There seems to be some difference on the development of symptoms depending on the route of uptake, but eventually poisoning with white phosphorus leads to kidney and liver damage.

Oral uptake leads to gastro-intestinal problems like abdominal cramps, nausea and vomitting, if you take up low doses chronically, this may lead to phosphorus laden stool (also called "smoking stool syndrome").

Since white phosphorus will ignite when it comes in contact with air, skin contact often leads to severe chemical burns. White phosphorus is also highly soluble in lipids and is therefore suspected to cross through our skin rather fast, leading to absorption in the body and subsequent poisoning by liver and kidney damage.

See reference 1 for a short overview and reference 2 for extensive information.

Regarding the exact molecular mechanisms is surprisingly little known and published. It is clear that poisoning with white phosphorus causes Triglycerides to accumulate in the liver, causing the fatty liver syndrome. Depending on the source it is also speculated that carbohydrate and/or protein synthesis in the liver is also affected (see for example here or here). Mostly this is explained by the high reduction potential of the phosphorus, which disturbs the fine balanced metabolic pathways. Finally this seems to leads to liver failure (see also reference 3).

According to the toxicology profile (reference 2) the damaged protein synthesis in the liver leads to fatty liver very fast.

  Liver damage in animals exposed to white phosphorus progresses
  rapidly. Four hours after receiving a single oral dose of white
  phosphorus, minimal fatty changes in hepatocytes were observed; by 12
  hours fatty changes were extensive (Ghoshal et al. 1969). Exposure to
  white phosphorus has been shown to damage the rough endoplasmic
  reticulum and cause a disaggregation of polyribosomes (Ganote and Otis
  1969; Pam et al. 1972). This damage results in impairment of protein
  synthesis, in particular, a decrease in the synthesis of the
  apolipoprotein portion of very low density lipoproteins (VLDL), which
  are required for the transport of triglycerides. A significant
  decrease in protein synthesis has been detected as early as 3 hours
  after oral exposure (Barker et al. 1963). The smooth endoplasmic
  reticulum is also involved in the formation of the VLDLs, and damage
  to the smooth endoplasmic reticulum also impairs the formation of
  VLDLs. The net result of these ultrastructural changes is an
  accumulation of triglycerides in the liver (Ghoshal et al. 1969). This
  results in steatosis and fibrosis, which is one of the mechanisms
  involved in the hepatotoxicity of white phosphorus. The mechanism
  behind the damage to the endoplasmic reticulum is not known; also, it
  is not known whether white phosphorus itself or a metabolite of white
  phosphorus is the damaging agent. In addition to these damages, white
  phosphorus or a metabolite causes damage to the mitochondria and
  nuclei in the livers of animals orally exposed to white phosphorus
  (Ghoshal et al. 1969). The damage to the mitochondria may impair the
  cell’s ability to produce ATP, thus resulting in necrosis of the cell.

Another possible (and additional) toxic effect may be traced to the (possibly enzymatic) generation of phosphines from phosphorus and water which are highly toxic to the central nervous system (here my source is only german, you can find it here). According to reference 4 phosphines are interfering with the COS gasotransmitter signaling. They can cause cardiac problems by this mechanism. Phosphines smell garlic like, this is an observation often made, when victims of white phosphorus poisonings are authopsied.

References

White Phosphorus Exposure
TOXICOLOGICAL PROFILE FOR WHITE PHOSPHORUS
Biochemical changes associated with acute phosphorus poisoning (in
humans)
Sulfurous Gases As Biological Messengers and Toxins: Comparative Genetics of Their Metabolism in Model Organisms


Decreasing the alcohol proof and faster in hangover, why?

I would argue that your central point is intrinsically flawed. Your claim is that starting at a high alcohol percentage, then gradually decreasing alcohol content, gets you intoxicated faster. @nico is correct that you will get drunk faster this way (more alcohol sooner rather than later, so this is trivial). If we allow only one variable to change, the alcohol content (and therefore the water content), then the first drink is the most potent, and each drink afterwards is getting progressively more dilute, then this implies you are able to rehydrate better the more you drink. This argues exactly opposite to your claim.

Since you offered up the example of vodka to wine, this introduces two new important aspects: fermentation impurities and sugar content. Vodka is distilled and relatively pure, so it offers little in addition to alcohol and therefore easy to process by the liver. Scotchs and whiskeys are low sugar, higher impurities, and so would be a bit more troubling to filter and process. As you move down to wine, impurities rise and sugar content is much higher. This added sugar load dehydrates faster as well as causes a cascade of hormonal changes that are more immediately troubling than the alcohol. Beer would generally be the extreme end of the impurity and sugar continuum.

Since you bring up the USSR and the KGB, I imagine that if they did stick to this regimen of interrogation, it could be more effective by power of suggestion. The victim believes they are more intoxicated than they are, and perhaps more likely to offer up their secrets.


The only "way" someone can have a 8-pack or 10-pack is due to genetics. Across the rectus abdominis muscle you have either 3 or 4 tendinous bands going over it, consequently resulting in either a 8 or 10 pack.


Have webs woven by LSD-intoxicated spiders ever been studied for their efficiency in fly catching?

Short answer
A low dose of LSD has been shown to lead to larger, more regular webs. This obsessive perfection of the web comes with an increased effort and likely an increased required building time. Whether LSD-affected webs are more effective or not has not been assessed as far as I am aware. Personally I think that, if anything, larger webs are more efficient for their purpose, regardless of their enhanced regularity.

Background
I traced down the experiments with d-lysergic acid dietheylamide (LSD-25) and web-building spiders to the experiments of [Peter Witt]*1 performed in the 1950's and 60's.

The original article of Witt (1951), dealing with the effects of LSD on the web building behavior of spiders (Zygiellax nohta) is not accessible to me. He reiterates on the data in a review (Witt, 1971). In this review he discusses the effect of a low dose of LSD on web building (Fig. 1).

Fig. 1. Web of an untreated spider (Araneus diadematus) (left) and a web of a spider (Zygiellax nohta) treated with a low dose of LSD-25. Source: Witt, 1971

Witt concludes that low dosages of LSD increase the regularity of the webs. Spiders which had received less than 0.05 pg LSD-25 built larger webs, with fewer oversized angles and significantly more regular central angles. The spiral was unusually regularly spaced. He did not investigate the effectiveness of these webs (Witt, 1971). However, I reckon that because of the larger size they may be more effective.

Witt notes that the normal web is far from a perfect geometric structure and that one can think of a web as a compromise between regularity, which serves to cover a wide area with a trap of a certain mesh size, and a quick construction. For example, Araneus diadematus makes a new web every morning before sunrise. It requires quite some labor producing and the webs are, arguably, structures of precision and beauty (Fig. 1). The webs take between 20 and 30 minutes to build. (Witt, 1971).

The balance between regularity and quick construction of the web is what may be distorted after relatively low doses of LSD (Witt, 1971). The spider seems to put too much and almost compulsory effort in making the perfect web, and likely without too much benefit in efficiency (The Guardian, 1971). But again, the author has not addressed this hypothesis directly.

Note that higher dosages of LSD (>0.05 pg) result in smaller and more irregular webs. The Guardian (1971) reproduced some figures on this (Fig. 2), showing an example of a grossly distorted and inefficient web.

Fig. 2. Web before and after a high dose of LSD. Source: The Guardian (1971)

References
- Witt, Experientia (1951); 7(8): 310-1
- Witt, Behav Sci (1971); 16(1): 98-113

Note
*Robert Pirsig is an American writer and philosopher who has not devoted his time to spiders as far as I know.


While it is true that some fossils can be radioactive, not all of them are. According to the ressources I have found, it depends on the place where these minerals are found and also the other minerals present at this place.

When there are uranium and or potassium rich ores available, the fossils seem to enrich these radioactive isotopes in the calcium matrix of the bone during fossilation. See the reference for some more details on this.

The isotopes which are occurring there are Uranium (U235 and U238), Potassium (K40)) and Rubidium (Rb87), all of them with half lives in the billion years. Carbon does not play a role in these very old fossils (millions of years old), as the half life of the relevant carbon isotope is to short. These elements are also used for radiodating these fossils, see the table below (from here):

Regarding the radioactive safety I think there are some fossils where you should be cautious and carry them around all day long in your pocket. Most of these isotopes release $\alpha$ and $\beta$ radiation, some $\gamma$. While the $\alpha$ radiation is relatively easy to shield, lead can have detrimental effects due to the occurance of retardation radiation of the slowed down particles. In the lab we use thick acrylic glass shields to protect us from $\beta$ radiation.

Additionally I have found some secondary sources for painting the dinosaur bones with lead paint, but no real first hand source from a museum or so. Additionally the rules for radiation safety are pretty strict. If the bones would be so radioactive that a short visit would endanger you (how long are you looking at such pieces, a few minutes at maximum I would say) than they couldn't be shown anyway. Let alone the dangers for the scientists which analyze them. So I would think this is an urban legend.

Reference:

Radioactivity in fossils at the Hagerman Fossil Beds National
Monument


It is White breasted Kingfisher also called White throated Kingfisher. Halcyon smyrnensis.

Why this is Halcyon smyrnensis?

Halcyon kingfishers are mostly large kingfishers with heavy bills.

According to wikipedia this genus has 11 species, some workers also include genera Pelargopsis, Syma and Todirhamphus.

Out of all the 11 species only two are comparable to H. smyrnensis; Halcyon badia and Halcyon coromanda.

Halcyon badia is an African resident.

Additional information:

They are “sit and wait” predators of small ground animals including large insects, rodents, snakes, and frogs, but some will also take fish.

The genus Halcyon in the current sense consists mainly of species resident in sub-Saharan Africa, with a couple of representatives in southern Asia, one of which, the white-throated kingfisher, occasionally reaches Europe. White-throated and Ruddy kingfishers (Halcyon coromanda) are at least partially migratory.


Link between pornography abstinence and hormone levels

In the context of breaking a pleasure producing habit, such as masturbation (with or without pornography), testosterone plays very little part.

There are two factors at play here:

Habitualisation - the tendency for an orgasm to repeat behaviours that it has become accustomed to.
Addiction/Dopamine Response - it feels good so I'm going to carry on.

The first bullet point is obvious, if you've always done something, it's going to make you feel different if you stop. If generally in society it is perceived as being a bad thing (thus making you feel guilty for partaking, even subconsciously), stopping that habit will make you feel good. Especially once you've gotten over the relapse stage.

The second bullet point is more involved. Orgasms, along with the viewing of sexually stimulating material, release dopamine into the blood. Over time, the dopamine receptors in the brain become desensitised and require more and more dopamine to get the same buzz. This is exactly why drug addicts need bigger and bigger doses of their drug. Consequently, once one has stopped partaking in the dopamine producing behaviour the receptors gradually begin to return to normal levels of sensitivity. This results in a generally better mood and a potentially higher libido. To those that don't know the root cause, this increase in mood and libido may appear as though testosterone levels had increased, however, this is likely not the case.


What kind of larva is this? (Southern CA, USA)

That looks a lot like a Common Southern California Termite. I would check any wood that you have around your home just to prevent any damage. If you want more information just look it up online, but that's most likely what it is.

Note the eyes, the short, segmented antennae, the mandibles (better seen in your second photo.)


Can fireflies species be identified with their wavelength?

In short: Yes it should be possible, but probably not for all species and as @anongoodnurse said there are probably easier methods of species-identification.

Elaboration:
I know (but could not find a reference) that there are currently hyperspectral cameras that are able to capture bandwidths as small as 2 nm.

And there are differences in the emission spectrum of fireflies.
Firefly luciferase bioluminescence color can vary between yellow-green (λmax = 550 nm) to red (λmax = 620). ( https://www.ncbi.nlm.nih.gov/pubmed/2801227 ) There are currently several different mechanisms describing how the structure of luciferase affects the emission spectrum of the photon and effectively the color of light emitted. (https://en.m.wikipedia.org/wiki/Luciferase)

However, it is likely that there are closely related species of firefly that have no (or very small) differences in emission spectrum. These will not be identifyable with spectral imaging.


Ventral stream pathway and architecture proposed by Poggio's group

This is a typical architecture of computation proposed as a model for ventral stream of visual processing in primates. It has a long history (e.g., Neocognitoron by Fukushima was 1980) and still widely accepted in machine learning (e.g., deep learning) and neuroscience.

It is motivated by the organization of V1 simple cells and complex cells. Simple cells in V1 can be approximately thought of as edge detectors at a specific retinal location. This is why on the figure you cite, they are represented as a circle with a bar (a cartoon receptive field). The simple cells can only detect things very locally, meaning if the edge appears at a different location in your field of view, it will not respond.

Mathematically, you can think of a spatial filter that detects an edge (e.g., oriented Gabor patch) multiplied to your retinal image, and summed. For example the filter below will detect match a 45 degree bar aligned on the hot-colored area, but will have less activity if the bar is shifted out of the specific position.

The complex cells in V1, on the other hand is still an edge detector, but has some location invariance. In other words, when the edge is slightly displaced, the response of complex cells does not seem to change. It is believed that this is because complex cells pull from multiple simple cells with the same orientation. This is what you see in your figure where a single complex cell pulls information from the same orientation simple cells but at different locations.

Mathematically, a soft-max operation or a max operation over the simple cell outputs can lead to a good complex cell model. But, it is not limited to such operations. In fact, quadratic or other nonlinear models are also widely used in computational neuroscience.

The full hierarchy for ventral stream is then simply obtained by extending repeatedly using the simple-cell-complex-cell analogy. For each stack simple cell layer extracts some local feature (by computing on the previous layer's complex cell's output), and complex cell layer makes it invariant over space. From edges in V1, one can get corners on the next layer, then complex contours, and all the way up to objects. At least that's how the story goes.


What percentage of fish are herbivorous vs. carnivorous?

I don't have an answer to this but there are a number of elements I think can be helpful for you in finding an answer.

First, a helpful word for searching here if you didn't know or hadn't thought of it is "trophic", as in "trophic level", as in "how high this organism is in the food chain".

Making searches related to fish and trophic levels I didn't find a single result for all fish; there are plenty of papers and graphs about the trophic distribution of fish but it's usually within a specific context or ecosystem. For example this graph gotten from Google Images, from a paper that looks at reef fish in Hawaii:

You can see in that graph, and plenty of other papers confirmed, that "herbivore/carnivore" may not always the most relevant distinction in terms of what a fish eats; unlike on land, where the base of the food chain is plants which are pretty big and visible and so are most of the organisms that eat them, in the ocean the base of the food chain is phytoplankton, which is eaten by zooplankton, both of which are what most of the fish we consider "at the bottom" of the fish food chain eat, so by that standard almost all fish are carnivores. But it doesn't seem to be how the word is used by everyone in the field; the graph in question being an example, distinguishing "Benthic carnivores" from "Planktivores" (Plankton-eaters) and "Piscivores" (fish eaters; presumably the "carnivores" eat non-fish animals).

See also this graph looking at reef fishes at various sites in the Caribbean:

Or this graph looking at the trophic structure in a stream

both of which similarly distinguish things more finely than "herbivore/carnivore".

And this, that I got from a search for "fish trophic histogram", ties the concepts to trophic levels (but on a local scale only again, this time the Mediterranean):

Otherwise the FishBase database seems to contain trophic pyramids but they need to be seen per ecosystem and there are a lot of available ecosystems, and given the shape of most pyramids they might include more than just fish.

As an aside, this paper might give a good explanation for why most of the fish we eat are carnivorous:
Trophic level scales positively with body size in fishes


Any examples of an organism's life cycle where the reproductive stage occur before the 'adult' stage?

There are two important points here:

The adult phase is defined as the phase during which reproduction occurs. It is therefore impossible for reproduction not to occur during the adult phase as you would immediately call this phase the adult phase. Because of this purely semantic issue (nothing to do with biology) the answer to your question is necessarily "no".
Only kin selection/group selection/lineage selection makes life after the reproductive age possible. It is therefore a pretty rare phenomenon. If this is unclear, you may want to read things about the evolution of ageing such as this post for example.

Maybe a question that would be of higher interest would be something along the lines of: "Can you list species that have non/reproductive phases in between a reproductive phase and death?" or "Are there any species that undergo different reproductive phases during their lives such as being first a sneaker and then territorial (yes) or such reproducing asexually at first and then sexually (probably but can't think of any examples)?".


If I graft two trees together while young, will they grow as one plant?

There are a couple of answers to this question.  Especially where trees are concerned, you can graft two or more trees onto the same rootstock, or even a single limb into a tree.

But if the graft takes, it won't behave too much more differently than just more branches of the same tree.  Structurally intertwining them will not be different than if you had just taken a single tree's branches to support each other.  The graft will usually only have a single set of roots, from the host tree.  They will not compete.  The tendency will be for the branches to grow apart so that they can independently get their own light.  This is very much like any other single tree.  Not sure about fusing two halves of a tree together - exposing the roots would tend to kill the tree or unsettle it.


Are there human-ingestible liquids that do not contain water?

Is there anything a human can drink that does not contain water?

Yes, there are a lot of liquids that do not contain water, but mostly they are not safe for human consumption.

Mercury is a liquid at room temperature. Can a person swallow it? Most assuredly. Motor oil has no water in it. It's not a satisfying beverage. Canola oil, olive oil, and many other food derived oils can be imbibed in even reasonably large amounts, but it won't do your digestive tract a big favor.

I've treated goats with propylene glycol (a liquid), parents treat their kids with mineral oil for constipation, etc. etc.

It depends on what you mean by "drink".


Do animals exist with an uneven total number of digits?

Coscinasterias calamaria, the Eleven-Armed Sea Star! (Although I doubt it has much to do with pi)

Image from Wikimedia Commons


From How Do Pine Cones Open (Nature):

  The scales of seed-bearing pine cones move in response to changes in relative humidity. The scales gape open when it is dry, releasing the cone's seeds. When it is damp, the scales close up. The cells in a mature cone are dead, so the mechanism is passive: the structure of the scale and the walls of the cells composing the scale respond to changing relative humidity.

As to the reasons why:

  Pine cones usually appear open because this is considered a more favourable condition for the seed dispersal and germination. This usually happens when the weather is warm and when they touch water or in cold conditions, they tend to close to avoid destruction.

As to the physics/biomechanics of the pine cone opening/closing, there is an interesting article titled Hygromorphs: from pine cones to biomimetic bilayers that discusses objects that respond to environmental humidity to change their shape.

  Using the pine cone as an example that opens when dried and closes when wet, we quantify the geometry, mechanics and dynamics of closure and opening at the cell, tissue and organ levels, building on our prior structural knowledge.


What is the origin of "melting" in molecular genetics?

The melting temperature (Tm) of a double stranded DNA tract is defined as the temperature at which 50% of the DNA molecules are dissociated into single strands (and 50% form duplexes). Sure, it has a different meaning than in physics... but it is a really common term in molecular biology and I doubt people will stop to use it anytime soon!

There is a vast amount of literature about the calculation of Tm, which is very important also for practical applications, such as designing PCR primers. This page has some explanations and references about the maths behind it.

I am not sure when the term first appeared, but it has clearly be used since the dawn of molecular biology.

DNA denaturation/renaturation dynamics were first studied in the '60s.

See for instance:

STRAND SEPARATION AND SPECIFIC RECOMBINATION IN DEOXYRIBONUCLEIC ACIDS: BIOLOGICAL STUDIES - J. Marmur and D. Lane - PNAS, 1960

Although Marmur and Lane do not talk about melting temperature, we can find the term already two years later in this 1962 paper:

Effect of Concentration on the Formation of Molecular Hybrids from T4 DNA - Andrzej W. Kozinski and Michael Beer - Biophys J., 1962

Evidently the term was already common there, as they don't care to define it (it's even in the abstract).

Who first used it? I'm not sure, if anyone knows feel free to add a comment or edit the answer.


mRNA with Pseudouridine and 5-methylcytidine?

After a couple months I got this working. I ordered the psuedouridine and 5 methylcytidine from Trilink. I also switched from the mMessage mMachine kit the the Megascript kit. Megascript has all the nucleotides separated while mMessage mMachine has them pooled. You have to dissolve Trilink nucleotides so that the concentration is the same as the natural nucleotides in your IVT kit. Then you just use the non-natural nucleotides instead of UTP and CTP. Let the IVT reaction run 4 hours. Be careful about RNAse contamination.


Expression/Mechanism of ROR1 in healthy tissue

Examining the literature it'd seem that the ROR pathways incl. ROR1 and ROR2 are critical for developing tissues in the majority of cases. We also see relevance in the expression of ROR1/2, more specifically ROR2, in cases where taxic cell types are required to migrate, branch, etc. Most of the literature determines much of this occurs through a noncanonical Wnt signaling pathway.

Wnt5a–Ror–Dishevelled signaling constitutes a core developmental pathway that controls tissue morphogenesis

Ror2 Receptor Mediates Wnt11 Ligand Signaling and Affects Convergence and Extension Movements in Zebrafish

Ror2 regulates branching, differentiation, and actin-cytoskeletal dynamics within the mammary epithelium

Notwithstanding the abnormalities we see in neonates with knocked down ROR, is it wrong to assume we'd see developmental defects of branching tissues in developing (or juvenile) organisms such as lung, mammary, neural, glandular tissue, etc.? Some data in that respect would be interesting, but it's also illuminating given the presence of ROR in cancer metastasis and EMT events.


What is the likelihood of a single human gene to the same gene from the other human?

Assumptions

Let's assume that we can perfectly align all human genome and therefore calculate such statistics of identity.

Let's assume that the probability of identity of 99.9% is the same for neutral sequences than for coding sequences. This assumption is most likely wrong but there is no other way to answer the question with the data that are given to us.

What is the question exactly?

Your homework question is a little unclear unfortunately. I don't know what is meant exactly by

  How likely is it that any single gene might vary from one individual to another?

Does it mean

  You randomly sample two humans and randomly sample one gene. What is the probability of perfect identity a this gene?

or does it mean

  You randomly sample one gene, what is the probability that all humans are identical for this gene?

I will assume it means the first one.

Step by step

I will go by subquestions to guide through the thought process! Try to answer the following questions one by one and you should be able to get to the final answer yourself

Randomly sample two individuals and randomly consider one nucleotide in their genome. What is the probability that this nucleotide is the same?
Randomly sample two individuals and randomly consider two nucleotides in their genome. What is the probability that these two nucleotides are the same?
Randomly sample two individuals and randomly consider n nucleotides in their genome. What is the probability that these n nucleotides are the same?
Randomly sample two individuals and randomly consider n nucleotides in their genome. What is the probability that these n nucleotides are different?
Randomly sample two individuals and randomly consider 3000 nucleotides in their genome. What is the probability that these 3000 nucleotides are different?

What answer did you get? If you got stuck somewhere, please let me know where!

Hints

No point about using a calculator, it will return Infinite or 0 at some point anyway!
Don't worry too much if you're not using all the numbers that are given to you!


Short answer: Mire them in a viscous liquid then leave them in there long enough for them to die, instead of immediate disposal.

Cooking oil is viscous, so yes you can viably use it to mire the fleas. You'll need to wait until they die though to dispose of them or else they'll come crawling back as you've stated. The DIY option is generally a water/dish soap mixture in a container: you'll put the fleas in and they sink to the bottom almost immediately. Just leave them in there and they'll eventually die in about 5 minutes. Some individuals suggest Dawn dish soap, much like here, where the claim is that the Dawn contains compounds which suffocate the fleas.

You can also make a flea trap for around the house, with a bowl of dish soap and water near a night light. They'll jump for the light and end up falling into the flea trap.


Specific mechanism behind lethality of yellow coat color in mice

Really interesting question: The lethal yellow mutation (also abbreviated Ay) affects the agouti signalling protein which plays a major role in pigmentation. Heterozygous expression of it leads to the dominant expression of pheomelanin (which is yellow), causing the mice to express this color (among other effects). To understand why it is homozygous embryonic lethal, we need to take a further look at the gene and its organisation.
Agouti is located on chromosome 2 of the mouse genome and downstream of a gene called "Raly" (synonymous also MERC)(Image from NCBI Genes)

The Ay mutation now deletes a large chunk of DNA, removing about 170kb between these genes. This removes parts of the coding sequence of the Raly gene and the complete promoter and (non-coding) exon1 of the Agouti gene and results in a fusion protein in which the agouti gene is put under the control of the Raly promoter. This leads to the expression of Agouti every time when Raly should be turned on.
Schematically, this looks like this (figure 4 from reference 2):

Raly is an RNA binding protein, which is highly expressed in embryonic tissues. The mutation leads to the expressing of Agouti there instead. According to reference 3 this leads to embryos which do not develop further than the blastocyst stage leading to premature death of the embryo.
So in short, the deletion removes the expression of Raly, a protein important for embryonic development. Im homozygous mice this is embryonical lethal, in heterozygous mice this can obviously be compensated. However, these mice tend to be obese and are more susceptible for certain tumors (reference 4).
References:

The embryonic lethality of homozygous lethal yellow mice (Ay/Ay) is
associated with the disruption of a novel RNA-binding protein
A molecular model for the genetic and phenotypic characteristics of
the mouse lethal yellow (Ay) mutation.
Pleiotropic effects of the mouse lethal yellow (Ay) mutation
explained by deletion of a maternally expressed gene and the
simultaneous production of agouti fusion RNAs
The molecular basis for dominant yellow agouti coat color mutations


What happens in a brain of a person suffering with apathy?

Starting your comment, first, apathy in itself is not a disease; it's not categorized as such by any medical or psychiatric organization. It is part of the symptoms of some disorders, including depression, schizophrenia and Alzheimer's.

Furthermore, apathy is not a simple symptom, but rather a constellation. That also makes it more difficult to address its brain correlates. From a review,  Moretti & Signori (2016):

  Apathy is an uncertain nosographical entity, which includes reduced motivation, abulia, decreased empathy, and lack of emotional involvement; it is an important and heavy-burden clinical condition which strongly impacts in everyday life events, affects the common daily living abilities, reduced the inner goal directed behavior, and gives the heaviest burden on caregivers. Is a quite common comorbidity of many neurological disease. [...] As a general observation, the occurrence of apathy is connected to damage of prefrontal cortex (PFC) and basal ganglia; “emotional affective” apathy may be related to the orbitomedial PFC and ventral striatum; “cognitive apathy” may be associated with dysfunction of lateral PFC and dorsal caudate nuclei; deficit of “autoactivation” may be due to bilateral lesions of the internal portion of globus pallidus, bilateral paramedian thalamic lesions, or the dorsomedial portion of PFC. On the other hand, apathy severity has been connected to neurofibrillary tangles density in the anterior cingulate gyrus and to gray matter atrophy in the anterior cingulate (ACC) and in the left medial frontal cortex, confirmed by functional imaging studies. These neural networks are linked to projects, judjing and planning, execution and selection common actions, and through the basolateral amygdala and nucleus accumbens projects to the frontostriatal and to the dorsolateral prefrontal cortex. Therefore, an alteration of these circuitry caused a lack of insight, a reduction of decision-making strategies, and a reduced speedness in action decision, major responsible for apathy. Emergent role concerns also the parietal cortex, with its direct action motivation control.


How far can parrots fly without needing to land?

Birds of flight were the original inspiration for the design of a machine that could fly and carry a person aloft, hence it's not surprising that the aerodynamics of avian flight and aircraft have much in common. Specifically, they both consume mass as the source of energy to maintain flight; jet fuel or gasoline in the case of airplanes, and stored body fat in birds, and they both have wings that provide aerodynamic lift as the air moves over them during flight. In addition, both share another characteristic of flight, the ability to glide, to continue flight without providing any of their own energy to maintain that flight. This energy is provided by the atmosphere itself in the form of rising air currents caused by a difference in temperature of a local 'pocket' of air; a pocket of air that is warmer than the surrounding air will rise because it has lower density, the Archimedes Principle in action. A similar process occurs when a parcel of moist air is surrounded by dry air at the same temperature as the moist air hence less dense than dry air. The third source of rising air is due to the local topography; the air on the windward side of a ridge or mountain is forced upward and is frequently used by birds as a source of lift.

Any discussion of gliding flight will unavoidably involve some aspects of atmospheric physics (a.k.a., weather), it's no different here. As stated above, a parcel of moist air surrounded by dry(er) air at the same temperature will rise. As long as that temperature is above the saturation temperature (the dew point) for that parcel of air, the water will remain in vapor form. We all know that as we go higher in the atmosphere the temperature drops; it's cooler at the top of a mountain than at its base. Therefore, as our parcel of moist air rises its temperature will drop, and eventually that temperature is the same as the dew point in that parcel leading to the condensation of that moisture, i.e., a cloud forms. As a surface of constant temperature in the atmosphere is nearly a level surface, we see clouds in the sky whose bases are all at the same level, the level where this condensation begins. Now, for a little of thermodynamics; when we boil water by adding heat (that is energy) to it, we are turning liquid water into a vapor (steam). Here's the thing, when we cool that steam down to the dew point it will condense back into liquid water, and in doing so, we get the heat (that was put in to make it boil) back again! That recovered heat shows up as an increase in temperature of the air that just gave up the water vapor. This increase in temperature causes that air to continue to rise, now due to a temperature difference with the surrounding air rather than a water vapor pressure difference; the cloud continues to grow upwards. This is the source of the cumulonimbus clouds we see in the sky that may eventually form thunderstorms. This discussion hi-lights a key fact about weather that relates directly to our discussion about gliding flight; if there are no updrafts, there are no clouds. That's correct, for a cloud to form, there must be updrafts containing moist air. No clouds indicates no updrafts. If there are no updrafts, there is no gliding flight. However, we note that really dry air is very hard to find; there still might be thermals around, but not likely, and those not very strong. The take away from this discussion is this: if we want to include increases in maximum range resulting from gliding flight, we need to be able to predict the weather (which hasn't happened yet, and I say this as one who has spent years as an undergraduate and graduate student active in atmospheric research.). Hence, long distance gliding flight will not be addressed any further here.

We begin our analysis of powered flight by considering a specific airplane, say a Boeing 787 passenger jet. To find its maximum range, the aircraft would be completely fueled up, take off and fly a level, constant speed flight path, as any accelerations (by changing altitude or going faster) would waist fuel. When the fuel tank goes dry, you have reached the maximum range of powered flight (assuming no head or tail winds of course).

From an analytic point of view, the fuel carried by the 787 is the source of energy, $E_s$, that powers its engines. These engines produce the thrust force, $\mathbf{T} = T\mathbf{\hat{T}}$ directed horizontally, parallel to the 787's longitudinal axis and to the flight path, that counteracts the effect of the atmospheric drag force, $\mathbf{D} = D\mathbf{\hat{D}}$ that opposes the 787's motion along its flight path. Under steady flight conditions (constant speed and altitude), the net horizontal forces on the 787 is zero so that $\mathbf{T} + \mathbf{D} = \mathbf{0}$, or $\mathbf{D}=-\mathbf{T}$. Taking the magnitude of both sides of this expression we find that $D=T$ so that $\mathbf{\hat{D}}=-\mathbf{\hat{T}}$. We find that the thrust generated by the engines has the same magnitude as, but directed opposite to the atmospheric drag.

Under the same flight conditions, we find a similar relationship for the vertical components of force acting on the 787, its weight, $\mathbf{F}_w = F_w\mathbf{\hat{F}}_w$ is balanced by the lift $\mathbf{L} = L\mathbf{\hat{L}}$ generated by the wings so that $F_w = m_p g = L$ and $\mathbf{\hat{L}}=-\mathbf{\hat{F}}_w$ where $m_p$ is the instantaneous mass (= takeoff mass of the plane, $m_{p_0}$, less the mass of fuel expended so far generating thrust) of the 787 and $g=9.8\, \text{m/s}^2$ is the standard gravitational acceleration on the surface of the Earth. We note here, that under these flight conditions, both $\mathbf{L}$ and $\mathbf{F}_w$ are perpendicular to $\mathbf{T}$ and $\mathbf{D}$.

If the thrust is removed so that $\mathbf{T}=\mathbf{0}$, then the drag force will no longer be opposed and will slow the plane down, reducing the speed of air flowing over the wing, which in turn will cause the wing to generate less lift, thus initiating the plane's descent (its weight is greater than the lift produced by the wings). If the plane is then 'nosed down' by an angle $\alpha$ from the horizontal, the projection of the plane's weight vector, $\mathbf{F}_w$ onto the plane's longitudinal axis will no longer be zero, but will instead be $\mathbf{F}_w\sin\alpha$ directed forward opposing the drag force. If $\alpha$ is chosen so that the sum of this projection and the drag vector is zero, then the plane will descend at a constant rate and the magnitude of the drag is given by $D = F_w\sin\alpha$. The projection of the weight vector onto the axis perpendicular to the plane's longitudinal axis, $\mathbf{F}_w\cos\alpha$, is balanced by the equal magnitude but oppositely directed lift vector, whose magnitude now becomes $L = F_w\cos\alpha$. If we form the ratio $D/L$ we find
\begin{equation}
\frac{D}{L} = \frac{F_w\sin\alpha}{F_w\cos\alpha} = \tan{\alpha} \tag{1}\label{1}
\end{equation}
The inverse of this ratio, $L_D = L/D = (\tan\alpha)^{-1}$, is known in aerodynamics as the lift to drag ratio while the angle $\alpha$ is called the glide slope angle. These two  parameters are important in the overall characterization of the aerodynamics of an air-frame. Once this ratio is known, it can be used to estimate the drag in level flight. But in level flight, the lift is equal in magnitude to the plane's weight, $L=F_w=m_p g$. Substituting this expression into Eq.~$\eqref{1}$ and solving for the drag
\begin{equation}
D = L\tan\alpha = F_w\tan\alpha = m_p g\tan\alpha  \tag{2}\label{2}
\end{equation}

We have reached the point in our analyses that we need to address the mass/energy budget for the plane's flight. It will be useful to separate the mass of the plane into its empty (no fuel) mass, $m_{p_e}$, and the mass of available fuel, $m_f$, with the initial, takeoff mass of fuel given by $m_{f_0}$. With these quantities defined, the initial takeoff mass of the plane is given by $m_{p_0} = m_{p_e} + m_{f_0}$ while the instantaneous mass is given by $m_p = m_{p_e} + m_f$. During flight, the mass of the fuel available, $m_f$, varies such that $m_{f_0} \ge m_f \ge 0$ while the mass of the plane, $m_p$, varies as $m_{p_0} \ge m_p \ge m_{p_e}$.

There are two additional constants required to determine the net effective energy available to do work against the drag force when consuming the (differential) quantity $\delta m_f$ of fuel while flying the (differential) distance $\delta \mathbf{r}$. The first of these, $\kappa$, determines the total (differential) energy, $\delta E$, available from the combustion of the quantity $\delta m_f$ of fuel
\begin{equation}
\delta E = \kappa \delta m_f   \tag{3}\label{3}
\end{equation}
For an American airplane such as the 787, $\kappa$ will have units something like BTU per pound of fuel expended.
The second, $\eta$, specifies the efficiency of converting the available energy into actual work, $\delta W$, generating thrust that counteracts the drag
\begin{equation}
\delta W = \eta \delta E = \eta \kappa \delta m_f = - \mathbf{T}\cdot\delta\mathbf{r} = - m_p g\tan\alpha \delta r \tag{4}\label{4}
\end{equation}
where $\delta\mathbf{r} = \delta r \mathbf{\hat{T}}$ is a differential displacement vector along the flight path during constant velocity, horizontal motion and the minus sign accounts for the fact that the plane's energy stores are consumed as that energy is used to counteract drag (a fundamentally dissipative process).

Letting the $\delta$'s become derivatives, dividing through by $m_p$ and using $m_p = m_{p_e} + m_f$ and replacing the integrated variables by primed quantities, , Eq.~$\eqref{4}$ can be rewritten in the integral form
\begin{equation}
\eta \kappa \int_{m_{f_0}}^{m_f} \frac{dm'}{m_{p_0} + m'}
= - g\tan\alpha \int_0^r dr'   \tag{5}\label{5}
\end{equation}
with the limits of integration evaluated at takeoff and the current downrange position a distance $r$ from takeoff.

Performing the integrations indicated in Eq.~$\eqref{5}$ and simplifying, we have the result
\begin{equation}
m_p = m_{p_0} e^{-\frac{g\tan\alpha}{\kappa\eta}r}   \tag{6}\label{6}
\end{equation}
We find that the mass of the plane, $m_p$, is an exponentially decreasing function of the distance flown, $r$. Letting $r=r_m$ be the maximum range of plane where all fuel has been expended (when $m_f=0$ so that $m_p = m_{p_e}$), Eq.~$\eqref{6}$ becomes
\begin{equation}
m_{p_e} = m_{p_0} e^{-\frac{g\tan\alpha}{\kappa\eta}r_m}   \tag{7}\label{7}
\end{equation}
We note the similarity of this expression to that of the Tsiolkovsky rocket equation.

Eq.~$\eqref{7}$ can be solved for the maximum range $r_m$
\begin{equation}
r_m = \frac{\kappa\eta}{g\tan\alpha}\ln\left(\frac{m_{p_0}}{m_{p_e}}\right)
   \tag{8}\label{8}
\end{equation}
an amazingly simple result, all things considered! This result remains valid for any aerodynamic system that obtains its lift via forward motion through the air provided by a propulsion system that consumes mass to produce thrust. It could be applied to a Cessna 172, or even a nitro powered radio controlled (RC) model of a 172. It could not be applied to an electrically (battery) powered model of the 172 because there is no mass loss from a battery, or to any type of glider (no thrust or mass loss). And it can, however, be applied to any bird of flight, including our parrot!

For the parrot, the energy source is the fat stored in its body. This mass is consumed through metabolic processes that convert it into $\text{CO}_2$ and water vapor that is expelled during respiration, and as sweat and urine as the parrot flies (the parrot's "exhaust" as it were!). The energy content of body fat ($\kappa$ as defined in Eq.~$\eqref{3}$) is 9 (food) Calories per gram. One food Calorie is equal to one kilocalorie which is in turn equal to 4184 Joules in SI units, see the Wikipedia article Food energy.

The efficiency of converting stored energy in the human body into mechanical work has been estimated to be $18\%$ -- $26\%$ (see Wikipedia page Muscle). One would expect similar numbers for other warm blooded vertebrates, so that, to one significant figure, we take $\eta = 20\% = 0.2$ (a dimensionless quantity).

There seems to be a very broad range for the percent of body mass that is fat. Some migratory birds have up to $70\%$ (see Obese super athletes: fat-fueled migration in birds and bats, however the parrot is not generally considered a migratory bird. The web page Comparison of flight mileage for various wild parrot species states a migration distance of 320 km for Thick-billed Parrots for example. Hence the $70\%$ number is likely far too large. At the other extreme, ground beef is considered lean if it contains $10\%$ fat, but more generally it is closer to $20\%$. We will select a value somewhat below the median of these extremes, say $35\%$.

A typical mass for a parrot is another difficult number to ascertain, as there is a very large difference in body mass for the various members of the parrot family. For example, the web page Average Bird Weights of Common Parrot Species gives data for 52 parrot species with links to four other species, each with several entries. These vary from 10 grams for the Zebra finch to 1530 grams for the Green-winged Macaw covering a mass range of over two orders of magnitude! Upshot: there is no such thing as a "typical" parrot! We will choose the Thick-billed Parrot as we have some long distance data to compare our result to. The Wikipedia page Thick-billed parrot gives its mass range as 315-370 grams, we shall use 370 grams so that $m_{p_0} = 0.37 \, \text{kg}$, $35\%$ of which is to be considered fuel so that $m_{f_0} = 0.16 \, \text{kg}$ leaving the parrot's 'empty mass' at $m_{p_e} = 0.24 \, \text{kg}$.

We have one remaining parameter to estimate, that being the glide slope angle, $\alpha$, used to find the lift to drag ratio above. Consider the order of magnitude estimates of $\alpha = 10^0 = 1\, \text{radian} \approx 60^o$, $\alpha = 10^{-1} = 0.1\, \text{radian} \approx 6^o$ or $\alpha = 10^{-2} = 0.01\, \text{radian} \approx 0.6^o$. Clearly $60^o$ is far too steep and $0.6^o$ is much too shallow, leaving $6^o$ as the only acceptable order of magnitude choice, hence we set $\alpha=10^{-1}$ radian, a number valid for most birds of flight.

Repeating Eq.~$\eqref{8}$ above,
$$
r_m = \frac{\kappa\eta}{g\tan\alpha}\ln\left(\frac{m_{p_0}}{m_{p_e}}\right)
$$
and substituting the parrot's values from above (including unit conversion factors)

$$
r_m= \frac{\left[\left(\frac{4184\,\text{J}}{\text{gm}}\right)
\left(\frac{1000\,\text{gm}}{\text{kg}}\right)
\left(\frac{\text{kg m}^2}{\text{J s}^2}\right)
\right] \left(0.2\right)}
{\left(\frac{9.8\,\text{m}}{\text{s}^2}\right)
\left(\tan\left(0.1\right)\right)}
\ln\left(\frac{0.37\,\text{kg}}{0.24\,\text{kg}}\right)
\approx 370 \text{ km }
$$

we find the answer to the question, "How Far Can a Parrot Fly [under power] in a Single Day?" to be

$$
\boxed{r_m\approx 370\, \text{km}}
$$

a number which is in close agreement with the (limited) data available which gave an actual (vs maximum) daily migration range of 320 km.

It's interesting to note that this maximum range for powered flight can be viewed as the minimum range when gliding flight is included. Under ideal weather conditions, the actual maximum range could be extended considerably if the parrot were to capitalize on any available thermals it encountered during its flight.


Why does yeast react the way it does to water combined with sugar?

Yeasts are living organisms, they do not evaporate. However it is true that in most fermented food we eat, yeast are no longer there. So why is it so?

It is not the reaction with sugar and warm water that makes them disappear. Most of the time they get killed later in the food making process. For instance, if you consider yeasts in bread, like french baguette for instance, after the dough raised, it goes to the oven where yeasts cells get heat killed.

For other processes, like brewering, yeasts used to stay in the final product. But then you had to drink it before it got spoiled by yeasts that were consuming all the sugar. So nowadays, industrially produced beers are filtered or pasteurized, or both, in order to get rid of the yeasts. Only artisanal beers are still "alive", with living yeasts in it.

EDIT:
As for the question "why/how do yeasts react with sugar?", sugar is actually fuel for yeasts. Yeasts oxidize sugar into CO2 in order to gain energy for their metabolism.


What does the acronym ‘PIN’ stand for referring to PIN proteins in plants?

Like many genes and gene products, PIN proteins were named for a mutant phenotype and PIN is not actually an acronym; the source in your link does actually explain this (emphasis mine):

  The significance and function of AtPIN1 was discovered through the phenotype generated by the loss-of-function mutation in the gene: mutant plants fail to develop floral organs properly and generate naked, pin-like inflorescences, which gave the name PIN-FORMED (PIN) to the family

Křeček, P., Skůpa, P., Libus, J., Naramoto, S., Tejos, R., Friml, J., & Zažímalová, E. (2009). The PIN-FORMED (PIN) protein family of auxin transporters. Genome biology, 10(12), 249.


What is this white-winged insect from Hong Kong?

I think these are planthopper nymphs. I can't be sure of the species, but Ricania speculum looks rather similar:

(image source)


Examples of healthy lifelong asymptomatic carrier of a severe infectious disease?

I am curious, is there any known disease/infection that is very severe normally, but ends up having little to no effect on the lives of asymptomatic carriers?

HIV is an obvious example, where so-called "long-term nonprogressors" successfully suppress HIV replication sufficiently that they do not develop AIDS but are unable to clear the infection entirely [1].

  patient suffers greatly and die easily without medical treatment

Since the comments below seem to suggest that HIV does not cause death without medical treatment, I'll point out that this is incorrect.  Over 30 million people have died from HIV infection.

  I am asking this as I am thinking whether this means certain disease symptoms are evolutionarily wired to protect the "greater good"

It does not.  Selection happens on individuals and not whole species, so the greater good is irrelevant.  Asymptomatic infection is a point on the spectrum of possible responses to infection between sterilizing immunity and death. Individuals who are chronically infected mount enough of an immune response to control the infection but not enough to completely clear it.  In the case of HIV, they are typically people who have exceptionally strong immune responses to a normally lethal virus.

Edit

The comments below suggest a deep misunderstanding of evolution. Since I think these are really the core of your question, I'll address them here.

  If traits really evolve only according to how much an individual reproduce sucessfully, it would be a different world today.

Which individuals reproduce is the sole determinant of which genes are passed down to the next generation.  This is because the genetics of each individual are determined at conception, and cannot be changed.  Hence, reproduction alone determines the traits of the next generation.

To quote wikipedia[2]:

  Evolution is change in the heritable characteristics of biological populations over successive generations. These characteristics are the expressions of genes that are passed on from parent to offspring during reproduction. Different characteristics tend to exist within any given population as a result of mutation, genetic recombination and other sources of genetic variation. Evolution occurs when evolutionary processes such as natural selection (including sexual selection) and genetic drift act on this variation, resulting in certain characteristics becoming more common or rare within a population

Evolution is the process by which some traits are passed down to the next generation while others are not though the mechanisms of selection (e.g. individuals with harmful traits dying) and genetic drift (e.g. random chance).

  Thank about a hypothetical super fast reproducing bacteria, using up all resources, which means extinction at the end, such traits would not be passed on. In fact some sort of "moderation" mechanism is needed to take care of the "greater good".

This is exactly what happens if you put a lot of fast reproducing bacteria in a closed environment with limited resources.  They will all eventually die.

You seem to be thinking of evolution as something that intelligently looks out for the wellbeing of species.  This is not the case.  Evolution is a random process by which different amounts of reproduction and survival between individuals alters the composition of the succeeding generations. As a random, emergent process it has no goals, no intelligence, and no sense of "good".  Rather, it simply happens as a result of individuals reproducing.  This frequently does lead to extinction, as evidenced by the fact that the vast majority of species no longer exist.

(1) https://academic.oup.com/cid/article/51/2/239/303856
(1) https://en.wikipedia.org/wiki/Evolution


Terrestrial locomotion of bats and pterosaurs

Quadrupedal means walking on 4 limbs, so yes bats can be considered quadrupeds. The scientific name for how an animal walks is gait. However, keep in mind that the same animal can have different gaits, think of a horse that can walk, gallop, etc. It seems that not all bats walk the same way, this here might be of interest, where they tell about a paper published in Nature in which they find a very different gait in Vampire bats, compared to 'normal' bats. In this paper they say that normal bats: "...shuffle  awkwardly from  a  sprawled  position." So I don't think they have a real name for a 'normal' bat gait.

For flying pterosaurs, it is hard to tell, we've never seen one walk.


What, other than genetic factors, influence which individual survives a parasite and which perishes?

I am neither a parasitologist nor an immunologist, so these suggestions are only provided as a starting point and may meet valid criticisms from others. However, as your comment mentions the 1918 flu epidemic, a couple of general suggestions.

Assuming that resistance to pathogenic organisms can involve the immune response, then at least two factors that might affect that — and hence resulting mortality or morbidity are:

Nutrition:
It is popular wisdom that undernourished individuals are more susceptible to disease. This might have diverse causes, but there would appear to be an extensive literature on the role of nutrition in the immune response, e.g. this article by  Chandra has been highly cited.

Previous immune challenges: There is, of course, the classic case of milk maids being resistant to smallpox because of immunity provided by the related cowpox. Thus exposure to previous strains of a virus may provide some protection. Speculating widely here, there may also be affects on the non-specific components of the immune response (macrophages and whatever).


It sounds like what you read and what your professor mentioned are different types of causation.

T4 is the primary form produced by the thyroid; T3 is metabolized from T4 in other tissues and more strongly activates thyroid hormone receptors. Metabolism from T4 to T3 then allows tissues to have control over how much active thyroid hormone there is - multiple levels of control are very common to hormones, and other signaling pathways as well.


What is this insect in Southern California?

This is a scarab beetle that belongs to the genus Cyclocephala, and has the nickname of "masked shafer" (gallery). There are over 300 different species within this genus, however, the species most common to southern California is C. hirta and C. pasadenae, with me leaning more towards the former.

C. hirta; San Diego County, CA (source)

C. hirta; San Leandro, CA. (source)

C. pasadenae; Vail, AZ (source)

  When it flies, it opens up its wings like a ladybug's.

Ladybug, left; masked chafer, right.


Yes, these sequences exist and they are called "silencers" (surprising, right?). There are different mechanisms by which this silencing of genes can happen.

In the "classical" way the silencer is bound by a  transcription factor which either passively suppress the gene by hindering the binding of specific transcription factors or by actively preventing the assembly of the general transcription factors. See the figure from paper 1:

Additionally there are non-classical negative regulatory element (NRE), which are usually elements upstream of the promoter which inhibit the binding regulatory proteins. NRE can also be enhancers depending on the proteins bound on them. Some NRE can induce a bend of the DNA, inhibiting the access to enhancer or promoter elements.

References:

Transcriptional control and the role of silencers in transcriptional
regulation in eukaryotes.
Transcriptional Regulatory Elements in the Human Genome


Origin, or source, of rhesus negative in human blood

Your question has many questions in it.

As for the evolution of Rh factor, Blancher and Apoil (2000) attribute the high level of sequence similarity (92%) of the two RH locus genes, RHD and RHCE to a gene duplication event in the common ancestor of human, chimps, and gorillas. Their analysis of the cDNA from these genes revealed "complex recombination events" after the lineages split.

Basically the most recent common ancestor of apes had the "human" RH genes, which then differentiated after the lineages diverged. Duplicate and differentiate is a common theme in evolution.

As for why it's called rhesus antigen, that's just as experimental artifact:

  The term "Rhesus antigen" was introduced by Landsteiner and Wiener,
  who found that rabbits (and later, guinea pigs) immunized with red
  blood cells (RBCs) from a rhesus monkey produced antibodies which
  agglutinated 85% of Caucasian blood samples (Landsteiner and Wiener
  1940, 1941).

They probably weren't even correct about the antibodies being rhesus:

  In conclusion, if the term "Rh" was coined by Landsteiner and Wiener
  because of the source of antigens (the rhesus monkey) they used to
  obtain anti-Rh in rabbits, it is highly probable that, in fact, they
  produced anti-LW antibodies.


By definition, the word "venomous" can only technically be applied to animals.  The most "poisonous" plant would be the gympie gympie tree, but if you want something "venomous", you might be able to find something similar within some species of carnivorous plants.


Are spiders part of the study of entomology?

Spiders are part of a taxon called Arachnida. Arachnida also contain scorpions, Oppiliones, acari, … The science of arachnids is logically called Arachnology

However, (wikipedia):

  Entomology (from Greek ἔντομος, entomos, "that which is cut in pieces or engraved/segmented", hence "insect"; and -λογία, -logia) is the scientific study of insects, a branch of arthropodology. In the past the term "insect" was more vague, and historically the definition of entomology included the study of terrestrial animals in other arthropod groups or other phyla, such as arachnids, myriapods, earthworms, land snails, and slugs. This wider meaning may still be encountered in informal use.

In other words, in the informal sense entomology include arachnology but the strict definition entomology does not encompass arachnology.

You will find here on tolweb.org more information about the systematics of Arthropoda


How does species diversity vs Earth total biomass relate?

I don't work in ecology, but my first thought is that I would not expect any relationship whatsoever between diversity and biomass. Biomass simply means the combined mass of all life on the planet. If that mass consists of one extremely fat goat the size of the moon, or several trillion different organisms doesn't make a difference, mass is mass.

Now, it is undoubtedly true that loss of diversity is a huge issue. However, the way this works is usually that we replace the local ecosystem with its several, varied species with a monoculture. For example, grasses like wheat and barley are taking over the world. Destroying a forest to plant wheat might easily result in no net change in biomass or even a net positive, but it will certainly be a significant loss in the diversity of the local ecosystem.

Finally, humans are a teeny tiny part of the world's biomass, most of which consists of unicellular life, plants and insects:

Note that the axes in the image above are logarithmic. You can get a clearer image, perhaps, from this:

(both images taken from Bar-On YM, Phillips R, Milo R., The biomass distribution on Earth, PNAS, 2018 Jun 19;115(25):6506-6511. https://www.pnas.org/content/115/25/6506)

See how all animals, let alone humans, are just a tiny part of the image on the right? That gives you a pretty clear indication of just how irrelevant we are in terms of global biomass. So yes, diversity is indeed decreasing, but there is no reason to think that the accumulated mass of living organisms will decrease, only the diversity of said mass will decrease.


What's this spring-like structure in the plant parenchyma cell?

It looks like a part of a xylem cell (particularly vessel). Take a look at pics in wiki article. Another good example is here on pic. 36. Possibly you have dragged a part of it during cutting. So it is presumably not a part of parenchyma cell.


How well can humans detect vitamin-richness?

Based on what I could search I guess that humans (and other organisms) usually do not have strong sensory mechanisms for micronutrients (Miyamoto et al, 2013).

There are some reports on sensing of metal ions, especially zinc and copper, by some organisms, including mammals (Bird, 2015; Ballou and Wilson, 2016). However, I haven't come across any study that talks about vitamin sensing.


Cat purring: What are some possible underlying mechanisms behind purring and bone remodeling and formation?

The author is likely referring to the mechanosensory behavior of bone (reviewed in Huang and Ogawa, 2010; lots of Google Scholar citations). Bone loading produces very tiny mechanical deflections (strain) which are translated into biochemical signals that promote bone growth through the action of osteoblasts. Burger and Klein-Nuland (1999) review possible mechanisms.

The low frequency soundwaves produced during purring overlap the frequencies that have been shown experimentally to induce bone formation (1-50Hz; e.g., Castillo et al., 2006; Xie at al. 2006). Although an interesting hypothesis, I don't think that osteogenesis in response to purring has ever been experimentally shown in cats.

Huang C, Ogawa R. 2010 FASEB J. 2010 Mechanotransduction in bone repair and regeneration. 24(10):3625-3632.

Burger EH, Klein-Nulend. 1999. Mechanotransduction in bone--role of the lacuno-canalicular network. FASEB J 13(Suppl):S101-S112.

Castillo AB, et al. 2006 Low-amplitude, broad-frequency vibration effects on cortical bone formation in mice. Bone 39:1087-1096.

Xie L, et al. 2006. Low-level mechanical vibrations can influence bone resorption and bone formation in the growing skeleton. Bone 39:1059-1066.


How are some people able to continue growing after reaching maturity?

Usually the cause is 'acromegaly' but there are numerous possible causes.

It is impossible to start growing in length after your bones have matured too much. This is because of the 'Epiphyseal plate' this is a anatomical structure in bones that is necessary for length growth in bones and it degenerates at the start of adulthood.

The most common cause, although still not a common disease, for gigantism is acromegalia. It's cause is an abnormally high amount of growth hormone in the body which is most commonly caused by a hormone secreting tumor.

When the onset of this disease happens before the epiphyseal plates have degenerated it can cause them to stay active in which case the patient will continue growing.

Note: When the onset is after the degeneration of the disks it doesn't cause gigantism but it still causes a very recognizable change in appearance and the model for Shrek in the movie suffered from this illness.

Edit: Sorry, I didn't notice your subquestions initially. Yes, another possible cause in men is the lack of testosterone because this hormone is normally responsible for the degeneration of the plates in men.

Edit 2: In women estrogen is the hormone that is responsible for this, which explains why the length of men and women isn't dependent on testosterone in both cases


Measure of diversity, accounting for known species

Simpson's estimator, which assumes that sample frequencies are not population frequencies, is unbiased on the probability scale. As @fileunderwater noted, it can be helpful to quantify diversity in terms of effective number of species, or Hill numbers. On this scale (the reciprocal of Simpson's concentration in this case), Simpson's estimator is no longer unbiased. Chao and Jost 2015 recently proposed some estimators for Hill diversity that formally rely on the total richness (of the sampled community) to estimate the true diversity of the community based on the sample, and argue that they have reduced the bias.

I sense, however, this is not exactly the same as your question. If I understand correctly, you have a known maximum diversity but not a known true cardinality/richness/total number of types within a given community/corpus whatever the pool you're looking at is called. In this case I might use maximum richness as a Bayesian prior; I might still use a Hill number as your metric but use the model to estimate that metric.

This 2014 review paper gets into these ideas a bit, or to take an Alan Turing perspective, you might find Zhang 2017 helpful.

Most diversity indices that ecologists use are not sensitive to total abundance, only relative abundance, so as Remi.b noted, classic indices (including Hill numbers) would all rank even communities with the same cardinality/richness identically; the only reason you're getting a difference between {1,1,1} and {2,2,2} with Simpson's estimator has to do with Simpson's solution to the bias in estimates of the community's diversity arising from using sample frequencies.


For how long and how cold should I perform ethanol/isopropanol precipitations of RNA or DNA?

I always did mine at -80 C, but I never compared the results to other protocols (I don't fix what's not broken). But, I was curious about the same thing, so I looked around. I found one paper discussing this: Paithankar and Prasad, Nuc Acids Res 19(6):1346 (1991)

It shows that at low concentrations, EtOH at RT actually outperforms the precipitations at both 4 C and  dry ice/ethanol bath. That difference is quite big at 100ng/ml DNA and lost when there is more than 10 ug/ml DNA. For typical extractions, based on this data, I'd do it at RT.

On the other hand, Hilario and Mackay say in their book that:

  for genomic DNA isolation, different DNA precipitation temperatures
  and incubation times have little effect on recovery rates. One can
  directly centrifuge after adding ethanol without the -20 C incubation,
  and, it -20 C ethanol is not available, room temperature ethanol can
  be used.

They do not, however, provide any citation for that statement.


In what circumstances does a mammalian egg copy its DNA?

The writers of the show may have been somewhat imprecise either by accident or intentionally to avoid excessive details.

There are several different stages of egg cells, with distinct names for each and for the process that leads from one to the next. The whole process of egg cell creation is called [Oogenesis].1 To quote Wikipedia:

  Oogenesis starts with the process of developing oogonia, which occurs
  via the transformation of primordial follicles into primary oocytes, a
  process called oocytogenesis.[4] Oocytogenesis is complete either
  before or shortly after birth.

To our current knowledge all primary Oocytes are present at birth. The next stage in the maturing process is called ootidogenesis, which produces an ootid.

  The succeeding phase of ootidogenesis occurs when the primary oocyte
  develops into an ootid. This is achieved by the process of meiosis. In
  fact, a primary oocyte is, by its biological definition, a cell whose
  primary function is to divide by the process of meiosis.[8]

  However, although this process begins at prenatal age, it stops at
  prophase I. In late fetal life, all oocytes, still primary oocytes,
  have halted at this stage of development, called the dictyate. After
  menarche, these cells then continue to develop, although only a few do
  so every menstrual cycle.

  Meiosis I of ootidogenesis begins during embryonic development, but
  halts in the diplotene stage of prophase I until puberty. The mouse
  oocyte in the dictyate (prolonged diplotene) stage actively repairs
  DNA damage, whereas DNA repair is not detectable in the pre-dictyate
  (leptotene, zygotene and pachytene) stages of meiosis

DNA replication is completed before Meiosis occurs. So oocytes do not replicate DNA after birth, but they do repair DNA to fix mutations that may occour after birth but before conception. If DNA repair fails, then mutations may persist. So the show would appear to be wrong about egg cells copying DNA in an adult bear, but right in that mutations might occur during its lifetime affecting its offspring.


Healing in the body is normally independent of the brain. Following an injury, a process of inflammation attracts lots of cells to the site of the injury (including platelets, white blood cells, clotting factors). There's also vasoconstriction (tightening of your blood vessels) to reduce blood loss from the injury site. Your skin cells continue to divide rapidly until new skin replaces the damaged one which later falls off. This is a highly simplified version of the process but hope it makes sense. So in summary, healing takes place by cell division (also known as mitosis).


Does reversion of resistant strains to wild-type only occur when no more drug pressure is exerted

I am not an expert on HIV but I am answering based on general principles.

This is a typical example of selection of individuals/populations with different fitness.

Reversion to wild-type (WT) would happen if the WT has higher fitness in that environment. Assuming that WT is the fittest under drug-free conditions, it is not difficult to understand that the WT population will outgrow other mutants.

For your question — "would a drug resistant HIV population revert to WT under treatment with other drugs", the simple answer would be no.

Explanation

HIV generally acquires resistance against different drugs quickly because it has a high mutation rate. In your example case, the HIV population that is resistant to the new drug will outgrow other populations if we assume that the selection is strong. There would not be any reversal to WT because WT would also be unfit in the new environment. If the selection is weak then the population genetic diversity would depend on the relative fitness of different genotypes.

There may also be pleiotropic effects: mutations that provide resistance against one drug can also possibly provide resistance against other drugs. This is well known in case of bacteria and there are many reports for HIV too (Rhee et al, 2010, Other Google Scholar Hits).


The Biopython 1.65 ABI parser should expose the chromatogram data, as of Biopython 1.66 it should expose everything.

UPDATE: Example using this for plotting here: http://biopython.org/wiki/ABI_traces


Microscope parameters for whole blood alalysis

As I found out in medical lab-groups, the most lab-workers use 100x Objective (oil or dry Leica objectices) and 10x ocular. This results in 1000x and the images like the below.

My idea was to use 20x objective (as it is much easier to handle) and 14MP camera. The erythrocyte should have the resolution about 60x60 pixels then, which should be enough for the differentiation.


How many different kinds of polypeptides, each composed of 12 amino acids, could be synthesized using the 20 common amino acids?

Judging from what you have said, I assume that combinatorics is not a problem to you.

I believe your problem is that you think Glu-(Met)x11 is equivalent to (Met)x11-Glu, just turned around. However, that is not a correct mindset. Amino acids are not symmetrical molecules, therefore reversed linear combination does not create a turned-around (be it chiral or not) form of a similar amino acid. My guess is that you write amino acid names in consecution when representing peptides. This method has a small problem that it does not incorporate directionality of molecules. Drawing the whole molecule may be a solution, but that is too much chore.

My solution is to add a small mark (perhaps an arrow, or a > mark) to represent a specific side of the amino acid molecule (amine group or carboxyl group), so that mirroring the sequence (so that the mark would be at the "other" side of each amino acid) would actually create a peptide molecule different from reversing the sequence (so that the mark is still at the "normal" side of each amino acid). If you think that doesn't look good, you can draw a frame around each amino acid, where one side of the amino acid has a dent and the other side has a bump (to represent the amine and carboxyl groups) so that only a bumped side can connect to a dented side. Mirroring the sequence would also reverse the positions of the bumps and dents, thereby creating a different peptide molecule than merely reversing the sequence while keeping the positions of the bumps and dents in place.


Are there ontologies for the description of the look of plants?

To transform an object in an ontology to an image of that object?  Sounds unlikely, I doubt that any botanical ontology is that developed and detailed.  It would be great if it worked.  Could be used to check the ontology.  The website https://www.ebi.ac.uk/ols/ontologies lists 251 biological ontologies.  There are several on specific plants or groups of plants (brassica, beet, oats) and several that might be more relevant to you: Plant Ontology, Plant Phenology Ontology, and Plant Trait Ontology,


Short answer

Yes, brain transplantation is technically possible, but only for short periods of time, and only in experimental settings.

Background

In terms of a full-brain transplant there has been only one group that have made serious attempts in doing this (according to wikipedia and a literature search on my end). In the 1960's White and colleagues transplanted canine brains from one animal to another (White et al., 1965). In total 6 brains were transplanted. However, the recipients' brains were not removed and the brains were merely surgically transplanted into the neck region of the recipient animal, and connected to the recipient's cervical vasculature (carotide arteries and jugular vein). Hence, the recipient canines ended up with two brains. The authors, however showed with these experiments that the transplantation of brains was feasible, and that the transplants survived and remained functional, which was evidenced by EEG activity. The brains survived from 6 hours up to two days.

Later, White and colleagues worked out a way to keep an isolated (but blood-perfused) monkey brain alive outside the skull, potentially allowing for a primate brain to be transplanted (White et al, 1975). The procedure could include longer-term 'storage' of the brain by cooling it, making the possibility of transplantation more feasible. However, White realized the difficulties with this approach, since, and I quote:

  [...] by definition the brain must be isolated before the transplantation, and thus requiring all nervous tissue connections to be severed (e.g. cranial nerves and spinal cord), the isolated transplanted monkey brain is without a mechanism to receive or transmit information.

To address this issue White et al. set out to transfer  the entire cephalon (head) of a monkey to the body of a recipient whose own cephalon had been removed at a mid-cervical
level. Under these circumstances the brain, being within its own cephalon, still connects to the cranial nerves:

source: University of washington

White et al. succeeded in transplanting a head, but the preparation rarely survived longer than three days due to haemorrhagic shock (White et al, 1975). Basically the recipient was quadriplegic, as the face was fully functional and White comments, and I quote:

  Observe the wakeful appearance of the cephalon and the obvious movement of the facial musculature with open mouth and eyes. This preparation gives every evidence of being in intelligent contact with its environment. [...] Cortical [EEG] activity in this preparation demonstrates awake recordings.

Hence, with the current available technology it does not make much sense to perform a brain transplant, as the transplanted brain cannot be functionally (neurally) connected to recipient body. However, strides are being made in re-connecting a severed spinal cord (Canavero, 2013), endeavors that could bring head transplants a little closer.

Quadriplegic people obviously face extreme psychological challenges (Sane Australia). However, even when they have become quadriplegic due to an event later in life, they are not mentally changed, in that they are still 'themselves'. Therefore, although human transplants never have been done, I dare to say that the transplanted head will determine the psychological 'self' of the recipient body, which includes memory and personal traits. At least, assuming the brain can be transplanted without inflicting neuronal damage.

References
- White et al. Science 1965;150:779-81
- White et al. Resuscitation 1975;4,197-210
- Canavero et al. Surg Neurol Int 2013;4:S335–S42

Further reading
- CBS News


What is the structure and function of chromosomes during interphase?

So the DNA in some chromosomes must have the pieces of information about how to do the DNA replication. - I am not sure about thing.

Genomes contain what is called the "origin of replication" - specific sequences in the DNA that tell DNA polymerase where to bind and to initiate replication.

As for your main question, I'm a little confused as to what you're asking. In a general sense, chromosomes function as carriers of genetic information. In eukaryotes, nuclear DNA is organized in the nucleus on linear chromosomes which carry most of the genetic information an organism needs to survive. In bacteria, the chromosome is a circular piece of DNA. In eukaryotes, the chromosome is also bound by histone proteins, which serves to regulate expression of certain genes and to help anchor the chromosomes to the inner nuclear membrane.


Yes, Sodium phenylbutyrate can upregulate the transcription of silenced genes by inhibiting the activity of Histone deacetylases (HDACs).
Histone acetylation performed by Histone acetyltransferases (HATs) helps in activation of genes, while deacetylation performed by HDACs is responsible for gene silencing. This makes HDACs a potent drug target to treat malignancies.

The inhibitors of HDAC regulate the chromatin structure which loosens the chromatin and hence effect the binding of transcription factors to DNA.  This binding modulates the expression of genes playing role in cell cycle and apoptosis, thus effecting cell growth and differentiation. (Reference)

But this is not similar to double negative. Double negative is term used in embryogenesis, where a particular repressor gene is activated in specific regulatory state. (Reference)


Natural examples of XOR functions at the cellular level

When I think about your question of natural examples of XOR, it pushes me to think about what type of natural environments (i.e., evolutionary pressures) would lead to the selection of an XOR equivalent.

When we implemented a synthetic XOR by "double flipping" one transcription terminator as a type of gene expression "check valve" it was the case that I did not know of any natural examples of flipping terminators, whereas I know of several examples of nature flipping promoters.

Why do we have plenty of natural examples of flipping promoters but (unknown to me at least) as yet no charismatic examples of naturally flipping terminators?

Perhaps we haven't been looking in the right environments to find them?

E.g., for a terminator to exist in nature, there needs to be something that must  be expressed upstream of the terminator, and also something that should not be expressed downstream of the terminator.  Since there are plenty of terminators there must plenty of examples of nature selecting for terminators.  My favorite example is the "Tø" terminator in phage T7 that is just downstream of the major capsid gene (highly expressed) but just upstream of a minor particle protein (weakly expressed).

But now reason thru what would need to be true in order to select for terminator flipping.  I'd need all the requirements of a static terminator (above), and then another such pairing of selective requirements under different environmental circumstances for additional gene products encoded in the opposite direction on the complementary strand of DNA. Phew!

I'm not saying that it is impossible to imagine such a complicated coupling of selection requirements emerging in nature, but it definitely seems a much more improbable aggregation of selective pressures to co-mingle all within a single genetic loci.

I'm still nevertheless very curious and would be grateful to learn of any natural examples.  -DE


Central of Dogma? reverse transcriptase says No

Go to wikipedia and look reverse transcriptase. All your questions will be answered. But to answer your question, reverse transcriptase is an enzyme that uses RNA molecules as a template to make a DNA version of said RNA. ie the flow of information from DNA to RNA is reversed.

The central dogma... is a terrible name. It was an idea state in the 1950s that information flows one way from DNA to RNA to protein. The use of the word dogma is an ill choice to use. Because science does learn new things. And given that DNA was only just discovered in the 1950s....ie the same decade... the word dogma is a bad idea. SHould have waited a few more decades first

Anyhow... the discovery of reverse transcriptase allow information to flow back from RNA to DNA. The discovery of siRNA.. mean RNA can control DNA. The discovery of prions... lead to current work now where pre-existing proteins can be templates for the folding of newly synthesised protein. DNA methylation allows epigenetic inheritance. Ie changes of certain protein levels (say during starvation) in your body can leave inheritable marks on your DNA (which will then affect the behavior of those gene in your children).

The central dogma now (if it still is used) has a lot more lines leading up and down the chain.


Is there a standard reference for the importance of tumor heterogeneity?

It's quite interesting that the first reference that come to mind is not a mathematical/theoretical one (which is, in all likelihood, going to be a lot older than the one I am going to mention) but a clinical one. That would be Gerlinger and Swanton and their paper in the New England Journal of Medicine.


The size, shape and leg arrangement as it hangs upside-down in the web, marks this spider as an Argiope, as previously noted.  The big white band on the front of the abdomen suggests A. argentata, but the photo is blurry enough that some of those spiders might be A. trifasciata.  I'd be happy to put it down as Argiope species, in the hope that more, and closer photos of this neat and completely harmless (to humans) spider are forthcoming.

https://bugguide.net/node/view/2033


How do you remove DNA/RNA from plastics?

Lab cleaning solutions can be bought which remove/destroy nucleic acids such as this one. UV is another technique for destroying DNA. And bleach is used to remove contaminant DNA in ancient DNA studies.

Searching for a DNA/RNA lab cleaning protocol would be a good idea to - something like this.


What is an explanation of the dual role of calcium hydroxide in teeth?

For more than 70 years calcium hydroxide has played a major role in endodontic therapy, although many of its functions are now being taken over by the recently introduced material MTA. Calcium hydroxide may be used to preserve the vital pulp if infection and bleeding are controlled; to repair root fractures, perforations, open apices and root resorptions [1].
Calcium ions released from calcium hydroxide stimulates fibronectin synthesis in dental pulp cells. Fibronectin might induce the differentiation of dental pulp cells to mineralized tissue forming cells that are the main cells to form dentine bridges, via contact with cells [2].
Calcium hydroxide ($Ca(OH)_2$) is known to cause internal resorption in the deciduous dentition. Though this has been attributed to chronic inflammation and odontoclasts, the exact mechanism has not been elucidated. $Ca(OH)_2$-induced odontoclastogenesis could be multifactorial. Odontoclasts may result from fusion of cells of monocyte/macrophage series either due to inflammatory mediators or through stimulation by stromal odontoblasts / fibroblasts. Pre-existing progenitor cells of primary tooth pulp because of their inherent propensity may transform into odontoclasts [3].

References:

Carrotte P. Endodontics: Part 9. Calcium hydroxide, root resorption, endo-perio lesions. Br Dent J. 2004 Dec 25;197(12):735-43. doi: 10.1038/sj.bdj.4811897. PubMed PMID: 15608732.

Mizuno M, Banzai Y. Calcium ion release from calcium hydroxide stimulated fibronectin gene expression in dental pulp cells and the differentiation of dental pulp cells to mineralized tissue forming cells by fibronectin. Int Endod J. 2008 Nov;41(11):933-8. doi: 10.1111/j.1365-2591.2008.01420.x. PubMed PMID: 19133082.

Ravi G R, Subramanyam R V. Calcium hydroxide-induced resorption of deciduous teeth: A possible explanation. Dent Hypotheses [serial online] 2012 [cited 2014 Jun 7];3:90-4.


Are omeprazole and other members estrogenic and/or antiandrenergic?

There is not a lot of evidence that the compound itself is estrogenic, but it may affect how estrogen is metabolized in the body, leading to feminizing outcomes.

Pubmed is a good source for information in the biomedical literature- here is a pubmed search that has more information on those terms.

Looking through some of the results of that search, I find that there seems to be a fair amount of evidence that omeprazole has something to do with gynecomastia, but the association is not strong:

A review of the literature has some conflicting information. One study of general practice in Britain suggested no detectable statistical relationship between taking omeprazole and gynecomastia. However, a smaller study suggested that in people who experienced gynecomastia who were also taking omeprazole, removing omeprazole helped in the majority of cases. I suggest reading the section of that review on omeprazole. The conclusion of the review is that omeprazole probably has a role in gynecomastia.
There is a literature of studies (mostly in Spain?) ascribing omeprazole a role in gynecomastia. One example.
There is evidence that omeprazole has a chemical effect on estrogen metabolism. However, it was much less strong than some other drugs examined.
There is evidence that omeprazole slows the metabolism of estradiol, an active estrogen compound (see Figure 2 in the review linked above).

Overall, people seem to say it (and related compounds) probably has something to do with gynecomastia, but it is not a principal contributor on average. Possibly it shows a synergy with some other drug or some lifestyle variable.


Why is SOC medium recommended for transformations?

To summarize from Hanahan's paper (see below for reference), he carried out a systematic review of conditions necessary to improve transfection efficiency. Among the conditions tested were the presence of various cations (Ca2+, Cs+, Mn2+, K+, Mg2+), DMSO, and growth temperatures (and a few other conditions not so commonly used these days). He worked with a strain that he subsequently isolated a derivative of, called DH1, which is now available commercially as DH1-alpha and other strain derivatives.

He defined transformation efficiency to be the number of transformed colonies on a plate, a measurement still used today. He found when the transforming media contained: certain cations, specifcally Mn2+, Ca2+, Rb+; as well as DTT, hexamine cobalt (III) and DMSO; greatly improved the transfection efficiency compared to the standard Ca2+ treatment. He also found that sucrose and K+ were useful, though not strictly necessary for his experimental strain. It was stated in this paper, though not explained, that sucrose acted as a stabilizer, possibly to guard against his initial use of 0°C incubation and/or freeze/thaw cycling. For the rest of his work, he did not use sucrose.

Among his conclusions, he states that DTT is necessary, as well as di-valent and mono-valent cations, but that they seem to be nonspecific. In other words, there is no strict requirement for having Ca2+, since Mg2+ and Mn2+ perform equally well, nor is there a requirement for K+, though it's admittedly easier to use than Rb+.

There are today a number of "rich" media broths that are available: SOB, SOC (SOB + MgCl2 and sucrose), 2xYT, NZY+, TB, etc. All of these are superior to LB for transformation purposes because of the refined salt balance and in particular the inclusion of these di-valent and mono-valent cations. Sucrose seems to be included for the ease of metabolism and stability of the heat shock process (though I can't find a paper explicitly explaining why it is used, other than tradition).

The two most common ways to transform bacteria are to have them chemically compentent (E. coli already in a rich media broth) or to electrically transform them (electroporation). The purpose of both of these is to induce holes into to cell membrane of the E. coli (chemical transformation relies on the heat shock process for this). Once these holes are made, DNA is free to enter into the bacteria. Naturally, this process is very traumatizing to the E. coli, especially since chemical transformation has the added insult of temperature shock (0°C to 42°C then back down to 0°C).

Substituting LB for any rich broth, such as SOC, will greatly improve transformation yield. If a protocol calls for SOC media, and you don't have any, you may substitute for another rich media. I have used 2xYT for SOC many times quite successfully, and as I stated earlier, only the valence number for the various ions seems to matter, so just make sure they are present.

It was my understanding that sucrose/glucose was added as an additional nutrient source for E. coli to expedite their recovery from the transformation protocol. I speculate that this is the case. Hanahan refers to sucrose as a stabilizer but does not define what it is stabilizing. I speculate that it acts as a cryopreservation aid and prevents ice crystal formation when undergoing cooling on ice in the heat shock method. Given the earlier bio.SE question about shifting E. coli feedstocks, it seems unlikely that sucrose will be used as a nutrient source in the one hour growth period immediately after transformation because that article quotes 4-12 hours as the common time range to shift metabolism from amino acids to carbohydrates.

Sources:

Hanahan D. Studies on transformation of Escherichia coli with plasmids. J Mol Biol 1983 166(4):557-80.


Glycolysis step 5: isomerization by triose phosphate isomerase

"Why" questions in biology tend not to make sense-
https://en.wikipedia.org/wiki/Teleology_in_biology

But perhaps if I narrate the reaction it will connect with your intuition.
Let's look at the reactions in question:

https://en.wikipedia.org/wiki/Glycolysis#Summary_of_reactions

Step 4 in glycolysis cleaves fructose 1,6-bisphosphate into two molecules that are isomers. One isomer (glyceraldehyde 3-phosphate, GADP) is a reactant in step 6, and fuels the “payout phase” where glycolysis reactions begin to yeild ATP and NADH. So what happens to dihydroxyacetone phosphate (DHAP), the other product from step 4? How can we extract energy from this?

Reaction 5 is the interconversion of GADP and DHAP. So as GADP is consumed by reaction 6, reaction 5 will, by Le Chatlier’s principle, lead to net conversion of DHAP to GADP. The GADP produced by this isomerization then also feeds reaction 6. In this way, both of the products of reaction 4, GADP and DHAP, are channeled down the chain to fuel NADH and ATP production.


Web spinning in spiders is a complex behavior and probably involves a number of different factors, genetic and environmental. Genetically there are surely many different genomic regions underlying the development and expression of the behavior.

Is the algorithm for web spinning directly encoded in the DNA? Not directly. There is not a single region of contiguous DNA sequence that codes for all the steps involved in building a web. Instead, there is a sequential and parallel developmental process beginning at fertilization (earlier if you include parental epigenetic modifications) - encoded and regulated by the genome and its products - that, without too many errors, generates a viable and fertile web-spinning organism. But the DNA sequence involved in that algorithm is spread all over the genome and includes coding genes, non-coding (ncRNA) genes, and regulatory regions. And the genome alone will not carry out an effective algorithm without proper environmental inputs like nutrition and parental provisions.

The act of constructing a web, when and where, and the design of the web is likely carried out via brain architecture and neuronal patterning, but of course these structures are built based on the DNA-based, developmental algorithm. In that sense, there are many nested levels of algorithms.

One of the best models used for studying behavioral genetics is the fruit fly Drosophila. Many different behaviors have been studied at the genetic and molecular level in Drosophila including courtship, foraging, sleeping, and memory-related tasks. A popular science book on behavioral genetics worth checking out is Time, Love, and Memory by Jonathan Weiner. It details the work of Seymour Benzer and provides a lot of background and easily understood explanations of how genes and their products can work together to exhibit complex phenotypes like sleeping patterns. It includes a detailed (though not up-to-date) description of circadian gene circuitry and how it develops.

At the moment, the best that I can think of for an algorithm directly encoded for by DNA is the sequential activation of HOX genes for animal body plans. But even in this case DNA code does not progress through correct development without other factors.


I don't believe this question is an exact duplicate of the question at Do bacteria die of old age?, however all of the comments and answers provided there are relevant, and you should read them before continuing to read this answer because I won't repeat what's stated there.

In addition to bacteria and yeast which produce certain "rejuvinated" cells that can divide indefinitely while other cells become senescent or "aged", all multicellular organisms actually employ a remarkably similar strategy. Under certain culture conditions, embryonic stem cells can propagate indefinitely (1).

During early embryogenesis they divide "symmetrically" to the extent that all of the daughter cells are fully undifferentiated until after gastrulation (2), but there is a certain degree of asymmetry that defines the axis along which gastrulation occurs prior to gastrulation (3). This asymmetry is mediated by a large number of signaling pathways (3), some of which become asymmetric during the very fist cell division of the embryo. Adult stem cells also divide asymmetrically primarily as a precursor to differentiation, but this is thought to also be involved in the asymmetric distribution of damaged components to their more differentiated daughter cells (4), as occurs in yeast and bacteria. Currently there is less research on this in adult or embryonic human stem cells than in bacteria or yeast, but it stands to reason that our embryonic cell line does the same thing beginning at its first division, and our germ line is immortal (we're no "older" at birth than our great-great-great-great-great-great-grandfathers) for the same reasons that unicellular cells are immortal.

References:

(1) https://en.wikipedia.org/wiki/Embryonic_stem_cell#Propagation

(2) https://en.wikipedia.org/wiki/Embryonic_stem_cell#Pluripotent

(3) https://en.wikipedia.org/wiki/Gastrulation#Loss_of_symmetry

(4) http://www.ncbi.nlm.nih.gov/pubmed/25966295


Difference between reciprocal inhibition and regular muscle movement?

What is the difference between reciprocal inhibition and regular muscle movement?

Reciprocal inhibition is part of regular muscle movement. It is controlled by the stretch reflex controlled by the muscle spindle. It's an important part of a functioning muscle and spinal cord, and not pathologic at all. However, this same reflex, in an excessively tight muscle on one end of a joint, would cause an excessively loose muscle on another end of a joint.

Here is an image showing this reflex, from Brust Practice of Neural Science, Chapter 6.

I can't give you any medical advice on this site, so I can't put that in context, but I think that answers your biology question.