What is the difference between conditional and inducible activation?

In my opinion the terms inducible and conditional are synonyms. Together with the term constitutive they refer to how transcription takes place, that is, the second phase in the central dogma that states that genetic information is propagated from replication to transcription to translation. The proteins that are produced during translation by ribosomes can have a feedback effect on replication and transcription.

When proteins bind to the promoter region of genes, they can induce or inhibit transcription. If a gene is preceded by a promoter region that always promotes transcription, it is said that the gene has a constitutive promoter. If the gene is transcribed conditionally, it may refer to proteins having to bind to the promoter region so that transcription can take place. There could be inverse situations and I believe the Cre/Lox technology is an example of such a situation.

Take the following as an example. A gene could be lethal meaning that if the protein it encodes is expressed it will kill the cell. It could have a promoter that promotes expression if a protein with an inhibitory effect is not bound to the promoter. Suppose I have these cells in a culture plate and I add some compound to the culture plate. The compound diffuses into the cells and binds to the inhibitory protein that is bound to the promoter region. With this binding of the compound to the protein that is in turn bound to the promoter region, the protein loses its ability to bind to the promoter region and inhibition of transcription is uplifted. Transcription then continues and expression of the lethal protein takes place after which the cell dies.

This could be used in practice as follow: if you were selling seeds to farmers, you would want them to buy seeds next year again, so you want the plant not to be able to produce viable seeds.

Coming back to your question, if you want to know more about the mice in question, you should contact the breeder as nomenclatures differ. See this article on interpreting mouse genetic nomenclature:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3039125/


It depends on species and situation.
There are a lot of different solitary wasps, the kind you are referring to are parasitic wasps, that lay their eggs in or on a host for the larvae to feed on before they pupate to reach the final stage of their lifetime.
Some larvae that consume a host in groups take as little as twelve days to consume their host and eat their way out.
However, this wasp species can even have their larvae remain in the larval stage through winter and adapt through seasons. it's entirely dependent on what sort of wasp you're asking for what the time span would be for a larva to mature.


A good software for agent based modelling?

My boss is a big fan of Repast HPC, but since Repast is a C++ framework it might not be the right choice for you. It takes a loooong time to write a good C++ program (even for someone who already knows the language fairly well), although it will run very quickly once it's written. A one or even two year long Master's program will end up going by surprisingly quickly, so if I was in your shoes I'd choose to start with the simplest thing possible (ie Netlogo). Once you have a finished product, even if it's somewhat more simplistic than you'd like, it'll be much easier to work your way up from there.

Really though, consider the choice of modeling framework to be part of your research project! Only you can come up with the right choice for your project, though as a practical matter you should heavily favor any framework that at least one person in your department already has some experience using. Things will go wrong, you will have questions, and Stack Overflow won't be able to answer all of them.

Here's a list of the more interesting agent-based modeling frameworks that I found from a few minutes of googling:

Repast HPC

pros:

C++ based
The only performance focused one of the bunch

cons:

C++ based
For simple models, would be like building a supercomputer to use as a pocket calculator

Netlogo

pros:

Focused on being accessible to non-programmers
Scripting language seems pretty straightforward

cons:

In my experience frameworks that try to implement their own scripting language in an attempt to be accessible to non-programmers ultimately end up being much more complicated to use than frameworks based around an established language. But I'm not the target audience.

Mesa

This one is Python based, so it's the one I would personally try first since I find Python to be the best language for quickly writing scientific programs of reasonable complexity. That's my own personal bias, so your mileage may vary

MASON


Why is the ingestion of salt and water beneficial to muscle cramp

Maybe it isn't.

  The standard theory: muscle cramps are caused by loss of fluids and electrolytes, which alters fluid balance in the body and increases the excitability of nerves.

  The "new" theory: muscles cramps result from "altered neuromuscular control," which can be triggered by a variety of factors, including genetic predisposition, damaged or fatigued muscles, starting too fast, and not tapering enough -- none of which have anything to do with hydration or electrolytes. [...]

  A few years ago, researchers at North Dakota State University published a study showing that dehydrating subjects by 3% of their initial body weight didn't change their susceptibility to muscle cramps (as measured by threshold frequency). Now, in a new British Journal of Sports Medicine study, they've extended those results to a greater degree of dehydration: their 10 subjects reached an average dehydration of 4.7% (greater than 3% is "significant" dehydration, while greater than 5% is "serious") after almost four hours of exercise in very hot conditions. Crucially, they exercised only with their non-dominant limbs, while the cramp testing was performed on their dominant leg, so that muscle fatigue/damage could be eliminated as a triggering factor.

  The result: no difference in cramp susceptibility or intensity, despite an extreme dehydration protocol that saw them lose about 4 g of sodium! The researchers conclude that their data supports the "altered neuromuscular control" theory.

Even the older research that did find it more plausible that electrolytes were a cause wasn't very adamant that's the [only] cause, e.g.:

  Consumption of a carbohydrate-electrolyte beverage before and during exercise in a hot environment may delay the onset of EAMCs [Exercise-associated muscle cramps], thereby allowing participants to exercise longer. However, it appears that dehydration and electrolyte loss are not the sole causes of EAMCs, because 69% of the subjects experienced EAMCs when they were hydrated and supplemented with electrolytes.

There are a few [not very well controlled, IMO] experiments from the 1920s and 30s (three papers to be more precise) that did find a role for sodium depletion in some cases of mild cramping. The most controlled of these (published in 1936) involved sodium depletion for 10 days (daily sweating and virtually no intake), which  is hard to argue is that common in most cramp suffers. The original paper notes that the level of sodium depletion involved led to quite a few other symptoms:

  Such deprivation led to aberrations of flavour, cramps, weakness,
  lassitude, and severe cardio-respiratory distress on exertion. The nitrogen balance became negative and the blood urea rose.

And despite the severe sodium depletion, the cramps were mild but generalized:

  These muscular cramps were not of the very severe localized type which are
  said to affect stokers and miners (Moss, 1923-24), but were widespread,
  frequent, not very painful, and generally controllable. Any muscle in
  the body was liable to go into spasmodic contraction, especially if some
  little effort was demanded of it (Moss, 1923-24). “ Coughed a little
  over something, cramps round chest, mild.” * R.B.N. experienced
  occasional cramps in the muscles lining the floor of the mouth but the
  extremities were most affected, and it was possible sometimes by suitable
  movement of the toes to alternate the spasms for hours on end between
  the extensor and flexor muscles. Perhaps the most characteristic of all
  were the manual cramps. R.A.M. experienced “ constant mild cramps
  of the fingers and thumb when using forceps at the balance,” * and R.B.N.
  found that he “ cramped quickly when working, telephoning, or using
  pipettes.” *

So that's why I say these types of cramps probably have little relevance for those experienced by most people.

I'm not sure there any studies for potassium. The paper reviewing the sodium evidence notes:

  Mechanisms in heat cramping remain murky. Sodium loss contracts extracellular fluid space and may alter ion channels to make neuromuscular junctions or muscle units hyperexcitable, thus evoking
  involuntary and sustained contractions, or heat cramping. And, not all camps buy salt loss for  cramps. Bananas, for example, remain popular in some football camps, to prevent heat cramping by ‘replacing potassium’. But here, bananas are yellow herrings because little potassium is lost in sweat. The same applies to calcium and magnesium. Sweat after all, is mainly water and salt (sodium chloride).

And do note that his latter paper is written by a Gatorade consultant.

One 2009 review in clear opposition to relevance of electrolytes-water for the usual exercise-related muscle cramps notes:

  In summary, dehydration and electrolyte depletion are often considered together (and recently together with muscle fatigue) as the “triad” causing EAMC. The key components of this hypothesis (fig 1) are that electrolyte (mainly sodium) depletion through excessive sweat sodium loss together with dehydration causes EAMC. However, results from prospective cohort studies consistently show that athletes suffering from acute EAMC are not dehydrated, neither do they have disturbances in serum osmolality or serum electrolyte (notably sodium) concentrations. Furthermore, sweat sodium concentrations measured during exercise in 23 reported cases with a past history of EAMC are not higher than those reported in many other studies. Both electrolyte depletion and dehydration are systemic abnormalities, and therefore would result in systemic symptoms, as has been observed in other clinical conditions. However, in EAMC, the symptoms classically are local and are confined to the working muscle groups. Thus, the available evidence to date does not support the hypotheses that electrolyte depletion or dehydration cause EAMC — therefore an alternate hypothesis for the aetiology of EAMC has to be considered.

Suffice to say that this field is still quite contested... and plagued by conflicts of interest. Witness a 2019 paper finding that a magic electrolyte formula (contents not disclosed) from a pharma company absolutely does lower the risk of cramps after exercise compared to water. Study funded by aforementioned pharma company, of course. And the press reported this as "water after exercise increases risk of cramps" (by diluting the electrolytes in your body, of course), arguably due to the authors' summary.

And while most of the previous material was about exercise-related cramps, even for the nocturnal cramps more often experienced by the elderly, the role of electrolytes appears uncommon; according to a 2007 review:

  Muscle cramps, notably nocturnal leg cramps, are common symptoms experienced by general medical patients, particularly the elderly. Their etiology is varied; most commonly, these cramps are idiopathic. With the notable (and relatively rare) exceptions of serious electrolyte imbalances including hypokalemia, hypomagnesemia and hypocalcemia, these cramps are typically benign in nature. [...]

  The second recent study to challenge the notion that diuretics [which promote a loss of electrolytes through urine] are a common cause of muscle cramps was a cross‐sectional survey of 365 general medical patients. Although the prevalence of leg cramps in this cohort was 50%, no associations were found between these cramps and any medication except analgesics that were used to treat the cramps. [...]

  Nevertheless, a review of the Physicians' Desk Reference database (available at www.pdr.net) suggests a consistent association between diuretics and muscle cramps. [...]

  The mechanism of diuretic‐associated cramping (if such an entity truly exists) is likely related to hypokalemia, hypomagnesemia, or volume contraction (with or without metabolic alkalosis). Hypocalcemia is a possible cause during therapy with loop‐diuretics such as furosemide, but is unlikely with the hypocalciuric thiazide‐type diuretics. Interestingly, potassium‐sparing diuretics, such as amiloride, are also associated with cramping. Thus volume contraction appears to be the one mechanism that is common to all classes of diuretics.

A 2012 new large-scale investigation did point to some epidemiological associations between cramps and diuretics:

  Cramp treatment was substantially more likely in the year following introduction of LABAs [long-acting β2-agonists], potassium-sparing diuretics, or thiazide-like diuretics, and 60.3% of quinine users (individuals experiencing cramp) received at least 1 of these medications during a 13-year period. In contrast, statin and loop diuretic associations were small. Physicians should be mindful that the use of these medications may worsen symptoms in patients experiencing nocturnal leg cramps.

And they also have some comments on putative mechanisms:

  Physicians may be surprised that potassium-sparing diuretics have a stronger link to cramp treatment than loop diuretics. Yet, hyperkalemia facilitates neuronal excitation, and hypokalemia suppresses motor neuron activity. β2-Agonists are known to have a stimulatory effect on motoneurons, and β2-adrenergic receptors are found on peripheral nerves.


Are there examples of Apis mellifera of different colors?

I've been reading a little more, and found a partial answer.

Not sure about albinoes, but Wikipedia lists a few different colors, arguably substantially different:

Under Apis mellifera subsp. ligustica (the Italian honeybee),

Leather
Bright yellow (golden)
Very pale yellow

Under Apis mellifera caucasia (Caucasian honeybee),

Dark with brown spots at times

In fact, both photos below are reported as Apis mellifera, here and here respectively.


Confusion about Lotka_Volterra model for two competing species

This is probably not a very satisfactory answer. The very next step in Murray's book (3rd Ed) there is a non-dimensionalised version of the model (eq 3.32) which looks like the one given in Boyce's book (10th Ed) except $\epsilon_i$ and $\sigma_i$ (eq 2, Ch 9). If you plug in $\epsilon_i = \sigma_i = 1$ in Boyce's book you get the same fixed point expression (eq 36) as Murray's book.

The idea is: in the RHS of a $\frac{dx_i}{dt}$ term the $x_i x_i$ represents intra-specific interaction and the $x_i x_j$ represents inter-specific interaction between species $i$ and $j$. You can put constants wherever you like to scale these terms with an interpretation. But the qualitative behavior of the system doesn't change and the coefficients persist in algebra, based on how you plugged them.

But to literally interpret the extra factor in the second set of equations: you can think of them like if $a_{ii}$ is the scaling of intra-specific interference, then $a_{ij}$ is a scaling of $a_{ii}$ for inter-species interaction, i.e. the species $j$ interfere with species $i$ with $a_{ij} a_{ii}$.


What is background signal in a Western blot?

In this context (and many others), the terms "background signal" and "noise" can almost be used interchangeably, if that helps.
Generally speaking, noise or background refers to any signal that isn't coming from the thing you're trying to detect (typically in reference to how that signal might interfere or be confused with your "true" signal). So non-specific binding could qualify as background, but it can also refer to regions of the membrane that shouldn't have any protein binding (with any number of causes). One exception I can think of in practice is if you have a specific non-target band that consistently shows up, that might technically fit the definition (sensu stricto) of "noise", but a molecular biologist will more likely refer to it as a "technical artifact" rather than "background".
That said, there are still a number of different kinds of "noise" or "background" that may show up on western blots, and the article you referenced does a pretty good job of describing them, but it could benefit from including some images. Here's a similar guide with more images and links to other Western troubleshooting guides. Hope it helps.


Why don't we breathe nitrogen when it makes up most of the air?

Animals use oxygen as a chemical energy source because oxygen gas can react with many other compounds to form oxides, which releases energy and happen spontaneously.

Both carbon and nitrogen can be made to react with oxygen, but otherwise they are pretty inert.  So of all the gasses in the air present at over a fraction of a percent, oxygen is the only one we can use for energy.

Hydrogen (and sulfer) are both possible substitutes for oxygen in the role of redox energy source, but are normally pretty small components of our environment.  On another planet they might well be the basis of biometabolism.

Of course the fact that plants can use carbon dioxide to fix carbon is a different case of biology using a gas out of the air.  Its the defining quality of plants!

The energetics of using CO2 is endothermic - it requires energy input. They have to use sunlight to get the energy to utilize this energy and its very costly energetically.  Animals can afford to move and grow because they use oxygen while they eat plants.


Can someone identify this tree from the Pacific Northwest?

It looks similar to a Cotinus coggygria, which is a shrub that we call a Smokebush in the UK. But given your location, it could be Cotinus obovatus, known as American smoketree.

See http://dendro.cnre.vt.edu/dendrology/syllabus/factsheet.cfm?ID=415

The leaves will start green and progressively change colour to deep reds in the autumn with sprays of pink-purple flowers in the summer that from a distance look like smoke, hence the name.

Here are some images I have found on the web.

http://www.cirrusimage.com/tree_American_smoke.htm

http://allthedirtongardening.blogspot.co.uk/2012/08/smoke-tree-smoke-bush-coninus.html


Are all/most/any membranes comprised of lipids from the smooth ER?

It sounds like we're mainly interested in phospholipids here, as they're the main component of cell membranes. Since your question didn't specify, we'll talk about Bacteria/Archaea and Eukarya separately

Bacteria/Archaea

Here, the answer is fairly intuitive. Bacteria and Archaea don't have endoplasmic reticulum, so they can't synthesize phospholipids in it. In this case, it seems like they create fatty acids directly from enzymes in the midst of the cytosol.

Eukarya

Here, the answer is a bit more complex. Fortunately, there are some good reviews about the topic that answer the question. Here, they talk about the entire phospholipid biosynthesis pathway and only mention the ER as an organelle, although it's worth noting that there are several sub-locations within the ER where specific groups are added. However, they fail to distinguish between rough and smooth. In another source, they mention not only the ER but also the mitochondria as having some ability to synthesize phospholipids. That's pretty cool, in my opinion.

TL;DR:

Bacteria and Archaea certainly don't rely on the smooth ER for lipid synthesis. In eukaryotes, there are several areas where lipids can be made but the smooth ER does seem to be the main source.


This paper is a compelling example of an effect of osmotic pressure on enzyme function. Restriction enzymes are normally very selective in the base sequences of sites at which they cut DNA, but in some conditions they show cutting at off-target sites, called "star activity." "Star activity" increased for some restriction enzymes almost linearly with osmotic pressure generated by a range of non-ionic solutes. Supporting the idea that the higher osmotic pressure was directly responsible, increased hydrostatic pressure reversed the effect of increased osmotic pressure.

Increasing the osmotic pressure is essentially decreasing the chemical activity of the water in the system. So it's not surprising that any enzyme reaction might be affected, particularly if the structures of active sites of enzymes are altered as suggested by the authors of the paper cited above.


What is the role of Aspartate Transaminase in gluconeogenesis?

I may have approached this problem from the wrong direction, so here's my attempt at an answer:

For gluconeogenesis to function, glycolysis needs to be shut off.  Glycolysis feeds the TCA cycle with Acetyl-CoA through the decarboxylation of pyruvate, and without glucose as a source, we need to look to other methods of generating OAA to make into PEP.  We can make OAA through Aspartate Transaminase by reacting Aspartate with α-ketoglutarate.


Fruit did not evolve from a single cell( except in the sense that plants did)  it evolved from seeds and their casing in angiosperms. Fruit is a means to disperse seeds. This will get you started on the different methods of seed dispersion.
https://www.britannica.com/science/seed-plant-reproductive-part

By enclosing their seeds in material animals want to eat, plants get animals to transport their seeds long distances and deposit them in a warm pile of fertilizer. Sugar is the easiest macronutrient for plants to produce so that is the what they pack their fruit with. animals tend to eat new growth which often contains seeds so it is easy to see how animals with seeds tough enough to survive digestion (which many seeds do) would quickly spread. Any adaptation that made animals more likely to eat these parts and spread their seeds would likewise spread.

I suggest familiarizing yourself with basic plant phylogeny first, since if you had you would know only one group of plants produce fruit, and so would not have asked half your questions. So please go do a few minutes of research and come back with a more coherent question.

If you want a complete retelling of the entirety of plant evolution you can do that yourself, show a little initiative and start here.

http://bmcevolbiol.biomedcentral.com/articles/10.1186/1471-2148-14-23

https://www.accessscience.com/content/plant-phylogeny/524400

Also rice is not a fruit. It is the plant's seeds you are eating, it did not evolve to taste good, you evolved to think it tastes good becasue it is nutritious, in much the same way meat tastes good. You are essentially murdering their offspring.

I also suggest learning what a theory is.


Does documentation exist that shows the evolutionary connection between common horses and the okapi?

tolweb.org is your friend!

Because the okapi and the horse are not so closely related you will probably find several articles on the subject. Okapi belongs to the order of artiodactyla while the horse belongs to the order of perissodactyla. They are both mammals, eutheria, ungalata (superorder).

Here is the tree of the eutheria (within the mammals) from tolweb. You have approximatively 150 references. You can click on perissodactyla and artiodactyla and you will find 100 more references.

These two references may help you (I only read the titles)

Graur, D., M. Gouy, and L. Duret. 1997. Evolutionary affinities of the order Perissodactyla and the phylogenetic status of the superordinal taxa Ungulata and Altungulata. Molecular Phylogenetics and Evolution 7:195-200
Xu, X. F., A. Janke, and U. Arnason. 1996. The complete mitochondrial DNA sequence of the greater Indian rhinoceros, Rhinoceros unicornis, and the phylogenetic relationship among Carnivora, Perissodactyla, and Artiodactyla (plus Cetacea). Molecular Biology and Evolution 13:1167-1173


Can neurotransmitter depletion cause short-term drug tolerance?

As I recall from textbooks I read as an undergrad, one mechanism of drug tolerance works by increasing the necessary thresh-hold at a synapse such that larger concentrations of neurotransmitter or more-frequent action potentials in the upstream axon were required to depolarize the membrane and propagate the signal.

Yes - usually through a reduced expression of receptors on the surface. Increasing the drug dosage merely increases the probability that one of the molecules will find the receptor. Chronic exposure of increasingly large doses can dramatically reduce receptor expression. In time, sans the drug, the receptor count will climb back up.

This is why a common cause of chronic drug addicts who have just gone through rehab is overdose: After months in rehab or free of a drug they immediately go back to the amount of drug they were doing before rehab - with some severe side-effects at the least, death at the worst.

  Does over-stimulation of a neural pathway (through the use of a drug or other stimuli that up-regulates a given neurotransmitter) shorten the half-life of the neurotransmitters it uses?

No. The half-life of a neurotransmitters is not a major concern; your body will construct them from stored resources if necessary, and healthy neurons have a significant store of neurotransmitters to prepare for multiple firings.

A neuron can be artificially over-stimulated and the neurotransmitter pool emptied (or all the neurotransmitters is bound to its receptor) - but only for Ach receptors at neuromuscular junctions. It hasn't been observed naturally, and not for other types of synapses. This does not result in the muscle no longer responding, but rather it will not respond any faster.

  Could a diet which is poor for necessary precursor nutrients cause a person's neurotransmitter concentrations to drop and reduce signaling along specific neural pathways?

Yes, but by that point you're not in good shape, if not courting death. Neurotransmitters are either very common in the diet - like ions - or are constructed from very common constituents of a normal diet - like Glutamine, the most common amino acid.

It would not be a therapy to treat drug addiction.

  Could lack of sleep or other physiological stressors have a similar effect?

You would die of lack of sleep first. Your body generally keeps a 30 day supply of absolutely essential vitamins and minerals, and will easily digest itself for precursors to construct neurotransmitters out of.

I have not heard of any physical or mental stress which has reduced the amount of neurotransmitters released into the synapse beyond absolute starvation or artificial scarcity.


The odds are that you're noticing the equality of patent nostrils in the middle of a changeover, when both are equally patent. Also, the shape of your nose may be permitting the congested side to still be fairly patent. Your nose is doing what it's supposed to be doing (and everybody suffers bilateral congestion during colds, allergies, etc.) If it were not, you would be plagued by dry, painful and bleeding nares (um... are you?)


Comments on Experimental result regarding Anti-Bacterial soap

After using soap, the pathogens that were previously present in hands are removed by the soap and water. But yes, bacteria from the water do attach themselves to our hands again, for that we should wash our hands with clean water, which may not be sterile but at least free from pathogens. Also if we wipe our hands to cloth after washing, the bacteria that may be present in the cloth adhere itself to human hands. The attachment of bacteria depends on the concentration of microbes, increase in microbial count increases the probability and risk of contamination. Unfortunately antibacterial soaps that use triclosan may kill more microorganisms while washing hands, but then they can't "protect us" from bacteria for some longer periods of time. Also it has been found that antibacterial soaps have the potential to create antibiotic-resistant bacteria, and some may even cause allergies.


How are geneticists able to isolate gene functions?

@LanceLafontaine suggested a few ways above, but I would recommend reading this section
in Alberts' Molecular Biology of the Cell, which gives a more descriptive overview of some approaches, but even that is not exhaustive.

An extremely simplistic and also not exhaustive summary:

observe mutants, see what processes are disrupted, and map these back to particular mutations
mutate a gene and see what processes are disrupted
biochemical studies to see, for example, which proteins (which are gene products) interact in vivo and things like where they're localized, which may hint at function.
analyze structure of proteins, see how similar they are to other proteins with known function, and infer that the protein of interest probably has a similar function

EDIT: The link to Alberts is to the 2002 edition (which is free online; the latest edition of the textbook costs around $200), so things have come a long way since then, but the underlying approaches are still in use.


With respect to your first question, that model isn't intended to take time into account, but is based on Hebbian learning with the goal of computability. It's generally used in simple pattern recognition situations where each case has no bearing on the next. The learning portion is performed ahead of time during the training phase. For example, a deterministic perceptron isn't permitted to change after training. In contrast, the Biological Neuron Model is much more complex, and uses a variety of ordinary differential equations to integrate the cumulative behavior of neurons over time. As such, those models are non-deterministic and don't see as much practical use outside of experimentation.

To address your second question, neurons themselves don't "learn." A single neuron is essentially meaningless. Learning is an emergent process created by the interaction of several systems at once. While one influencing factor is connectivity (zero for no connection, non-zero for the inhibitory or excitatory connection which emulates both synaptic and non-synaptic), what you might call short term learning can also be performed by existing clusters of neurons, without any change in connectivity. Biologically, this is what must occur before any of the comparably slow process of tissue remodelling can take place, and the computationally equivalent process is only possible in time-aware models like the aforementioned Biological Neuron Model.

Take, for example, someone who wishes to learn to play guitar. When they begin playing, existing clusters emulate the desired behavior as best as they can. These neurons act as the functional scaffold that initiates and drives the neuroplastic process. Playing becomes easier because this scaffold becomes more efficient as new connections (shortcuts) are created, existing connections are strengthened, and irrelevant connections are inhibited. The improved scaffold in turn allows further improvements. Newborn neurons may also migrate to the area, though the how, why, and when of that process is unclear to me. This "behavior emulation" or "short term learning" process used in practicing the guitar, or whenever a novel situation is encountered, must be primarily governed by excitatory and inhibitory neurons' influence. Otherwise the whole process cannot even begin.

Further reading

Parameter estimation of a spiking silicon neuron.
Synaptic plasticity, memory and the hippocampus: a neural network approach to causality
Signaling mechanisms in cortical axon growth, guidance, and branching


Why is the 4.4 kb band barely visible in this HindIII digest of lambda DNA?

First of all, the 4.4 kb HindIII band is derived from the right end of λ DNA, so during storage it anneals to the 23.1 kb left arm fragment via λ's 12 bp cohesive ends. You can solve this problem by preheating the markers to 65°C for a few minutes then cooling rapidly (i.e. on ice).

In a stained gel the intensity of a band is proportional to the amount of DNA in that band. This is why the heavier bands are more intense. The fragment X in lane 2 is similar in intensity to the 0.5 kb λ fragment so DNA content of the two bands is similar.

The amount of DNA in the 0.5 kb band is 250 ng *(0.5/48.5) where 48.5 is the size of wild-type λ DNA. I'll leave it for you to complete the calculation.


How to find Exons in mRNA Computationally

The only information you are missing is a way to identify the splice sites. There are many ways of doing what you need. The simplest, assuming you are sure of the origins of the mRNA, is to use a BLAST flavor, either plain BLASTn or, even better, BLAT, to compare your mRNA sequence to the genome of interest. BLAT really should be all you need if the mRNA comes from the genome you are aligning it to.

BLAT however, has no knowledge of splice sites and will simply cut your mRNA so as to maximize local alignment scores. If you need something more sophisticated than BLAT, use a specialized aligner as @SteveLianoglou suggested. These programs include a model of splice sites (both canonical and non) and will align exons correctly. My personal favorite is exonerate.

Assuming you are using Linux (which you should be if you are planning on doing a lot of this type of analyses), you can install it on a Debian based distribution (such as Ubuntu and its variants) with this command:

sudo apt-get install exonerate

Then, to align the mRNA to its gene do:

exonerate -m est2genome -n 1 mrna.txt dna.txt > out.txt

-m is the model that exonerate will use to align your two sequences. Since the important thing in your case is to correctly model splice sites, you should use either est2genome or, if you are comparing different species, coding2genome, or if you have a full length cDNA including UTRs, cdna2genome.
-n 1 means find the best match only. Assuming you are aligning an mRNA to its coding gene, this is all you are interested in.


What is the metagenome like for other classes of animals?

There are multiple parts to an answer for this.

1) There is not only a microbiome in the gut. So microbiomes in general are very diverse. A fish microbiome on the scales will of course be very different to the one on a human skin.

2) Gut microbiomes are also quite different both in taxonomic and functional content, as they are in different ecological niches.

3) There are microbiome studies for nearly every type of organism I could imagine now. Fish, insects, snakes, you name it. They differ in diversity and composition of their microbiome, but also the used methods and databases do differ, so it is hard to compare them.

4) The further away from well studied microbiomes we get, the less specific will be our assignment of taxonomy and function, because we have not seen enough comparable microbes before. So more information will be hidden in the "dark matter" (in metagenomics: reads not assigned to a taxon and/or function).

Unfortunately I don't know of any jellyfish microbiomes so far. Their body (as far as I know ) seems to be much more "permeable" for sea water (-> their environment) and thus I would think that they generally would have aquatic bacteria in whatever corresponds to their gut. The sea microbiome is said to be very diverse and far too little studied, although there are cool projects like the Global Ocean Sampling Day to try and close this huge gap as best as possible.


How does repair take place on leading strand in eukaryotes?

I'll keep the answer to this as concise as possible. The major mismatch repair (MMR) pathway used by eukaryotes is the MutS$\alpha$-MutL$\alpha$-dependent MMR. See the diagram below for its mechanism:

The pathway initiates when MutS$\alpha$ (Msh2–Msh6) binds to a mismatch. This is followed by binding of MutL$\alpha$ (Mlh1 and Pms2). PCNA then activates MutL$\alpha$ to incise the nascent strand and the DNA ends are used for removing the replication error. After this, the repair is completed by correct DNA synthesis and ligation (note that this pathway works in both leading and lagging strands). DNA replication and MMR are temporally coupled in a manner that may be related to the regulation or appearance of the signals used for MMR. Also, pay attention to the point that the opposite strand is used as reference strand for repair and the strand to which MutL$\alpha$ binds is the one at which Pol$\epsilon$ (or Pol$\delta$) replicates as the DNA polymerase and the PCNA act as the signal for MutL$\alpha$ activity.

See this paper (also the image source) by Kunkel and Erie (2015), they describe this process and a lot of things related to it, including its regulation and signals, in much more detail. I haven't talked much about the details here as the paper is a much better source to understand them.

References:

Kunkel TA, Erie DA. Eukaryotic Mismatch Repair in Relation to DNA Replication. Annu Rev Genet. 2015;49:291–313. doi:10.1146/annurev-genet-112414-054722


Why don't half of us have situs inversus?

In the Wikipedia article linked to in the question, one will note that there are several medical conditions associated with situs inversus, including congenital heart disease, primary ciliary dyskinesia, and Kartagener Syndrome. These can easily lead to reduced fitness for reproduction, especially PCD/Kartagener Syndrome, as one effect is male infertility due to lack of functional cilia on sperm.

Therefore, there likely is a negative pressure on the alleles responsible for this condition, explaining why it is so rare.


Do B/T cells form from lymphoid tissue or bone marrow?

This is a good question and I can see where some confusion can arise. Lymphocytes are a class of cells that include both B and T cells among others. They both have the same precursor cell that being a small lymphocyte [1,2]. The small lymphocyte will grow into a large lymphocyte then differentiate into a pro-B-cell or a pro-T-cell [3]. After differentiation the pro-B-cells are "trained" in the bone marrow and the pro-T-cells are "trained" in the thymus [4,5]. The processes of training for both B and T cells are active areas of research and are quite interesting if a bit confusing.

from [6]
"Lymphoid tissue has several different structural organizations related to its particular function in the immune response. The most highly organized lymphoid tissues are in the thymus and lymph nodes, which are well-defined encapsulated organs with easily identifiable architectures. In the spleen (a soft, purplish organ lying high in the abdomen), the lymphoid tissue is a cylinder of loosely organized cells surrounding small arteries. In the bone marrow this tissue is mixed with the blood-forming cells, and no organization is apparent."

It is true that red blood cells are produced in the bone marrow and are somewhat related to lymphocytes. They are cousins to each other in some way [7].

I hope this helped show the differences in the maturation of T and B cells and cleared up some confusion for you. If you would like to know more I would recommend picking up an immunology book. I used this one [8] and quite liked it when I was taking immunology.

[1] https://en.wikipedia.org/wiki/Lymphocyte

[2] https://medical-dictionary.thefreedictionary.com/small+lymphocyte

[3] https://www.researchgate.net/figure/Life-and-death-decisions-during-B-and-T-cell-developmenta-This-panel-is-a_fig2_8014354

[4] https://www2.nau.edu/~fpm/immunology/Exams/Tcelldevelopment-401.html

[5] https://www.researchgate.net/publication/6196234_B-cell_anergy_From_transgenic_models_to_naturally_occurring_anergic_B_cells

[6] https://www.britannica.com/science/lymphoid-tissue

[7] https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0022042/?figure=1

[8]https://www.amazon.com/Basic-Immunology-Functions-Disorders-Immune/dp/032339082X/ref=sr_1_7?ie=UTF8&qid=1524514359&sr=8-7&keywords=immunology


Are there any animals that gradually approaches the predator to search for food?

The behaviour that you describe is common in most animal species, as part of the natural trade-off between access to food, minimizing risk, habituation and hunger. Animals usually choose to forage in high-quality habitats that has a low risk of predation, but if food sources are depleted (or competition and/or territoriality is high) they will move to other areas with lower food quality or higher risk (since they are desperate for food).

In general, the effect of predators are both direct (killing of prey) and indirect (changes in prey behavior to avoid predation). The indirect effects means that prey will often choose to feed in habitats that are suboptimal from the perspective of forage quality, which will have negative effects on their foraging efficiency. These types of indirect effects of predators are often labelled as 'The landscape of fear' or the 'ecology of fear' (see e.g. Brown et al, 1999). However, as food resources run out this will trade-off against the fear of predators (along with possible habituation effects), which will lead to the behaviour you are asking for. You might also be interested in Gamelius et al (2014), as an example of how prey behaviour can be influenced by the presence of predators (here, roe deer and lynx), but there is a large number of studies looking into these issues. The review "Fear in animals: a meta-analysis and review of risk assessment" by Stankowich & Blumstein (2005) will also give you a good background and many examples.

The use of scarecrows is a simple way to understand the 'landscape of fear'. By placing a scarecrow in a field you strengthen the "landscape of fear" (by adding an artificial 'predator'), which will modify the behaviour of perceived pest species (prey), so that they avoid the areas around the scarecrow. However, if the animals you want to scare away ("pests") run out of food they will take larger risks and venture closer to the scarecrow to forage. Over time, they will also become habituated to the scarecrow, and will discover that it doesn't seem to pose a big threat, which will decrease the effectiveness of the scarecrow.

References

Brown et al. 1999. The Ecology of Fear: Optimal Foraging, Game Theory, and Trophic Interactions. Journal of Mammalogy
Gamelius et al. 2014. Habitat Selection and Risk of Predation: Re-colonization by Lynx had Limited Impact on Habitat Selection by Roe Deer. Plos One
Stankowich & Blumstein. 2005. Fear in animals: a meta-analysis and review of risk assessment. Proceedings B


Why is it that drinking caffeinated tea does not help one to stay awake?

It could be tolerance if other caffeinated beverages are usually consumed, however it also depends on the type of tea itself, and other properties, such as how long the tea has steeped for.

For example, brewed black tea can have anywhere from 14-61 mg of caffeine, which is a large range and depends on which tea you are drinking specifically.  Whereas if you were drinking green tea that has not been steeped for long, it can have 24-40 mg of caffeine, which at the lower range will probably not help you stay awake.

From MayoClinic.Org:

  The actual caffeine content of the same coffee drink can vary from day to day — even at the same coffee shop — because of various factors, such as roasting and grinding, as well as brewing time. The caffeine content of tea also is affected by how long it's brewed.

Caffeine beverage levels can be found here:

http://www.mayoclinic.org/healthy-living/nutrition-and-healthy-eating/in-depth/caffeine/art-20049372


Explanation of the meaning of high-throughput

High-throughput sequencing specifically refers to sequencing techniques like Illumina that allow you to sequence massive amounts of DNA at once (hundreds of thousands of strands), as opposed to older techniques such as cloning the cDNA in plasmids, followed by sequencing.


When discussing the control of gut motility there is more to mention than the use of serotonergics and opioids - a number of peptide and nonpeptide neurotransmitters are important. Somatostatin and nitric oxide are two examples which each happen be inhibitory of intestinal motor function, but by two completely different mechanisms. A bit of understanding in cell biology, specifically cell signalling would be helpful to fully grasp this, but the former acts by inhibiting the release of Acetylcholine and Substance P while the latter increases levels of cAMP/cGMP. And don't forget about the basics when it comes to motor control - the cholinergics and adrenergics (including dopamine) are logical opposites.

References
Leung, P.S. 2014, The Gastrointestinal System: Gastrointestinal, Nutritional and Hepatobiliary Physiology, Springer, 19/03/2018, http://www.springer.com/cda/content/document/cda_downloaddocument/9789401787703-c2.pdf?SGWID=0-0-45-1491980-p176563984


Is it possible to prove that a hand sanitizer can kill 100% of a person's germs?

There's no realistic way to prove that your hand sanitizer can kill 100% of a person's germs. In fact there's probably no realistic hand sanitizer that can do that. The reason is that there are just so many germs. There are billions of germs on your hands. To compare, there were only a few hundred thousand people in Hiroshima when it was hit by the atomic bomb in 1945, and even that did not reach 100% fatality.

It's because it's hard to kill all germs that antibiotic resistance is a problem.


Is there evidence to suggest that nutrients in vitamin capsules are not as readily absorbed as the same nutrients in whole foods?

The answer probably varies for different nutrients.  An informal article by ConsumerLab.com indicates that many vitamins are better absorbed from natural sources, but a few are actually more readily absorbed from supplements.

Looking at Vitamin C specifically, a 2013 review article by Carr and Vissers concluded as follows (emphasis mine):

  Overall, a majority of animal studies have shown differences in the comparative bioavailability of synthetic versus food-derived vitamin C, or vitamin C in the presence of isolated bioflavonoids, although the results varied depending on the animal model, study design and body compartments measured. In contrast, all steady state comparative bioavailability studies in humans have shown no differences between synthetic and natural vitamin C, regardless of the subject population, study design or intervention used. Some pharmacokinetic studies in humans have shown transient and small comparative differences between synthetic and natural vitamin C, although these differences are likely to have minimal physiological impact.

In other words, with vitamin C natural and synthetic sources appear to be equally bioavailable for humans.  The authors do note that "Although synthetic and food-derived vitamin C appear to be equally bioavailable in humans, ingesting vitamin C as part of a whole food is considered preferable because of the concomitant consumption of numerous other macro- and micronutrients and phytochemicals, which will confer additional health benefits."

References:

Carr, Anitra C.; Vissers, Margreet C. M. (2013). "Synthetic or food-derived vitamin C—Are they equally bioavailable?". Nutrients 11 (5). pp. 4284–4304. doi:10.3390/nu5114284. PMC 3847730.


What is the difference between the glycolate pathway and photorespiration?

The simple answer to the question posed in the title of the question is as follows. The glycolate pathway is the series of reactions converting phosphogycolate to reusable carbon intermediates + CO2. Photorespiration is the combination of two processes:

The oxidation of the enodiolate intermediate on Rubisco to phosphoglycoate + 3-phosphoglycerate.
The processing of the phosphoglycolate produced by the glycolate pathway.

You cannot use the two interchangeably as there is no respiration (use of oxygen) in the glycolate pathway. The glycolate pathway is just the latter part of photorespiration. I'm not sure what the text books are that confuse the two, but Stryer presents this quite clearly in Figure 20.6 and 20.7 at http://www.ncbi.nlm.nih.gov/books/NBK22344/#A2795.

I am not familiar with the term "conservation pathway" in your final question. I would call the glycolate pathway a "salvage pathway" (although this term is more commonly used for recycling the skeletons of the products of macromolecular, esp. DNA, degradation). It does not salvage all of the carbon skeleton of phosphoglycolate as some carbon is lost to the atmosphere as CO2.


The answer is both yes and no, depending on how often and how hard one rubs his or her own eyes.

Occasional light rubbing is not a problem-- it stimulates tear production and relieves stress by lowering heart rate via the oculocardiac reflex.

Frequent hard rubbing is a problem-- it can worsen eyesight in people who already have progressive myopia, and worst-case-scenario lead to retinal detachment. For those with glaucoma, can interrupt blood flow and even cause nerve damage. It can (but rarely) scratch, tear, or deform the cornea leading to pain and distorted vision. It can lead to damage of small delicate vessels, causing a subconjunctival hemorrhage, which is benign despite its worrisome appearance.

It is generally recommended to just avoiding rubbing the eyes altogether!

References:

www.abc.net.au/health/talkinghealth/factbuster/stories/2012/09/18/3592456.htm
http://www.visioneyeinstitute.com.au/dangers-rubbing-eyes/


What are the obstacles to a quick survey of statin usage in COVID-19 patients?

The problem with your setup is that by targeting an ICU ward you are already narrowing your study to those who developed severe COVID-19. A more robust design would be a retrospective cohort study, where the exposure of interest has already been recorded.
E.g. the UK Biobank (~500,000 participants) has recently incorporated SARS-CoV-2 test results into its dataset, so you could use this to:

create a case/control split based on exposure (i.e. patients' historic use of statins)*
study the effect this has on outcome (i.e. development of severe COVID-19)

In  this  study,  we implemented rapid dynamic linkage, which allows us to provide a regular feed of new COVID-19 (SARS-CoV-2) test results to UK Biobank to facilitate rapid and urgent research into the epidemiological and human genetic risk factors for severe infection in the cohort.

Dynamic linkage of COVID-19 test results between Public Health England’s Second Generation Surveillance System and UK Biobank, Microbial Genomics (2020) **

* Or any of the other thousands of variables recorded in UKB.
** Disclaimer: I have worked on this project.


If the covid-19 appeared once, could it reappear anytime?

Frame challenge answer: you are jumping to the conclusion that they really hope the virus will "die out". But it's more likely they adopted those measures to slow its progression to a manageable degree. See e.g. this conceptual image from ECDC

Even if there are new outbreaks of COVID-19 in the future, when they happen is not irrelevant, as we could be much better prepared given the current/ongoing research on both (antiviral) treatments and possibly a vaccine as well.

Regarding the "meat" of the question, it's a matter of probabilities, not certainties. It was and is generally assumed that other [bat etc.] coronaviruses will jump hosts to humans in the future.

Besides SARS, another (much) lesser known cross-species jump actually occurred in China in 2016 with SADS-CoV, which killed thousands of pig[let]s, but was not infectious to humans. Annoyingly enough for the Chinese pig farmers, SADS-CoV re-emerged in early 2019 despite the fact that there were no cases reported between May 2017 and January 2019.


Hydrogen sulfide can be toxic at high concentrations, however, the amount that your columns will make is likely very low, and will almost certainly degrade/oxidize into something safer before it hurts anyone (who isn't a small organism in the column!). It will noticeably smell bad at levels well below what is dangerous. So maybe just make sure that the columns are in a ventilated space.
Remember, what is happening in the column is basically just rotting organic matter, like leaving a bunch of food waste in a highly compacted, sealed environment. It is sort of intrinsically gross, but it isn't any more dangerous to your health than forgetting to take out the garbage for a month (actually, it's probably a lot less dangerous than that!).
For example, this guide says the following (after constructing columns with different inputs such as e.g. eggs):

You may have seen worms, snails, shrimp or other small organisms in the water, but probably not many (if any) in the bottle with the egg yolk, because hydrogen sulfide is toxic to most organisms!

So, depending on what you put in there, a very H2S-productive medium is likely to create enough H2S to kill tiny animals that are trapped inside the column. But apparently not enough to hurt large animals like you, as long as you don't huff the column.


Plant Cell

In the case of plants, shriveled cells are a huge problem. When plant cells are put in a hypertonic solution, the cell wall remains turgid and stays that way but the plasma membrane doesn't, it shrinks as you already know with the other organelles as well. This is known as plasmolysis. If this situation continues it causes death.

Shrivelling  causes the plant to wilt too.

Animal Cells

Well it does have affects overall and at cellular level

It changes the RMP(resting membrane potential) across the cell because of change of sodium ions outside the cell
-It decreases rate of metabolism


What does the immune system do to stop pathogens that aren't killed by macrophages?

There are two broad types of infection classified by their persistence: acute and chronic infections.

I find that most courses on immunology nicely cover acute infections and their detection, and resolution. In the case of S. typhi, which has the ability to invade host cells such as phagocytes and inhibit their ability to properly function, the case isn't so pretty (1). The same can be said for some viruses like HepC and HIV, or other bacteria like Mycobacterium.

Salmonella spp. have a number of virulence factors. The flagellum of the bacteria actually acts as a TLR agonist that activates phagocytes like monocytes/macrophages and neutrophils, which are often first-responders. Then, the bacteria can facilitate the injection of some of its own proteins into the host cell which does a number of things like modulate vessicle trafficking, suppress cellular functions, induce apoptosis and promote overall survival of the bacterium inside the phagocytes (2).

So normally, and referring to the below figure, the overall reponse to a Salmonella infection is adaptive in nature, presumably because your innate effectors have been stunted:

SRC

You can see in healthy phagocytes that through one of two pathways, protein antigens end up displayed on HLA molecules for cellular immunity to take over. Option B is that another cell like a macrophage detects distress signals from the infected cell and induces cell death in it through receptors or oxidative burst. In the case of Salmonella, HLA expression is down-regulated and oxidative burst can be inhibited so localized, infected antigen-presenting cells cant mount an effective response.

That's not to say everything is de-regulated early on. If you succeed in antigen presentation or innate killing (perhaps a non-pathogenic strain), you will resolve the infection as seen in the above figure: a combination of T-mediated killing, B-mediated killing, NK-mediated killing, and generalized inflammation.

In the chronic case, the pathogen will have escaped the primary immune response, but the system will attempt to continue to resolve the infection. This can lead to a number of things: cellular anergy, cellular hyperactivity, sequestration (see granuloma), chronic inflammation & tissue damage, and so forth. The following diagram is predicated upon viral infections but the immunology is largely similar:

SRC

There are changes to the system that are a result of over-exposure to antigen, and an inability to clear that stimulation. The best way to explain it is that chronic stimulation leads to both hyperactivity and suppression. The constant presence of effector molecules like TNF-a leads to a persistent state of tissue inflammation, which is bad for the tissue, but taken together with the persistent presence of antigen, this may lead to dysfunctional responses by lymphocytes (3).

A particularly virulent infection may be impossible for your immune system to clear without assistance, then, requiring the intervention of gram-negative antibiotics, for example.


Does the magnitude of gene-expression changes decrease the more downstream a gene is from the origin of change?

Gene expression can be very well described by Hill functions, i.e.:
$$c_Y(c_X) = \frac{c_X^n}{1+c_X^n}$$
when $X$ activates $Y$ and
$$c_Y(c_X) = \frac{1}{1+c_X^n}$$
when $X$ represses $Y$ (omitting units and all sorts of constants for simplicity). For the common case that $n>1$, these functions look like this:

As you can see, they are far from linear, but sigmoids. For $n→∞$, these become perfect step functions.
As a result, gene regulation mostly works like a switch:
As long as you are not close to the critical concentration ($1$ in the above example), changes in the regulator have a less than proportional effect.
For instance in the above example, it doesn’t matter whether the concentration of your activator is $2$ or $10$, the protein production is pretty much $1$.
Therefore, “signals” in gene-regulation networks get stabilised instead of diluted.
There are also some other self-regulation effects contributing to this such as genes that self-regulate, the availability of amino acids, and the limits of the translation apparatus.
Note that without these sigmoidal relationships, you would also have big influences of the inevitable fluctuations of the regulator.
As a result, it would be impossible to keep the metabolism in some stable state – the only stable state in a linear system is death.
Simply put, you would have to keep a very precise and regular diet, lest your body stops working.


What is the function of dendritic cell in immunity?

Dendritic cells are so called professional antigen-presenting cells (APCs) as pointed out by Sleepes in comment section. They express both MHC-I and MHC-II receptors on their cell surface on which they present small peptides. These small peptides come from digested proteins of their own (MHC-I) or antigens that were phagocited or taken up by receptor mediated endocytosis (MHC-II). They also express costimulatory molecules necessary for the activation of T-cells (eg. CD80/CD86).

source: http://journals.cambridge.org/fulltext_content/ERM/ERM2_09/S1462399400002143sup004.htm

As you can see in image above, activation of a T-cell requires two distinct signals: the recognition of an antigen and a co-stimulatory signal.

source: http://www.mhhe.com/biosci/ap/dynamichuman2/content/gifs/0158.gif

After activation T-cells undergo rapid division and diversification.

Details of T-cell activation by dendritic cells can be found in this article for example:
Immunol Cell Biol. 1997 Jun;75(3):223-30.
The role of dendritic cells in T cell activation.
Ni K1, O'Neill HC.


Fatigue on exercise is proportional to unmet demand for oxygen and glucose (sugar/fuel).

In people who are "fat":

They typically do less exercise. Therefore their cardiovascular system is not conditioned with the heart being able to cope with increased exercise i.e. it is unable to beat more efficiently and instead must beat A LOT more faster to cope consuming more oxygen and glucose. Even at rest, they will typically have a higher resting rate. They also have less efficient muscles (i.e. the muscles themselves can't breakdown energy as well, use it as well and the body isn't as great at picking the right set of muscles)
The fat itself can compress vessels carrying blood. This pressure increases blood pressure. This is worsened by a typical high diet of salt and again by typical lack of exercise. Higher blood pressure means the heart has to beat harder and faster to pump blood around the body
They weigh more so each movement requires A LOT more energy. Their resting metabolic rate is higher than a thinner person as is any exercise they do.
On exercise they do not lose heat fast enough. This impairs the breakdown of glucose and also more energy is required to lose the excess heat
They may be subclinically diabetic. Their body may have lots of glucose floating around in the blood but they can't use it because their muscles can't absorb it.
They have far increased rates of build up of fatty plaques on the blood vessel walls. This narrows the vessels and only multiplies with all the other problems
Then there's lots of other more minor but very important reasons like psychological (reduced capacity to brave through fatigue), reduced sleep meaning a higher baseline of tiredness (in the extreme side caused by obstructive sleep apnoea), increased rates of smoking (which does millions of things to reduce exercise capacity)


As usual, a rant from Joe Felsenstein's webpage seems relevant. Specifically, this:
"There is no consensus, even among systematists, as to what the word "cladistics" means."
Everyone seems to have agreed that phenetics--which is to say the blind faith in the results of clustering algorithms such as neighbor-joining etc.--is on its own not very useful, compared to a principled dedication to placing organisms taxonomically into monophyletic groups.
However, the hard-line cladistics point of view (e.g. Willi Hennig society) is that no method of inference other than maximum parsimony (in one of its various flavors) is acceptable, for obscure philosophical reasons that no one cares about. Frankly, for any realistic purpose, cladistically unacceptable methods such as Bayesian inference and likelihood methods perform the best. From cladistics wiki:

Although traditionally such cladograms were generated largely on the basis of morphological characters and originally calculated by hand, genetic sequencing data and computational phylogenetics are now commonly used in phylogenetic analyses, and the parsimony criterion has been abandoned by many phylogeneticists in favor of more "sophisticated" but less parsimonious evolutionary models of character state transformation. Cladists contend that these models are unjustified.

In other words, cladistics is more of a philosophical point of view than a group of methods. There are "soft" versions that everyone pretty much agrees on, namely the principle that monophyletic groups are preferable to paraphyletic groups. But methodologically, it's just a lot easier and more workable to use non-cladistic or even phenetic techniques rather than the (computationally frequently more onerous and not necessarily more accurate) parsimony techniques of cladistics.
For a (fairly) recent apologia specific to neighbor-joining, see here.
In short, given the highly heuristic nature of most science, most workers aren't really paying attention to these debates, and just use the tool that works for the problem they're working on. And in many cases those methods are phenetic, even if cladists claimed a victory of principle.


Why aren't more prostate glands just removed?

Your question is along the lines of "Many women will develop breast cancer, especially later in life. Why don't they just remove their breasts after menopause, because they won't need them for breast feeding?" There are a lot of disadvantages and only questionable advantages.

Chief among the effects of removing the prostate are urinary incontinence and erectile dysfunction. That area of the body is very highly innervated, and it is nearly impossible to just remove the prostate without damaging anything else. While it is true that many men will develop prostate problems as they get older, they can frequently be treated medically, or just observed for any dangerous changes. Benign prostate hyperplasia is just that - benign - so there's no need to undergo a major operation with significant side effects. Additionally, many prostate cancers are so slow-growing that they never metastasize or pose any threat, so they are simply monitored and treated medically as needed.


How hot can a beverage get without burning the tongue?

Afaik the tongue is not more heat tolerant than other parts of the body, so the minimum temperature to cause burn is about drinking a beverage having 45°C temperature for a long time (more than 5 minutes). The pain threshold of tongue is around 47°C, so you will feel when it really burns.

According to studies the hedonic value of coffee has a maximum by 60°C, and it is significantly lower by safe levels (45°C). Frequent burns of mouth increases the risk of oral cancer. So I think this will be a hard choice... ;-)

  A burn is an injury which is caused by application of heat or chemical
  substances to the external or internal surfaces of the body, which
  causes destruction of tissues. The minimum temperature for producing a
  burn is about 44°C for an exposure of about 5-6 hours or about 65°C
  for two seconds are sufficient to produce burns.

Thermal injuries

  I. With the object of producing standard low-temperature burns in
  animals, and of studying the area of tissue only partly damaged in a
  burn, a burning iron has been made capable of applying temperatures
  from 45°-80°C. to the skin; with this the amount of heat and
  temperature causing skin damage has been studied, and the macroscopic
  and microscopic damage due to graded temperatures have been
  delineated.

  Graded temperatures of 45°-80°C. have been applied to the skin of shaved, anæsthetised guinea-pigs, and in some cases rats, for times
  varying from 10 sec. to 6 and 10 min. Observations have been made of
  the development of erythema, flare, blanching, blueing, heat fixation,
  incipient blister formation, œdema, and edge wheal, as also upon the
  later scab formation and rate of epithelium regeneration.
  Applications of 47°C. up to 6 minutes produce no visible change.
  At 50°-55°C. applied for 1 minute and over, there is a critical temperature for the development of permanent and irreversible damage;
  in animals good scab formation occurs after burning at this
  temperature.
  After temperatures of 60°-65°C. the epidermis can be peeled off from the exposed area, leaving a punched-out exposed surface area
  somewhat like the exposed human blister.

1943 - EXPERIMENTAL THERMAL BURNS, ESPECIALLY THE MODERATE TEMPERATURE BURN
According to Green the pain threshold of tongue is around 46-48°C.

1985 - Heat pain thresholds in the oral-facial region

  In all experiments, the chosen mean preferred temperature for drinking
  was around 60 °C (140 °F). Black coffee drinkers chose a slightly
  higher mean temperature than drinkers with added creamer, and they
  also chose a slightly lower mean temperature when the flavor was
  stronger. In all cases, consumers tended to choose, on average,
  temperatures for drinking coffee that were above the oral pain
  threshold and the burn damage threshold.

2006 - At What Temperatures Do Consumers Like to Drink Coffee?: Mixing Methods

  Overall, the available results strongly suggest that high-temperature
  beverage drinking increases the risk of EC. Future studies will
  require standardized strategies that allow for combining data, and
  results should be reported by histological subtypes of EC.

High-temperature beverages and Foods and Esophageal Cancer Risk -- A Systematic Review


DNA is not the only thing in biology that determines a phenotype (observable trait, e.g. fingerprint). Far from it.

Traits can be affected by the environment (a very good example, temperature-dependent sex determination), stochastic (random) phenomena - these are know to occur in transcription ("reading DNA") or the decay of mRNA (messenger molecules which instruct protein building) - and by epigenetic phenomena. The degree to which DNA is actively read, or silenced, does not wholly depend on the DNA. In fact, this depends on the exact state of the cell or nucleus. Roughly speaking, cells in your brain (e.g. neurons) and the cells that line your lungs have identical DNA, but they are shaped, look, behave and react differently to the outside world. This is due to epigenetics, think of it as the life history of the cell.

Here's an analogy: reading the exactly same book can have different effects on people. The book is the DNA, its information unchanging, but the person and their exact status are the complicated world of the environment and the cell that is using its DNA for some purposes. PS. Terrible analogy but it may help.

By no means is my list exhaustive. Hope you can see how that identical twins with identical DNA can have a different shade of skin color (tanning!), different fingerprints (subtle and complex differences during digit development), or a different sense of fashion (psychology, cognition, what have you).


Copper is toxic, however from a copper device insufficient levels enter the bloodstream to cause any harm. The released copper is however toxic to sperm. Nevertheless at the site of insertion, they can cause inflammation (especially in the first 21 days and during menstruation) and thus they also recruit white blood cells and the increase in levels of prostaglandins. However, this isn't that common.


Yes, we should. But Ebola doesn't completely immunosuppress us, or there would be no survivors.

Ebola kills by overwhelming the body before enough antibodies are formed to fight it.

If you're one of the survivors (as about 40-50% are, more with good care), you'll have antibodies to Ebola in your blood which might help someone else infected with Ebola.

If you're not one of the survivors, it's still likely you'll have some antibodies, but the shock your body goes into from all the dead cell products in your blood (which - overly simplified - causes a cytokine storm -> leaky capillaries -> fluid balance problems -> end organ failure -> death).


Can humans shorten their sleeping patterns?

Polyphasic sleep can allow people to sleep at multiple regular intervals throughout the day and allows people to get by with less total sleep. I don't know of any training that can help people reduce the amount of monophasic sleep they need without a negative impact.


Why cytotoxic T cells don't kill dendritic cells when they present antigen?

The presentation of antigens on the cell surface is done by two different molecule complexes: The MHCI and the MHCII complexes. These are coupled to different pathways and are recognized by different T cell populations.

The MHCI molecule presents all proteins which are present in the cell on the surface. To do so, peptides coming from the proteasome (where long proteins are digested) are transported in the the endoplasmatic reticulum (ER) by a special transporter called Transporter associated with Antigen Processing (TAP). By doing so, a profile of all proteins expressed in the cell is presented on its surface, including proteins which arise due to an infection of the cell. MHCI is recognized by cytotoxic (or CD8 positive) T cells which subsequently kill all cells which show foreign antigens on their surface (since this is a sign for an infection).

The MHCII complex only presents proteins on its surface which have been taken up by phagocytosis (so here only external proteins are presented). To prevent binding of cellular proteins in the ER (like for MHCI), the binding pocket of the receptor is blocked by the invariant chain. This chain dissociates only when the MHCII complex enter the phagolysosome with its acidic conditions. This makes sure that only proteins which have been taken up by phagocytosis are presented. MHCII complexes are recognized by helper (or CD4 positive) T cells, which in turn can activate B cells to raise a proper immune response.

In theory this should prevent all problems. In the practical life this is different for dendritic cells in a mechanism called "cross presentation". In this mechanism antigens which are taken up by phagocytosis are exported from the phagolysosme and imported into the ER. This pathway also involves the TAP protein. By choosing this way, APC can activate naive CTL which will kill all cells which present this antigen. See references 1 and 2 for more details.

This pathway is important for the immune response to a number of viruses as well as tumors which evade the MHCII mediated immune response by suppressing the MHCII antigen presentation. See references 3 and 4.

It is also important for the stability of the self-tolerance by the deletion of auto-reactive CTL. See reference 5 for details.

References:

Outside looking in: the inner workings of the crosspresentation
pathway within dendritic cells
Cross-talk between the endocytic pathway and the endoplasmic
reticulum in cross-presentation by MHC class I molecules
Role of bone marrow-derived cells in presenting MHC class I-restricted tumor antigens.
Cytotoxic T-cell immunity to virus-infected non-haematopoietic cells
requires presentation of exogenous antigen.
Exogenous class I-restricted cross-presentation of self antigens can
lead to deletion of autoreactive CD8+ T cells.


I think you are misunderstanding "color" here. When applied to cats, it doesn't literally mean a color shade as used in color theory, but "coat color" which can in fact also be a "coat pattern".

The cats above are two-colored, not three-colored. One color is white. The other color is what is called "tabby" in English and is a pattern of dark spots arranged in regular stripes on a lighter background. These spots are not considered a third color in cats.

This is a calico cat. Her three coat colors are white, orange, and grey tabby. See how the orange and grey are irregularly interspersed, this is the pattern of paternal and maternal chromosome expression on her body. Again, the grey and black patches within the tabby part are regularly placed. They don't make two separate colors, grey and black, but a single coat coloring, grey tabby. There are also other color combinations in calico cats, for example white-orange-black, and they are more straightforward to recognize.


What is the mechanism responsible for the 'delay' in delayed rectifier potassium channels?

These channels are slow to respond. After depolarization they are activated, but only after a relatively long time. Their closing kinetics are also relatively slow. A definition is give here.


Definitely an arachnid and mite (subclass Acari), and very likely a member of the order Parasitiformes, of which there are more than 100,000 species!!

Your specimen brings to mind the family Argasidae (the "soft ticks" -- so called because they lack a hard scutum).

Specifically, your specimen reminds me of Argas reflexus, the pigeon tick. (which has been found to be an increasing pest and human concern in urban settings).

 Credit: Milan Kudlička

Based on the size of your specimen, I would guess you're looking at a non-adult stage.

However, this is just a guess, and I will try to explore other species in this general group to see if I can come up with a better-supported guess.

(By the way: any pigeons living nearby??)


Can Fluoride be absorbed into the blood from within the mouth without swallowing?

Although I'm having a hard time finding a source that provides specific information on fluoride in toothpaste, this review explains that fluoride is most readily absorbed through intestinal epithelia and that fluoride absorption through other tissues, such as oral epithelia, depends strongly on other chemical properties of fluoride-containing compounds: their

  "reactivity and structure, solubility, and ability to release fluoride
  ions."

This suggests that you would need additional information concerning the overall toothpaste formula.

This review shows the rates at which fluoride ions are released from various toothpaste formulations. Figures 2 and 3 show that the highest discharge rate is roughly 1.7ppm and the lowest was just under 0.5ppm, both occurring after a 24hr period. The authors note in the discussion that these measurements are likely higher than what would occur in the mouth, since they had to use deionized water for their experiments, in which fluoride is more soluble than in saliva.

Wikipedia lists fluoride toxicity levels as being between 0.5 and 1.0mg/L. Fluoride's molar mass is 18.9984 g/mol and this calculator shows that 0.5mg/L of fluoride translates to about 0.5ppm. While at first this makes the above results sound a dire, it's important to note that toothpaste remains on your teeth for far less than 24hrs and to remember that less fluoride is released into saliva than into deionized water.

Wish I could find better results on how much fluoride might be released during a typical toothbrushing session, but I'm inferring from the linked review that it would be small enough to not merit a health concern.

I emailed a dentist friend for more info and will update this post as I hear back from him.

As for the comment about glands, it's important to understand that the glands found in the mouth are secretory glands, which means that they are optimized for discharging fluids and not for accepting them.

--Update--

My dentist friend wrote back, confirming that no significant fluoride absorption occurs through the gums. From him:

  the only significant absorption would be through swallowing fluoride.
  Any that was just in the mouth would not be well absorbed...
  that is why we do the high dose swish and spit treatments is to avoid
  fluorosis but deliver sufficient fluoride to the teeth.

In short, it looks like the answer to your question is: no, fluoride is not significantly absorbed into the blood from within the mouth without swallowing.


Are enhancers and silencers considered as epigenetic modifications?

No.

Epigenetic information is (by definition) NOT included in the nucleotide sequence, but affects genetic expression.

Enhancers/silencers are themselves nucleotide sequences, and therefore not epigenetic information.

Methylation is an example of epigenetic information, but a DNA sequence itself is genetic information, even if it affects a gene.

CgATgCCAg= Genetic

Acetylation of a histone/DNA methylation= epigenetic

Hope that helps!

Further reading: http://www.whatisepigenetics.com/fundamentals/


Why would eating the meat of cows fed with antibiotics trigger an immune response to the antibiotics?

It's difficult to know how to answer this question because it is unclear why you think that this might not happen.

As skymningen has said in comments, any foreign molecule is capable of acting as an antigen,  in principle. We know that people develop allergic reactions to penicillin. And if you do a Google search for immunoassay [insert name of antibiotic] you will probably find results indicating that there are commercially-available kits for assaying the antibiotic based upon antibodies directed against it.

It is however worth noting that these anti-antibiotic antibodies were certainly not raised directly by feeding, or even injecting, the antibiotic. This is because the immune system doesn't really respond to small molecules. If you want to make antibodies directed against a small molecule you have to tag it on to a protein - this is called haptenisation. Then some of the antibodies that develop against the modified protein will recognise the hapten (the small molecule). Another example of this is the development of immunoassay for steroid hormones.

So we have to imagine that a fed antibiotic enters the bloodstream and then reacts chemically with a blood protein - essentially the antibiotic has haptenised itself. I seem to recall reading that β-lactam antibiotics are fairly reactive against lysine residues. The propensity of different antibiotics to provoke an immune response may be simply a function of their reactivity.


Is excessive hydration a risk factor for cancer in humans?

In the most technical sense, yes. In a practical sense, no. Average background radiation dose from food and water sources is ~.3 mSv according to the UN. Given that it takes 1 full Sv to increase cancer risk by ~5-6%, it seems unlikely that, under normal conditions, variability in consumption of water will change risk in a significant fashion.

Now, when dealing with highly contaminated water, there may be a more exaggerated effects, scaling with an increased concentration of radioactive particles per unit of water. Of course, in highly radioactive situations the risk of radiation poisoning may be a more immediate worry.


Plant cell question in age 12 science test

From a picture like this one cannot actually say whether "part-A" is a mitochondria or chloroplast. That could even be some random vesicles or, to think even crazier, assembling viruses.

The question is really bad and the kid isn't really incorrect. Mitochondria as a guess is pretty reasonable too. However, the second answer is incorrect. I don't know what the kid wants to imply by "to absorb photosynthesis"; it is unclear to me.


First, the correlation between canine teeth and carnivory isn't absolute. Gorillas have fearsome canines, and they're herbivores. Humans are the only primates capable of rotary chewing, thanks to our small canines. (Encyclopedia Britannica: Canine Tooth)

Even with our small canines, some groups of humans live almost entirely on meat. However, humans are clearly omnivores in general.

Our closest living relative is the chimpanzee. Chimps are primarily herbivores, but they love meat.

Mastering the art of tool (and weapon) making, made our ancestors more efficient hunters. Meat became an especially important source of food for people living in colder climates, where plants were scarce in winter or year round. It was thus presumably more important during the Ice Age, which was an important chapter in our evolution.

But humans remain adapted to an omnivorous diet, ranging from herbivory (veganism) to carnivory.


advantages of shivering in cold environments

Firstly, movement by shuddering or shivering, in simplicity, effects the conversion of potential energy into kinetic energy. This is achieved by expending ATP in muscular tissue, causing rapid bursts of contraction.

Brown adipose tissue, although located within most mammals ranging from infants to elderly, is predominantly found in infants differing from white adipocytes insofar as brown adipose tissue has a greater capillary network. Due to the higher surface area to volume ratio of the infant comparative to adults, the rate of heat loss is appreciably greater than a human adult. Thus a more efficient means of thermogenesis is required, namely, when the BAT detects body temperature below the homeostatic norm, the hormone norepinephrine is released, reacting with lipases to form triglyceride. This may subsequently decomposed further, to be converted into heat energy around the body (there are of course various intermediate stages).

Additionally, located primarily in brown adipose tissue is a protein named UCP-1. This allows the cells respectively to undergo 'non-shivering thermogenesis', heat generation without shivering by uncoupling the respiratory cycle in the mitochondria to oxidise more rapidly the substrate. As a consequence, fewer molecules of ATP are produced but heat production is increased.

Therefore, the differences may be rested on 1) the required efficiency of heat generation between infants and adults; 2) the act of shivering per unit of muscle area generates more heat.

You can find further information regarding the UCP-1 uncoupling mechanism in BAT from, https://www.ncbi.nlm.nih.gov/gene?Db=gene&Cmd=ShowDetailView&TermToSearch=7350


Use cases of RNA secondary structure prediction

Short answer

I can think of at least a dozen applications for which it would be useful to know the secondary structure of a given sequence of RNA off of the top of my head. In no particular order:

Simulation/visualization of RNA
Riboswitches
MicroRNA
RNA interference (RNAi)
RNA-RNA interactions
RNA-DNA interactions
RNA-protein interactions
Ribosomal protein expression
Ribozymes
Forced evolution of RNA aptamers
Synthetic tRNAs with four and five base-pair codons
Termination of transcription (the process that makes mRNA from DNA)

Basically anything to do with RNA, which is one of the fundamental building blocks of all living creatures.

More in-depth

Simulation/visualization of RNA

Secondary structure (2°) forms the second (yep) level in the standard 4 level hierarchy of macromolecular structure, and consists of short-range interactions between and among residues. In RNA, 2° is usually thought of as being loosely identical with base-pairing interactions. In order to do a proper simulation/visualization you'll probably also need at least the 3° information, but 2° is important too.

Riboswitches

As an mRNA gets translated by a ribosome, in many cases it can form into a complex 3D structure that will affect the translation process. For example, some of the mRNAs that encode proteins related to the metabolism of metal ions have a riboswitch that will themselves bind to metal ions and inhibit/upregulate expression of the related protein. For various reasons it's usually extremely difficult to get the full 3D structure of a riboswitch, so getting to know the 2° remains an important source of information about them.


A parasitic interaction is when one species has a fitness increase (benefit) from the interaction while the other has a fitness decrease (cost). Note: you don't need to have physical contact to have an interaction. As soon as the presence of one specie influence the fitness of the other, it is enough to consider that there is an interaction.

In the case of Batesian mimicry, I think it is obvious to understand why the non-toxic species gain from this interaction. Let's imagine the toxic (model) species is blue. Predators learn to avoid blue species because they feel very sick right after eating it. In other words, the predators have a bad experience or even better we can say that the predator receives a punishment or a negative reinforcement (instrumental conditioning). In consequence the predator that got this negative reinforcement will probably avoid blue individuals in the future.

When a predator eats an individual from the mimic non-toxic species, he got a positive reinforcement. In consequence the predator learns that the prey tastes good and in consequence it is more likely to eat a blue prey next time it encounters one, which obviously has a negative impact on toxic model organism.

Now, I have two issues with this concept.

The interaction is not one-to-one and we can consider that the presence of a species that use Batesian mimicry influence the variance in fitness of the toxic species only if (actually you might argue differently by not assuming infinite population size) the distribution ranges are not completely overlapping or if there are some kind of population structure.
If the toxic species causes death to the predator, then the predators never get the opportunity to learn. But one can consider the same mechanisms at evolutionary timescale than at the time of the lifespan of the predators. It is also possible that the predators have higher cognitive abilities allowing them to gain insights concerning the toxicity of one species without having to taste it.

EDIT

  What if predators can tell the difference between the two prey species?

Your point, if I understand it, is that if the predators manage to sense (or to evolve sensing) the two prey species differently (in consequence the non-toxic species does not mimic the other prey species anymore), then the toxic species will not suffer anymore from the mimicry. So in other words, mimicry is a parasitic interaction but predators might evolve ways to sense the two species differently in which case there would have no mimicry anymore. Note: the predator is more likely to evolve good sensing abilities if it forages on few species only.

I think your issue is that you should not consider a species to be mimicry if the predator can tell the difference between the two prey species. It is not to the human eyes that the mimicry makes sense but only to those of the predators. So, batesian mimicry is a parasitic interaction and if the predators evolve so that they can sense the difference between the two species, then there is no more Batesian mimicry and there is no more parasitic interactions between the two prey species.

  Why do you say that  "physical contact" not necessary for two species to have a parasitic interaction?

The interactions between species are defined as follow:

The benefits and costs (harmed) are defined in terms of fitness. These definitions do not involve any physical interactions. And to the eyes of the evolutionist at least, that would not make much sense to add a notion of physical interaction into these definitions.

  In the case of Batesian mimicry the ± effect is not always certain (while it is certain in common parasitic interactions)

The point is interesting. I think it just mean that the non-toxic organism is a facultative parasite (a species that can live with or without the parasitic interaction). Statistically speaking, if you have enough preys of each species and especially enough predators, then the consequence is certain.

Consider the common Ivy. It is a parasite of other plants but can also live on human-made walls in which case the negative effect on other plants is not always certain either. The difference between the Ivy and the non-toxic prey is that the fitness of the non-toxic prey depends on whether it parasites the other species while the Ivy is doing just fine on human-made walls.

You can think about the interactions between rabbits and wolves. They share a prey-predator interaction which is a special case of the parasitic interaction according to above diagram. In a particular environment the wolves might be absent and so predation does not occur, just like the non-toxic species might be absent species might be absent and so the parasitic interaction does not occur anymore.


Mice that have been reconstituted with geneX-transduced cells

Your second interpretation is correct.  The mice have been reconstituted from stem cells that were "transduced" (using a viral vector) with a construct containing the appropriate geneX. The link gives comparison of transduction vs. transfection.

https://www.vectalys.com/blog/what-are-the-differences-between-transfection-and-transduction-222


How many, and how severe, are known single gene polymorphisms for obesity?

MC4R, TMEM18, GNPDA2, KCTD15, NEGR1, BDNF, ETV5, MTCH2, and SH2B1 have also been identified as being associated with adult onset obesity risk, however FTO currently appears to be the one with the strongest evidence. For example see Thorleifsson et al. (2009), Elks et al. (2010) and Willer (2009)


What are the factors to consider when determining the sample size for a given study?

Could be as much as possible – using multistage sampling. But it all depends on how much you are willing to spend, and your time constraint.


Do all fungi dislike acidic environments?

Fungi that grow in acidic media are well known, here just one reference: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC518635/pdf/jbacter00651-0183.pdf

About their spread, they are less common in mild environments (like you hands, or your garden soil) but of course in acidic environments, they will be predominant.


How do detergents get in hydrophobic membrane interior?

It depends on the concentration, but at higher concentration the detergent molecules build so called micelles, where the hydrophobic "tail" is orientation into the inner part and the hydrophilic "head" is orientated to the outside. This allows the micelle also to fuse with the membrane and then to desintegrate it.
This illustration from the Wikipedia shows the schematically:

Its from the surfactant article, which has more details.


A study has found that cell phones cause infertility, is this something to worry about or is the study flawed?

The study is basically worthless.
First, the study was not constructed to test this hypothesis, so it's just something interesting that may point to future studies. It does not provide sufficient evidence.
But the biggest problem is that the study was of 52 individuals with only one or two samples, which makes it statistically useless.
Any uncontrolled variable could account for all the difference detected. If one person had low sperm count because they wore tight underwear it would completely account for the difference.
This would barely qualify as an exploratory study, much less anything conclusive. This study would need to be reconstructed with a minimum of thousands of people, or control the participants' behavior (preferably both), to produce useful conclusions.
Any study with a really small N that deals with human behavior is basically worthless as far as any certainty goes.
The questionnaire is not any better — cellphone position is just binary: 1 belt and/or pocket, 2 anything else. Since most of the people are going to fall in the first category, there are very few degrees of freedom to work with. They just ran all the numbers hoping to get something. This is barn door statistics at its worst.


Why should benzalkonium chloride (an antifungal agent) be used during your laundry machine's "rinse" cycle, not its "wash" cycle?

The label of the veterinary product Fung-A-Way, which is Benzalkonium Chloride 0.15%, states that "Efficiency is neutralized by soap or detergent residues."

The website http://www.mpbio.com has the following under its description for Benzalkonium Chloride:
"Incompatible with anionic detergents, such as soap, and with nitrates."


Are there organisms that "branch more" near the leaf?

I can't say that your question is very clear to me, but perhaps something of interest to you would be a common type of inflorescence called an umbel. specifically, a compound umbel with associated umbellets.

Compound Umbel:

 Source: Educational Technology Clearinghouse

Some examples can be found here

Again, since your post is not clear to me, I'll also include images of other complex inflorescences:

 Source: texaswildbuds.com   [the compound cyme might be of interest to you]


Why myelin sheat does not cover the whole axon?

The nodes of Ranvier (the gaps between myelin sheath segments) speed up the action potential because the electric current can jump from node to node (or gap to gap). If the myelin covered the entire axon, the signal wouldn't have the gaps to speed up the signal. As for optimal length, the gap is 1μm long, but can be longer, on the order of millimeters depending on the type of cell. The length of the myelin doesn't matter so much as the length of the nodes of Ranvier because they are where the Na+/K+ channels are found so the ion exchange can occur. This is how an action potetial can occur, so the myelin not covering the entire axon is crucial for the ability of neurons to propagate a signal.


Is hydrochloric acid suitable for pickling food?

Short answer
Weak organic acids are more effective for food preservation then strong mineral acids, mainly because undissociated weak acids can cross the cell membrane and disrupt cell physiology from within.

Background
Natural fermented, or pickled materials are traditionally cured in a brine solution (salt, water, sometimes spices and sugar). Desirable anaerobic bacteria convert carbohydrates to acetic acid that “pickle” and preserve the food. The brine protects the vegetables from aerobic organisms. However, most contemporary pickles are not fermented at all; instead they rely upon the direct addition of acetic acid (vinegar, a product of fermentation), and usually heating for additional preservation. This way the acetic acid production through the fermentation process is simply bypassed.

So the basis of the traditional and contemporary pickling is the addition of organic acids like lactic and acetic acids. These small organic acids are known to be more effective against bacteria than inorganic mineral acids like HCl (Rode et al., 2010)

Acetic acid is a weak acid. In undissociated form, it is lipid soluble and able to rapidly diffuse through the plasma membrane (source: World Nutrition Science blog). It is thought that diffusion of acetic acid and other organic acids into the bacterial cell is the main mechanism of action behind its preservative effects. Preservation by acidification is especially effective in certain species of pH-sensitive bacteria such as E. coli and Salmonella. In contrast, strong mineral acids are nearly completely ionized in solution and ions do not pass the cell membrane's hydrophobic lipid bilayer.

The mechanism of action of small organic acids in food preservation are thought to be at least threefold:

Once diffused in the cell, organic acids will dissociate because the internal pH is near or above neutrality and thereby lower the bacteria's internal pH and disrupt cell physiology;
The anionic part of the organic acids, which cannot escape the bacteria in its dissociated form, will accumulate within the bacteria and disrupt many metabolic functions. This is one advantage of using organic weak acids like acetic acid, because they are normal constituents of the cells. Acetic acid and lactic acid for example are both intermediates in glucose metabolism. Accumulation of these metabolites will disrupt the glucose metabolism essential to the cell's survival.
Eventually, upon progressing accumulation, osmotic pressure increases become mechanically incompatible with bacterial life.

Another advantage of acetic acid is that it is a natural metabolite in human metabolism, and because it has been used in food preservation for thousands of years it is not classified as a food preservative, at least in the EU, and can be freely added to foods. Last but not least, acetic acid has a certain taste to it that may be preferable over inorganic acids.

Reference
- Rode et al., Can J Microbiol (2010); 56(9): 777-92