i) = \frac{24}{5} - \frac{23}{5} = 1/5$

(3) Finally we have $\Delta z =  z' - z = \frac{2.1(10) + 3(1)}{13}-\frac{3\cdot 1+2\cdot 2}{5} = \frac{29}{65} $

and $w = \frac{3\cdot 1+ 2\cdot 5}{3+2} = \frac{13}{5} = 2.6$

So $$w \Delta z = (2.6) \frac{29}{65} = 1.16 $$

$$= \text{cov}(z_i,w_i) + E(w_i \Delta z_i) = 0.96 + .2 = 1.16 $$

  $n_i$ is the number of elements in group $i.$

  $n_i'$ is the same for the filial generation.

  $z_i$ is the value of a character for group $i.$

  $z_i'$ is the same for offspring of $z_i.$

  $w_i$ is a fitness weight, often the number of offspring an element $z_i$ will have.

  $w$ is the average fitness for the parental generation.

  $z$ is the average value of z for parental generation;

  $z'$ is the average of z for the filial generation.

  $z_2' - z_2$ (for example) is the average value of $z_2$ in the second filial
  generation minus the average of $z_2$ in the parent's generation.

$^1$ This site condenses some critical discussion of the Price equation. I have not worked through it yet but it addresses some lingering doubts I have about just what this equation means. Strongly recommended.