I searched a bit and could not find any such format, but I am not a specialist in taxonomy.

From what I understand, the structure you want is that of either a tree or a DAG (Directed Acyclic Graph). Both are straightforward to store in a variety of formats.

One possibility is to use a format similar to other biological data that has a similar data structure. For example, Gene Ontology is a widely used dataset that has the structure of a DAG and has a number of formats including XML listing the parents and additional data of each node in the graph. See here for their formats.


Why is funnel web spider venom so lethal to humans and not so much for other mammals?

First, we need to understand that neurons have special proteins embedded in their membranes called ion channels. These allow dissolved ions such as sodium, potassium, and calcium to pass from one side of the membrane to the other. Neurons use these channels to control their electrical activity.

Peptide neurotoxins such as the one produced by funnel spiders (robustoxin) work by having a shape and charge configuration that is complementary to ion channels, and thus they will bind to these channels and affect the way they operate (often by simply blocking the channel). Robustoxin seems to operate by removing sodium-channel inactivation.

There is a bit more information about the primary toxin on the Wikipedia page for delta atracotoxin. The intended target of this toxin seems to be insects, where it interferes with potassium and calcium channels. In mammals it interferes with sodium channels, but it seems to be particularly potent in primates. Why are some species affected more than others?

Not all ion channels are built the same. From species to species, we see a huge array of genetic differences that affect both the shape and functional properties of these proteins. Ion channels which happen to have a shape and charge configuration that is highly complementary to robustoxin will adhere to it more firmly, and thus be more affected by it.

So did we just get unlucky and happen to have sodium channels that perfectly fit robustoxin? That seems to be the most likely answer, given that Australia probably has no native spider-consuming primates. Perhaps someone else can suggest other arachnid predators that might be an intended target for robustoxin?


Does octopus eye presents the equivalent of fovea in primates?

Yes, they do have an area of densely packed receptors, although not point-like as the human fovea.

Talbot and Marshall (2011) performed a retinal topography analysis in three species of cephalopods: a cuttlefish, a squid and an octopus.

According to the authors:

  It was found that all species possessed an increase in photoreceptor density in a horizontal streak approximately placed at the position of a potential horizon in the habitat.

Here is an image from the same paper:

The retinal topography of each of the three species in this study: (a) S. plangon and (b) O. cyanea show a prominent, horizontally orientated band of increased photoreceptor density across the horizontal equator of the retina; (c) S. lessoniana shows a more centrally positioned area of increased photoreceptor density.

Source: Talbot, C. and Marshall, J. (2011). The retinal topography of three species of coleoid cephalopod: significance for perception of polarized light. Philosophical Transactions of the Royal Society B: Biological Sciences, 366(1565), pp.724-733.


Alternatives to TBE buffer for denaturing polyacrylamide gel electrophoresis of DNA and RNA?

You can try SB (sodium boric acid), LA (lithum acetate) or LB (lithium boric acid) buffers. Thex generate must less heat then TAE or TBE buffers and can be run on much higher voltages and are much cheaper than TAE or TBE. Also they do not interfere with standard applications such as band excision and they last longer.

For more info try this sites:

http://www.fasterbettermedia.com/products.html
http://ddgehelp.blogspot.com/2008/01/alternative-electrophoresis-buffer-to.html


What will happen if one keeps the photosynthesis plant active 24x7?

Ideal conditions for photosynthesis
You mention ideal conditions to carry out photosynthesis, I would just like to point out that this includes carbondioxide levels, temperature, and nutrients as well as light.
Flowering
As anongoodnurse mentions performance might be measured by blooming which, in most flowering plants, has a day-light related component. However, for general growth increasing daylight over the 'natural' day length can often increase yield.
Daylight Cycles
The important point to note is that plants do 'ramp up' at dawn getting ready to start photosynthesizing (for some plants with temporal photosynthesis mechanisms (see CAM photosynthesis) this can be even more important). The reason plants do this is because plants can suffer from 'photobleaching' which can be considered similar to sunburn in humans, if they are not ready for sunlight. Getting 'ready' can involve lots of things including opening stomata (pores) to let CO2 in, changing which metabolic pathways are active,  and moving about chloroplasts inside cells. Plants 'figure out' how and when to ramp up based on circadian rhythms which work well on 24 hour clocks and slight changes over time. Thus 12 hrs to 16 hrs can be a big change, particularly if the change happens by lights coming on earlier. Additionally, the 24 hour 'clock' means that plants will do better with 18hr light then 6hrs dark cycles than 36hrs light 6 hrs dark, because the total cycle length should be about 24hrs.
Photosynthesis Side Effects
Finally, constant photosynthesis does take its toll on plants as photorespiration accompanies photosynthesis. In C3 plants (most crops) this can reduce photosynthetic output by 25% whilst creating ammonia as a byproduct. The ammonia needs to be detoxified as a build up in the cell can cause cell death. Thus plants need enough 'respite' from photosynthesis to deal with photorespiration byproducts or they will suffer.


How does the flow of ions along voltage-gated channels lead to nerve conduction along axons?

The flow of current during action potential generation is perpendicular to the axon length. The channels that transmit ions in neurons are often voltage-gated. Voltage-gated Na+ channels (VGSCs) open when the membrane depolarizes. So when excitatory neurotranmitters (e.g., glutamate) open up channels (e.g., AMPA receptors) in the dendritic region, anions (e.g., Na+) flow in. The ensuing membrane depolarization opens up VGSCs in the axon hillock, that subsequently opens VGSCs adjacently in the axon, that opens up VGSCs a little further up in the axon etc etc. Hence, while the flow of Na+ is perpendicular to the axonal membrane, the net effect is a wave of VGSCs opening up along the axon length. With some delay, voltage-gated K+ channels open that allow K+ to flow in, repolarizing the membrane, preparing the neuron for another action potential (fig. 1).

Fig. 1. Action potential mediated by step wise activation of voltage-gated ion channels. Source: Human Medical Physiology

Hence, although neuronal ion fluxes and networks can be modeled by electric currents flowing in electronic circuitry (Fig. 2), nerve conduction is not anything like it. Current flow in electronic circuits is a flow of electrons. In action potentials in neurons it is ions that carry the transported charge.

.
Fig. 2. Hodgkin & Huxley's axon model. The power sources are the electric gradients of Na+, K+ and a leak current source. The conductances are represented by those same ions. The cell membrane is modeled by a capacitor. Source: Bonabi et al. (2014)

Reference
- Bonabi et al., Front Neurosci (2014)


Why do recessive lethal genetic diseases continue to exist?

Firstly, sorry if this is not so much an answer as a comment, but it is too long to put in the comments section, although I'll try keep it concise...

I can see exactly what you're doing however my math differs at points, and would appreciate you looking over it.

"The expected number of healthy children per couple: 4*(1-p)^2 + 2*2*p*(1-p) + p^2 = 4 - 8*p + 4*p^2 + 4*p - 4*p^2 + p^2= 4 - 4*p - p^2 = (2-p)^2"

Is it not: ... =  4 - 8p + 4p^2 + 4p - 4p^2 + p^2 = 4 - 4p + p^2 = (p-2)^2

Furthermore: "The expected number of carrying: 2*p*(1-p) + 2*p^2 = 2*p - 2*p^2 + 2*p^2 = 2p" - why for the probability of carriers in mixed couples - "2*p*(1-p)" - why have you not multiplied through by two (as with expected healthy children), given that as you said "a mixed couple will have, on average, 2 healthy and 2 carrying children"?

Is it not: 2 *2p(1-p) + 2p^2 = 4p - 4p^2  + 2p^2 = 4p - 2p^2 = 2p(-p + 2)

In this respect I got different expectations. Lastly "Dividing to get the new probability for carrying the gene..." You have done (no. healthy) / (no. carriers). Is the probability for carrying the gene not (no. carriers)/(no. carriers + no. health) - that is the no. carriers as a fraction of the entire population to give a probability?

Using my expectations this would be: [2p(-p+2)] / [2p(-p+2) + (p-2)^2] = [2p(-p+2)] / [-2p^2 + 4p + p^2 - 4p +4] = [2p(-p+2)] / [-p^2 + 4] = [2p(-p+2)] / [(-p + 2)(p + 2)] = 2p / (p+2)

Therefore, with a new probability for carrying of 2p / (p+2), for our "hypothesis" of the diminishing probability of carrying to stand, we need the condition 2p / (p+2) < p to stand, solving for p:

2p < p(p+2) -> 2p < p^2 + 2p -> 0 < p^2 -> p > 0

Since, as a probability, p must be <= 1, and assuming (as we are) that carriers exist and so it must be > 0, p always satisfies this condition - ergo I would conclude that for any value of p - not just small, the probability of carrying will diminish in the next generation. Just as we "hypothesised". However a quick google of "plot y = 2x/(x+2)" would indicate to me that as p approaches 0 it's rate of "diminishing" actually decreases, and it does not get exponentially smaller as you indicated. But solving for y = 0 gives x = 0 so this model would suggest the gene is never actually fully eradicated?! Which of course confuses me, although on a macro scale it might make sense, as you can't have, for example, 0.1 children "carrying", and 99.9 "healthy", only 1 and 99 or 0 and 100.

Thanks for reading this far, any response would be really appreciated, especially given I might be miles off.

Philip.


Tea that makes everything taste like dirt

This sounds like gymnemic acid, which can be isolated from the leaves of Gymnema sylvestre. It’s an “anti-sweet” compound, which wouldn’t necessarily make everything taste like dirt but might do so for you particularly. When I had it, it made my tongue slightly numb and candy tasted like nothing rather than sweetness, so it may not be what you’re looking for.

Lactisole (from coffee beans) is another option, but I haven’t tried that one personally so I’m not sure what its taste effects are like.


Are Purkinje Action Potentials Neuronal and Cardiac?

The His-Purkinje fiber system is a network of one type of specialized conducting cardiac cells that carry an action potential in the heart. There are other cells which perform this function in different parts of the heart. The initiation time, shape, and duration of the action potential are distinctive for different parts of the heart, reflecting their different functions. These distinctions arise because the myocytes in each region of the heart have a characteristic set of channels and anatomy. You can completely dissociate the nervous system from the heart, and the heart will still pace itself. Think of what happens with heart transplants. This completely eliminates neuronal influence. See the following brief excerpt which explains one type of cells conduction method. Please note there is no reference to neurons.

  The positive charge that enters cell A not only depolarizes cell A but also produces a flow of positive charge to cell B—intracellular current. This flow of positive charge discharges the membrane capacitance of cell B, thereby depolarizing cell B and releasing extracellular positive charges that had been associated with the membrane. The movement of this extracellular positive charge from around cell B toward the extracellular region around cell A constitutes the extracellular current. The flow of intracellular current from cell A to cell B and the flow of extracellular current from around cell B to around cell A are equal and opposite. It is the flow of this extracellular current in the heart that gives rise to an instantaneous electrical vector, which changes with time. Each point on an electrocardiogram (ECG) is the sum of the many such electrical vectors, generated by the many cells of the heart.

This has been extensively studied, so much so that cardiac electrophysiologists can pinpoint the location of a small group of cells that are misfiring by the nature of the impulse they are giving off. The annual median salary for an electrophysiologist in the US is $480,000. :-( There is a lot of grant money in this area. It's a big deal.

For in-depth study of electrophysiology of cardiac cells, please see Electrophysiology of Cardiac Cells or any other of a number of reliable sources.


Intrinsically disordered proteins as potential drug targets

IDPs are indeed attractive drug targets and there are ongoing efforts to develop drug molecules that block interactions between a disordered and a structured protein. According to this relatively recent paper, however, these efforts have not brought a drug on the market, yet.

A few promising studies have shown drug-like molecules that inhibit protein-protein interactions based on intrinsic disorder of one of the partners and target:

oncogenic fusion protein EWS-FLI1 and RNA helicase A. A small molecule has been found that targets the disordered region of EWS-FLI1, blocks the interaction with the helicase and inhibits growth of Ewing's sarcoma.
p53 tumor supressor and its interactor Mdm2. Mdm2, by binding to an intrinsically disordered region of p53, targets p53 for ubiquitination and also causes it to be transported out of the nucleus. Promising small molecules  have been found that associate with Mdm2 and thereby block its interaction with p53.
c-Myc oncoprotein and the interaction with its partner Max protein. This study demonstrates two small molecules that bind to c-Myc and stabilize its disordered conformation, which inhibits its interaction with the Max protein.

The challenge in targeting protein-protein interactions for therapies stems largely from the fact, that the protein-protein contact surfaces are much larger than those involved in protein–small-molecule interactions (1,500–3,000 Å2 and (300–1,000 Å2, respectively) [2]. They are often flat and have no defined binding pocket. Also, IDPs often don't bind natural small ligands, that could act as starting points in developing drugs.

You may find this paper helpful:

Metallo SJ, Intrinsically disordered proteins are potential drug targets, Curr Opin Chem Biol. 2010 14(4): 481–488.

BTW: for a comprehensive, manually curated list of disordered proteins and regions, please check the Database of Protein Disorder.


How does the matter that makes up the fat of your fat cells ultimately leave your body--following weight loss?

Yes, they are mostly exhaled. The carbon, hydrogen and oxygen that the fats are made of recombine to become $CO_2$ and $H_2 O$ and are exhaled.

It's the same overall chemical reaction as if the fats / carbohydrates were burnt, except it's by a different pathway, and the energy produced goes (mostly) towards driving other chemical reactions rather than becoming light and heat.


Why does the human brain not overfit when training at some task?

I would say the human brain overfits all the time! Gambling addiction,  superstition and anxiety disorders are all examples of overfitting. We are optimized for seeking patterns and avoiding threats. Our brains mess this up all the time! But having said that, one of the major differences between the human brain and a neural network is the amount of information that's being supplied. Neural networks overfit in part because of limited data sets. Our brains have nearly unlimited data sets available, and this provides us at least the opportunity for some self correction.


Can the dietary fibres as chemical compounds be regarded as polymers?

Dietary fibers are the indigestible portion of food derived from plants.

Most of these are indeed polymers of sugars (that is, a chain of repeated basic unit of carbohydrate), for example cellulose, alginate or pectin. They have glycosidic bonds that cannot be broken down by enzymes found in humans, and are thus indigestible.

But there are exceptions, for example raffinose, a trisaccharide found in beans & cabbage, is also categorised as a dietary fiber, as it is not breakable by human enzymes.


How much nucleoside triphosphate is required to form one peptide bond during protein synthesis?

Although the question shows considerable effort to achieve clarity, the way it is phrased as:

  How many molecules of nucleoside triphosphate… [does] it take to release enough energy

still allows ambiguity, as I would not really regard the NTPs involved in protein synthesis “releasing energy”. So let us consider two reformulations of the question, as the explanation of the answers is of more scientific interest than the actual answers.

1. How many molecules of NTP are hydrolysed in the reactions causing the formation of one peptide bond on the ribosome?

  Answer = 3

Formation of each peptide bond involves a cycle consisting of the introduction of a single new aminoacyl-tRNA to the A site of a ribosome carrying a growing polypeptide chain (or initiator tRNA for the first peptide bond), the peptidyl transferase reaction, and than translocation of the extended peptidyl-tRNA from A- to P-site. (See, e.g. Berg et al. online — Ch. 29)

1 ATP is hydrolysed in the aminoacylation reaction:

                Amino Acid + tRNA + ATP → Aminoacyl-tRNA + AMP + PPi

1 GTP is hydrolysed in the aatRNA binding reaction catalysed by EF-Tu/EF1.

1 GTP is hydrolysed in the translocation reaction catalysed by EF-G/EF2

No NTP is consumed directly in the peptidyl transferase reaction — the energy for bond formation comes from the ‘activated’ aminoacyl-tRNA.

2. What is the total energetic cost in molecules of ATP for the formation of one peptide bond?

Here one might argue that:

  Answer = 4+

The additional ATP occurs if one considers the total energetic cost of the aminoacylation reaction as 2 ATP, not 1 ATP. This arises from the fact that the ATP is hydrolysed to AMP (+PPi) and not ADP. Recycling of the AMP involves first the use of 1 molecule of ATP in the adenylate kinase reaction to produce ADP:

                                 ATP + AMP ⇄ 2ADP

followed by the energy (from membrane ATP synthase) to regenerate ATP from ADP:

                                 ADP + Pi ⇾ ATP

Why 4+? Certain amino acids (e.g. val and ile) are sufficiently similar to one another that the aminoacyl-tRNA synthetases have evolved a proof reading capacity, in which any incorrectly aminoacylated tRNA is hydrolysed. This only occurs for certain amino acids and at a rate that is difficult to determine, so the wastage of the ATP in this manner cannot be calculated precisely.


What's the proper term for "brain waves" read from an EEG?

The terminology around EEGs is variable, dependent on the context;

Brain wave is fine, but has a bit of a popular undertone;
Oscillation, as per the deleted answer,  implicitly refers to a longer-term behavior, i.e., something periodic (EEG);
Waveform is often used to describe a single event with a recognizable shape (ERP, compound action potentials, etc.);
EEG signal/recording/trace is more than fine too, it doesn't carry any implicit meaning about its nature, it does carry relevant information on the method used;
EEG is fine too, EEG means electroencephalogram, the 'gram' suffix comes from Greek, where it means “something written,” or a “drawing”, so literally it means something like "graph of the electrical brain". So simply speaking of 'the EEG' is OK as well.

This list may not be exhaustive, merely illustrative


Eating rarely but a lot, or often but little

Eating many small meals or eating large meals is irrelevant. The only thing that matters is getting the right amount of calories needed for your body to function properly.
Fat accumulation does not happen if you do not go over your daily calorie limit.
After a big meal your food is not only stored as fat but as a polysaccharide form of glucose called glycogen that is stored in the liver and or muscles for later use.
Therefore, there is no better way to eat, it depends on what size you like your meals to be as long as you stay within your calorie range.

See http://www.choosemyplate.gov for more information.


Bananas seem to contain lots of dietary fiber that help move consumed food through the intestines (popular article) thereby promoting digestion. Whether one should eat bananas before or after dinner is probably a debatable subject (Yahoo forum).


doing more assays I found what was the trouble. I used an oligodT for the rtPCR and then I amplified with my polymerase. Probably my RNA sample had not a linear conformation in the region that my reverse primer must join. The oligo dt bint to the polyA region, typical of this type of potyviruses.


How exactly are game theoretical evolutionary models described during implementation for computer simulations?

The field most closely associated with game theoretic models in biology is evolutionary game theory. If modeling is required, then the typical paradigm is agent-based modeling, and a good introductory book is:

  Yoav Shoham and Kevin Leyton-Brown
  [2009], "Multiagent systems:
  algorithmic, game-theoretic, and
  logical foundations", Cambridge
  University press.

As for actually building the model, and what to describe/how, I will take you through my usual procedure since this is a field I specialize in:

Define what type of strategies you think are relevant to the interactions you are modeling. Select what you expect the payoff of those strategies to be. For instance, if you are studying the evolution of cooperation, you might select 'Cooperate' and 'Defect' as your strategies and the Prisoner's dilemma as your pay-off matrix, but maybe you will pick something more general. Unfortunately, in most of EGT a clear distinction between genotype and phenotype is not drawn, and they are usually equated. At the end of this step you have a game matrix G. Sometimes when mutation or innovation are explicitly necessary even in the inviscid model, further analytic approaches are taken at this stage. I recommend Hofbauer & Sigmund (2003) for a broad treatment of step 1.
Now you need a basic intuition of what the 'default' behavior in this interaction is, so solve the replicator dynamics of G.
The main interest in EGT right now is structured populations. This is where computational modeling is typically used. However, before I turn to simulation, I first try the best analytic approach I know. I use the Ohtsuki-Nowak transform on G to analytically solve the interaction for random graphs (Ohtsuki & Nowak, 2006).
If I am still interested in the question, and steps 2 and 3 didn't capture all the subtlety of the system I want to study, then I start building a multi-agent computational model. I make sure that my model has some way to scale to the completely inviscid case of replicatory dynamics, and the simply-structured case of ON-transform. If my computational model disagrees with the analytic approach in these regimes, then I become worried. Otherwise, I continue with standard agent-based modeling techniques. Personally, I code in Matlab. I have never seen a modern EGT simulation that required the performance of C/Fortran. As suggested in another answer, if you don't have a programming background then you can use NetLogo. However, my experience is that the models are typically simple enough to implement from scratch, and NetLogo models typically hide from you some very important subtleties (like which reproduction rule to use: death-birth, birth-death, immitation?) and usually lead to weaker papers.

Note the broad theme. These models are typically described as differential equations, and this approach is preferred to agent-based models. However, if a clean differential equations approach does not capture all the subtleties of what you are studying, then an ABM paradigm is adopted.


Is this answer about the limiting factor correct?

I agree with you, and think that there is a mistake in the "Correct answer". The interpretation in the "Explanation" seems to be correct though ("Algae at locations 4 and 5 exhibited growth in response to fertilization with nitrogen."), so I think that there is a typo/mistake in the "correct answer". The answer should be D.

Normally within ecology (and especially in reference to nutrients, such as  nitrogen and phosphorus), limiting factor refers to the substance/nutrient that is in short supply within a particular environment, and is therefore limiting the potential growth of organisms. For examples, see any ecological textbook or Blumenthal et al (2001) (as an article example, picked at random). The concept of limiting factors is related to Liebig's_law, which states that growth of organisms is determined by the scarcest resource, and not the total level of resources.

When performing a couple of searches now, I see some instances though where the term limiting factor is used on the opposite way, in reference to toxic substances. One example of this is Imadi et al (2016), where monomeric aluminum reduces root growth due to aluminum toxicity. This is not the most common use of the term though.


Helium is not as dense as air, and when your vocal cord vibrate with the helium, it vibrates at a higher frequency, making your voice higher. sulfur hexafluoride Is Denser than air, making your voice deeper.


For how long can influenza survive on a piece of paper?

Perhaps just eight to 12 hours.

  Both influenza A and B viruses survived for 24-48 hr on hard, nonporous surfaces such as stainless steel and plastic but survived for less than 8-12 hr on cloth, paper, and tissues. Measurable quantities of influenza A virus were transferred from stainless steel surfaces to hands for 24 hr and from tissues to hands for up to 15 min.

--Survival of influenza viruses on environmental surfaces.

Or, perhaps, up to 17 days, when in the presence of "respiratory mucus" (i.e. snot), although even then a couple days was more plausible. Note that this was on Swiss banknotes, which isn't standard paper.

  Influenza A viruses tested by cell culture survived up to 3 days when they were inoculated at high concentrations. The same inoculum in the presence of respiratory mucus showed a striking increase in survival time (up to 17 days)....  When nasopharyngeal secretions of naturally infected children were used, influenza virus survived for at least 48 h in one-third of the cases.

-- Survival of influenza virus on banknotes.


As far as I am concerned the intra-assay CV is the average of individual CVs found in an assay.

So let's assume you have a data set of 40 samples, and for each sample you have 2 replicates (results), like the one below.

You would first calculate the mean for each sample, so in the sample above that would be: $$\frac{0.132 + 0.128}{2} = 0.130$$

Then you would calculate the standard deviation for each sample, so going back to our example above, the standard deviation for sample 1 would be as follows: $$\sigma=\sqrt{\frac{1}{2} ((0.132-0.130)^2 + (0.128 - 0.130)^2)}=\frac{1}{500}=0.002$$

Next you would calculate the Coefficient of Variation, so in our case:

$$CV = \frac{\sigma}{\bar{x}}\times100=\frac{0.002}{0.130}\times100\approx1.6%$$

Afterwards you would repeat the aforementioned procedure for each sample.

In the end you would calculate the average of all individual CVs, so: $$CV_{intra} = \frac{\sum_{i=1}^{40} CV}{40} \approx 5.2% $$

I have stolen the example from Salimetrics, I think this document explains inter-assay and intra-assay CV very nicely.

Please note: The usefulness of inter and intra-assay CVs are somewhat disputed, as this Wikipedia article mentions.


Understanding of the saturation function in the Monod-Wyman-Changeux Model

I don't have access to Sneyd's Mathematical Physiology, but in Wikipedia's description of the Monod-Wyman-Changeux model, they call Y the "fractional occupancy of the ligand binding site". Other references refer to it as the "fractional saturation".

In other words, it's simply the fraction of the binding sites which currently have ligands bound to them. The denominator, then, is the total number of binding sites, which is equivalent (for a unit volume) to the total concentration of the protein (i.e. the sum of every protein form) times the number of binding sites per protein.

The numerator is the number of ligand-bound binding sites. Which is equivalent (for a unit volume) to the concentration of each form, multiplied by the number of ligands bound to it. So the zero-ligand forms are multiplied by zero, the one-ligand forms are multiplied by one, the two-ligand forms are multiplied by two, etc. (This doesn't reflect "doubly concentrated", rather it reflects the stoichiometry: for each protein molecule in the 2-bound state, there are two ligand molecules bound to it.)

So the answer to your boxed question is yes: that would be the appropriate form for a cooperative protein with three binding sites.


Can bacterial RNA be degraded at -80⁰C in a SDS solution?

I think it is relatively unlikely that the RNA will degrade under these conditions. For the future, I would handle this differently:

You can centrifuge the cells and snap freeze them in an appropriate
buffer in liquid nitrogen and then store them at -80°C. I would not freeze the dry pellet, as these are often hard to re-dissolve after freezing.
Alternatively, you centrifuge them, break them up with Trizol (or whatever you use for this purpose) and freeze them in this solution. This will be
safer as it completely denatures all proteins including all nucleases.

I would choose (and have done this already several times with cell samples that I couldn't process without problems) the second method.


What said by ebrohman is correct. In fact there are two factor that led to leaves falling when fall approaching: photoperiod and the circadian rhythm (24 hours) of the plant.
In the circadian rhythm is possible observe oscillation in proteins expression. Some of the proteins that regulate leaves abscission (aka falling) have an oscillations in their expression and present a pic of the expression in the late afternoon. Moreover to be active this protein need to be on "a dark" condition because the light will lead to proteins degradation.

For exemple

Imagine that in summer there is a long day condition with sunlight present from 7am until 20am (photoperiod) and that the proteins that lead to leaves abscission is expressed by the plant around 6pm (circadian rhythm). Due the presence of the sunlight the proteins will be degrade.
When the hour of sunlight decrease (with fall approaching) the proteins is day by day less degraded and this could led to the plant to prepare itself for the winter, also with the leaves abscission.

If you are interested to know more about the argument I can suggest you an interesting review write by Pin and Nilsson (2012)

Cold
Is possible that a decrease in the temperature lead to a leaves falling. However I think that temperature has to decrease significantly over more day to allow any changes in plants structure.

I hope that my answer could help, if you do not understand something let me know. I will try to explain it in a different way.


Cell growth conditions for preparing electrocompetent cells

I'm new so I can't make this a comment, and I don't think the other commenter addressed your questions so here it goes: I don't think there will be much difference, if any, between 0.2 and 0.3 OD. Once you get higher and the cells start transitioning into a stationary phase is a different story. Did you mean to ask about 0.03 OD as well (you wrote 03.)? I'm not an expert in E. Coli, but they would probably be less likely to produce proteins that are contact inhibited. Sub-optimal temperatures may have a minor effect on growth, but I don't believe this will initiate much change or induce production of large amounts of cold shock proteins.


Why are high levels of epinephrine and low levels of cortisol signs of stress?

So it seems to me that signs of stress would be high levels of both of these things.

Yes. Wikipedia claims [1] the same:

  Stressors [...] activate the HPA axis, though via different pathways. [...] Stressors that are uncontrollable, threaten physical integrity, or involve trauma tend to have a high, flat diurnal profile of cortisol release (with lower-than-normal levels of cortisol in the morning and higher-than-normal levels in the evening) resulting in a high overall level of daily cortisol release. On the other hand, controllable stressors tend to produce higher-than-normal morning cortisol.

The same on a webpage of Society for Endocrinology [2]:

  In addition, in response to stress, extra cortisol is released to help the body to respond appropriately.

Yet, there are conditions in which stress can lower cortisol levels. One of them is psoriazis [3]:

  [...] patients with persistently high levels of stressors seem to have a specific psychophysiological profile of lowered cortisol levels and may be particularly vulnerable to the influence of stressors on their psoriasis.

And some psychiatric disorders [4]:

  Several stress-associated neuropsychiatric disorders, notably posttraumatic stress disorder and chronic pain and fatigue syndromes, paradoxically exhibit somewhat low plasma levels of the stress hormone cortisol.

References:

Wikipedia contributors, "Hypothalamic–pituitary–adrenal axis," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Hypothalamic%E2%80%93pituitary%E2%80%93adrenal_axis&oldid=619115237 (accessed August 7, 2014).
Society for Endocrinology. Hormones. Cortisol (2013). Available from http://www.yourhormones.info/hormones/cortisol.aspx (accessed 07.08.2014)
Evers AW, Verhoeven EW, Kraaimaat FW, de Jong EM, de Brouwer SJ, Schalkwijk J, Sweep FC, van de Kerkhof PC. How stress gets under the skin: cortisol and stress reactivity in psoriasis. Br. J. Dermatol. 2010 Nov;163(5):986-91. doi: 10.1111/j.1365-2133.2010.09984.x. PubMed PMID: 20716227.
Yehuda R, Seckl J. Minireview: Stress-related psychiatric disorders with low cortisol levels: a metabolic hypothesis. Endocrinology. 2011 Dec;152(12):4496-503. doi: 10.1210/en.2011-1218. PubMed PMID: 21971152.


Is the number of nucleoli in a nucleus fixed?

I'll directly go to your fourth question, as all of them can be answered with a yes. This rather old mouse paper already got to the point. Sadly, only the abstract is freely available. Briefly, the number can be variable in the smallest unit you are interested in, the cell type. From the abstract:

The distribution of the number of nucleoli in many diploid cells
exhibited a mode of two or three nucleoli per nucleus, and a range
from 1 to 6 nucleoli.

In the paper, there are histogram of different cell types of mouse and all of them seem to be variable in their number of nucleoli.


Why does no one get vaccinated against plague in Europe?

Ask yourself when was the last time that you went to a friend's home and had to worry about getting flea bites? Modern cities still have lots of rats, but modern construction, pesticides, and hygiene have greatly reduced the number of encounters between fleas and people. Contrast that with the early 18th century. When the young George Washington wrote an essay on civil behavior, he felt it worth while to include this item:

  13th Kill no Vermin as Fleas, lice ticks in the Sight of Others, if
  you See any filth or thick Spittle put your foot Dexteriously upon it
  if it be upon the Cloths of your Companions, Put it off privately, and
  if it be upon your own Cloths return Thanks to him who puts it off.

Plague is almost exclusively transmitted to humans by fleas (the pneumonic form of the disease can be transmitted by aerosols but is rare). Few encounters with fleas, few cases of the Plague.

Mumps and measles (for example) are transmitted by human to human contact. No fleas needed. Modern life may have done away with flea bites, but it has only increased the number of persons we come in contact with each day. If you think about it, all the diseases we commonly get vaccinations for are ones spread by direct human to human contact: smallpox, polio, diphtheria, whooping cough, mumps, measles, flu. Tetanus vaccines are an exception, but that's a bacteria that is ubiquitous in the environment, and causes a very nasty disease.


Experiments in vitro vs those with dead organisms and fixated tissue

Does the term in vitro necessarily imply that the organism/organs/cells of study are dead?

No, in vitro studies are often carried out with living cells - just think of in vitro fertilisation. The nearest I can come up with for what you want is histology, but I think even this encompasses studies of living cells and tissues.


What is this snail? (Location: Bangkok, Thailan; size: 3 cm long, 5 mm wide; color: mostly black)

Possibly Macrochlamys indica or another species in the same genus, based on shell morphology.

Source


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

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


Is mate choice in non-human primates MHC-dependent?

tl;dr It's messy for non-human primates too. Winternitz et al. (2017) ("Patterns of MHC‐dependent mate selection in humans and nonhuman primates: a meta‐analysis", Molecular Ecology 26(2)) review studies of MHC-based mate choice in human and non-human primates. Some of the take-home messages, mostly from the abstract:

  [abstract] the overall effect sizes of primate MHC-based mating preferences
  are relatively weak ... calling for careful sampling design in future studies.

There is a

  "systematic trend" for primates preferring MHC diversity (p. 679)

(I think this means "not significant" ...)

  (p. 680) Nonhuman primates tend to consistently prefer MHC-dissimilar mates (Fig. 4a), but our power to detect a significant average effect is limited by our small sample size (N=6) and by the addition of random effects to control for pseudoreplication.

For MHC-diversity preferences:

  Examined separately ...  nonhuman primates had a non-significant trend for mate choice for diversity (primates = 0.110 (-0.207 to 0.456), N=7, Fig. 1b)

Here are some of the key figures (these figures also include data for humans, omitted here). However, note that the overall estimates in this figure do not account for the effects of study ID and phylogenetic relatedness (see Figure 1 in the paper), which tend to make the confidence intervals wider/weaken the statistical significance.

Figure 4a, preference for MHC-dissimilar mates [disassortativity] (overall CI is [-0.01, 0.18], consistent with the "almost significant" comment referenced above)

Figure 4b, preference for MHC-similar mates [assortativity]:

For reference, the species included here are: Rhinopithecus roxellana (golden/Sichuan snub-nosed monkey); Cheirogaleus medius (fat-tailed dwarf lemur); Papio ursinus (Chacma/Cape baboon); Microcebus murinus (gray mouse lemur); Mandrillus sphinx (mandrill); Macaca mulatta (Rhesus macaque).


Notice: the only select agent I've worked with is VSV which was a USDA select pathogen (not as big of a concern for humans).

TLDR:  It would provide some protection, but I would be most worried about a false sense of security.  It would unlikely be up to rated standards, but it would likely be better than a t-shirt.

First let's start with ebolaviruses.

Ebola, like HIV and many other viruses, doesn't do well outside a host.  This might be because the protein structures beneficial in the host are not the same as needed for stability in exposed air and room temperature.  A counter example of a very stable virus would be something like human rhino virus (HRV).  If HRV was compared to be like a rock, ebola would be over cooked spaghetti.

Certainly the virus has to maintain some stability in the environment, otherwise it wouldn't succeed evolutionary.  As I'm sure you've heard on the news, ebola is spread by contact with contaminated fluids.  I would like to point out a wonderful info-graphic that was made for public consumption, especially the image on viral life cycle:

Assuming that you're not going splunking in bat inhabited caves in West Africa, it's safe to assume that what we are worried about is human to human transmission through infectious fluids.  Ebola actual isn't that stable in water, so just soaking a surface in water and a little oil might help you out (if you don't have bleach handy).  I want to be clear that I'm not recommending this, in reality you should just avoid contaminated objects.  I think that we have clearly established that what we're really concerned about is infectious bodily fluid.

This leads me to the wonderful note by Jose Martin-Moreno titled "Is respiratory protection appropriate in the Ebola response?"  I don't think I can express the problem better than he can, so hopefully I will be allowed a substantial quote:

  This transmission [of ebola] occurs via close family contact or in
  health-care settings, particularly when placing orotracheal intubation
  or when caring for a patient who is vomiting or bleeding. Ebola is
  rarely transmitted via an airborne route. Although these routes of
  transmission are well known, most agencies, including governmental
  agencies responsible for repatriating western patients, apply
  infection-control measures appropriate for airborne diseases.
  Excessive precautions could offer reassurance to those responding to
  Ebola, yet complete respiratory protection is expensive,
  uncomfortable, and unaffordable for countries that are the most
  affected. Worse, such an approach suggests that the only defence is
  individual protective equipment, which is inaccessible to the general
  population. Moreover, the image of workers with spectacular protective
  clothing might contribute to the panic in some communities. If this
  leads people to flee affected areas it could increase the spread of
  infection.

With that said, all your full face gas mask is going to help with is prevention of fluids from hitting your head.  You could probably take the actual filters out to breath more easily (I find breathing in them a giant pain).  And as @Chris pointed out, they are easily clogged which could necessitate the need to take off the whole mask (which might be doing some good) to prevent suffocation.

Moving to hazmat suit.

It's actually good news that you don't need the air containment of the suit, as that's the hardest element to maintain.  To state the obvious, the main purpose of the suit is to prevent your body from coming in contact with infectious fluids (in this case).  To do that you don't need to be in positive pressure personnel suit (PPPE), or follow BSL4 considerations.  The respiratory concerns from in an BSL4 environment come from other select agents, and the personal working in such a facility are going to be doing very different activities from what you should be doing as person trying to avoid an outbreak (they could be purposefully growing up purified high-titer virus stocks and running around with pointy things as an example).

Here I'm going to run into citation problems because no one (that I could find) has tested the kind of scenario I'm about to discuss, so it should be seen as informed conjecture.  Assuming yous suit is actually an analog of a Tychem QC suit, it's probably not a rated OSHA unit (A-D), but that doesn't necessarily matter.

On it's first use it would likely be sufficient to protect against incidental exposure.  Let's assume for the sake of argument that you didn't run into any Ebola when you used it as a costume, and don't the next time you put it on.  At this point decontamination (decon) isn't the concern, failure of the material is.  In other words, are you sure you don't have any holes, tears or cracks in the material?  I think this is going to be the real limiting factor in the life of the suit.  Using good old fashioned duct tape will be give you a few more uses, but the suits are just not designed to last through prolonged use.

Now let's assume the worst and that you get substantial blood splatter on you (while wearing your suit) from an ebola patient.  And not a little that could easily be wiped of with a spray bottle of 10% bleach and a paper towel (how most decon could be done).  Instead let's assume you're standing next to someone who suffers a traumatic injury on top of having ebola virus disease (EVD).  I'm imagining something like a point-blank shotgun wound or, given the probability of this scenario, a falling grand piano. In this case, you're going to want to decontaminate the suit before you take it off, which is the same thing professionals are going to do.

If you're friends with your local fire department, and you live in an area with a large enough population to have a HAZMAT team, you can probably get them to at least give you a run through of how it's done in ideal conditions.  YouTube videos are also not hard to find, just search JESTC and decontamination.

Presumably you would have a hard time going through several rinse and wash steps, but you would want emulate this as much as possible.  With ebola, you would be fine to decontaminate with a 10% bleach solution (or if you use bargain/cheap bleach 15%).  The trick is that you would want to do it a few times, and with a friend (also hopefully in a suit).  Thus if you got two generic soap sprayers, filled one with 10% bleach, and the other with water, and then alternated spraying your partner with bleach and water, wiping down as you went, you should be able to decon the suit pretty well.  If possible you're going to want to collect all the run off an rinsate.  Again professionals tend to use actual kiddie pools for this.

But just the act of using so much bleach on the suit is going to weaken the fabric, again leading to the principle problem of failure of the fabric. Thus I would be worried that such a suit would provide a false sense of security, leading one to go into dangerous infectious environments when one shouldn't.  Just avoiding and going away from contaminated individuals is going to be the best solution, regardless of a suit.

I considered going into why I think it's highly unlikely that any of the ebolaviruses would evolve to be airborne, but I consider that outside the scope of the question.


The IC50 is the concentration of an inhibitor at which you observe the half maximal inhibition. See the figure from the Wikipedia:

The IC50 can be seen as a way to measure the effectiveness of an inhibitor on a biological function as an enzyme. In the case of PD180970 you have an inhibitor which inhibits the p210 Bcr-Abl tyrosine kinase. The IC50 is the concentration at which 50% of the kinase is inhibited.

In table 1 different mutations of the tyrosine kinase are tested against the inhibitor to see, if the mutations have an influence on the IC50. This is important as PD180970 is considered as an anti-cancer drug and possible mutations would make it less effective here.


Are SNPs or SSR copy number variation mutations more prominent?

It's not really clear to me what you're after when you ask about how prominent or dominant these two kinds of variations are. But let's look deeper.
Guichoux et al. (1) say:

There are two main differences between SSRs and SNPs. First, SNPs are more numerous than SSRs in the genome of most species. On average, in the human genome, there is one SNP every 100–300 bp (Thorisson et al. 2005), com-pared to one SSR locus every 2–30 kb (Webster et al. 2002), depending on how SSRs are defined (Kelkar et al. 2010).This can be important for genome-wide association studies but not necessarily for other applications. Second, the mutation rate per generation differs drastically between the two marker types. SSRs have mutation rates ranging from $10^3$ to $10^4$ per locus per generation (Ellegren 2000), compared to about $10^9$ for SNPs, i.e. several orders of magnitude lower. As a consequence, SNPs are typically diallelic: In humans, < 0.1% of SNPs are triallelic (Lai 2001).In contrast, SSR loci generally have high allelic richness, often in excess of 10 alleles.

Based on these numbers, SNPs occur perhaps 80 times as often as SSRs.  Is that more prominent?
An SSR is larger than an SNP, covering perhaps one hundred to several hundred bases versus one base (by definition).  An SSR locus also occurs in multiple variants, e.g. having a copy number from a wide range, versus only two possible variants that usually occur for an SNP locus.
The mutation rates are substantially different, apparently typically 5 orders of magnitude more frequent for SSRs than for SNPs.  Note, though, that mutation rate does not directly affect the frequency of variants seen in the genomes of extant organisms: the variants present are a result of the filtering of mutations by the forces of selection.
Note also that all bases are subject to mutation, thereby producing an SNP, but SSR mutations only occur where a repetitive sequence already exists.  (Also, the likelihood of mutation becomes significant only when the existing sequence has more than a few repeats, as the mechanism of mutation depends on this.)
A main question, though, is what is the significance of the variation?  Are you interested in variation just because they mark individual genomes within a population, or are you interested in the variation of the phenotypes of individuals?  Some genetic loci are irrelevant to phenotype and some can affect the phenotype to lesser or greater degree.  SNPs can occur anywhere so can be presumed to have a "fair" chance of affecting phenotype.  On the other hand SSRs can occur where only where repetitive sequences can occur (and persist where they survive selective forces). With SSRs, varying copy number in some contexts such as protein coding sequences, may have larger phenotype effects than an SNP, and thus be subject to stronger selection forces.
My view is that both SSRs and SNPs are important and it's not terribly productive to worry about general prominence or dominance of one over the other.
Reference:
(1) Guichoux, Erwan & Lagache, Lelia & Wagner, Stefanie & Chaumeil, Philippe & Léger, Patrick & Lepais, Olivier & Lepoittevin, Camille & Malausa, Thibaut & Revardel, Emmanuelle & Salin, Franck & Petit, Rémy. (2011). Current trends in microsatellite genotyping. Molecular ecology resources. 11. 591-611. 10.1111/j.1755-0998.2011.03014.x.


Fasting gastric pH versus normal gastric pH

The stomach linings generally secrete gastric acid (HCl, KCl and NaCl) and the native pH of the stomach is around 2. The longer you fast, gastric acid levels keep increasing until it reaches around 1-1.5. The food that you eat increases the pH levels of your stomach because the acid reacts with the food while digestion. Depending upon the type of food you eat, the pH levels of your stomach vary, but it is generally around 4-5 (again it varies depending upon the type and amount of food there is in the stomach).


Are the human genes' promoters all known?

Nope. The human genome is still quite unexplored, new genes are still being discovered and the annotation of non-protein-coding regions (that include promoters) is still far from being complete. For example, look at the Statistics comparison of the current and previous Human GENCODE Release, it clearly shows that the annotation of the human genome is still an ongoing process.


The condensation is not done in water alone - the enzymatic function of the ribosome plays the essential part here. And in the active center of the ribosome where the formation of the peptide bond takes place, no water is present, only the growing peptide chain and the single amino acid (bound to the tRNA). See this schematic image from the Wikipedia:

If you make x-ray crystallography, this looks like this (from here). You can see that the tRNA with the unbound amino acid is actually inside the ribosome and protected from the outside:


How does the muscle return to its resting state after muscle contraction?

ad 1. : In skeletal muscle, contraction of the antagonist stretches the agonist to its original position (Fig. 1).

ad 2. : Yes, ATP generates a fixed amount of energy that limits the force generated.

Fig. 1. Agonist/antagonist pairs in the skeletal musculature have opposing actions. source: wikipedia


Why there is no vaccine against Human Immunodeficiency Virus (HIV)?

One of the reasons we don't have an HIV vaccine yet is we've only been trying to make one for a little over 30 years. It can take a long time to develop a vaccine. Beyond that, there are a number of specific challenges.

One of them is that, yes as your teacher said, the virus is highly variable. Specifically, the parts of the viral proteins involved in binding and infecting a host cell are highly variable. There are a number of other challenges. One important and related challenge is that, unlike with many vaccine preventable diseases (e.g., measles), an successful HIV vaccine will have to entirely prevent infection  rather than just control and clear infection without developing disease. Once a reservoir of infected cells is established, the opportunity for clearance is gone. This makes the production and maintenance of high titers of neutralizing antibodies that much more important.

There is a very good review of the challenges and current directions of HIV vaccine development here


Is it possible to see the microbes on your hand without using UV light or a microscope?

Given your constraints, the only solution available would require some amount of preparation. If you are so inclined, you can purchase sterile, ready-to-use agar plates online, which you can then inoculate with microorganisms from your hands by simply touching the agar surface with your palms, and letting the plates incubate at room temperature. A day or two's time should be sufficient for plenty of microorganisms to grow, allowing you to demonstrate that your hands have "germs" (although some of the microorganisms you'll find on your agar plate may very well be airborne contaminants if you don't take some precautions).


I saw, it has long (about 1 inches) long hair on his body.

The hairs you refer to may be urticating hairs, which can cause extreme itching & irritation. Without a picture of the caterpillar, I can't say for sure though; out of extra precaution, let's just assume they are (until an image is provided).

  Are they dangerous?

As long as you don't let the caterpillar hair come into contact with your bare skin/body, there should be no risk of harm. That being said, be mindful of indirect contact; i.e., perhaps picking the caterpillar up with your shirt sleeve, the hairs now being on the sleeve, then you wiping your face with your shirt sleeve later in the day. See here for more information, including treatment, should said exposure ever occur.

  Do they bite?

Caterpillars do have the ability to bite, however, their bite isn't strong enough to pierce human skin. Nothing to worry about here..

  How to get rid of them?

To "get rid" of the caterpillar, I recommend getting a hard, thin surface - such as a piece of cardboard - ushering the caterpillar onto the surface, and then placing the caterpillar somewhere safe outside. If the caterpillar is in the process of molting, relocation can easily kill it, so please be diligent when attempting to relocate.


Please help identify insect found indoor in Malaysia, south east Asia

In the USA we call these insects crickets. Because they make a noise that sounds like the pronunciation of their name. This one looks like a male with two cerci.


How could this molecule affect the body? (Lysergic acid derivative)

That is lysergic acid piperidide, an analog of lysergic acid diethylamide (LSD). According to Wikipedia, it is an agonist of the 5-HT2A receptor, but is much less potent than LSD.


Humans cannot hibernate. There are a number of reasons why we would not expect them to do so.

Hibernation is thought to be an evolutionary adaptation to cold temperatures, and food scarcity, (perhaps also predator avoidance). Humans evolved in tropical regions with an abundance of food, and are also considered apex predators. There was thus no evolutionary pressure.

If we were to induce sleep with the relevant pitutary hormones. Humans would likely die, if they do not have any life support.


Can hepatitis B also infect vaccinated persons?

It is possible but the chance is somewhat low - 10%.

You can check to be sure that the level of surface antibody in your blood is efficient by a simple blood test.

The Hepatitis B vaccine is very effective at preventing Hepatitis B virus infection. After receiving all three doses, Hepatitis B vaccine provides greater than 90% protection to infants, children, and adults immunized before being exposed to the virus.

In highly endemic areas, Hepatitis B is most commonly spread from mother to child at birth (perinatal transmission), or through horizontal transmission (exposure to infected blood), especially from an infected child to an uninfected child during the first 5 years of life.

Find more about this here:

http://www.who.int/mediacentre/factsheets/fs204/en/

You can find all about Hepatitis B vaccine on the CDC's website:

http://www.cdc.gov/vaccines/vpd-vac/hepb/public/index.html


Your question is relative to the species concept that you are using. Mayr's biological species concept (BSC) is based on the ability to interbreed; a process-based definition. Most biologists use it, but most taxonomists, who are the people who actually describe species, use some variation of the phylogenetic species concept. The phylogenetic species concept is not based on process, but on fixed differences. Fixed differences are evidence of a lack of interbreeding, but the concept is not explicitly based on reproduction. Fixed morphological differences have been used to classify microbes, most often in culture. But currently, microbes are most often classified with a combination of morphological and genetic characters. The small subunit rRNA is sequenced and put through an algorithm for estimating species based on genetic distances. In short, your question depends a lot on which species concept you are using, and whether you would accept a distance-based DNA definition. But species need not be defined reproductively.


How long does it take to form a peptide bond?

Alberts et al, Molecular Biology of the Cell, say that eukaryotic ribosomes add about 2 amino acids per second, and bacterial about 20 per second (5th edition, p 275). These should be taken only as ballpark estimates: the rate certainly will vary from species to species, from cell to cell, from protein to protein. Some cells (reticulocytes, for instance) are professional protein synthesizers. Others, for instance bacterial endospores, do almost no protein synthesis at all.

These authors estimate the translation rate in mouse embryonic stem cells at around 5.5 amino acids/second. There is a lot of variation from gene to gene, even within this one cell type. They even see systematic variation depending on where you are in the gene.


Can viruses be reintroduced to humans from ice sheets?

Yes, pathogens have been shown to survive freezing temperatures under ice and still remain potentially dangerous after the melting of ice.
This has not only happened for relatively simple molecules such as the ones that viruses are made out of, but it has also even happened with larger pathogens such as bacteria (anthrax outbreak in 2016).
Unlike high temperatures which can cause molecules to dissociate due to excess kinetic energy, freezing temperatures usually preserve molecules and even cells such as with the aforementioned anthrax outbreak. This means that viruses can survive cryogenesis.
In 2015, researchers in Tibet discovered 28 'new' species of viruses in (melting glaciers).
These sort of discoveries lead many to believe that with global warming, previously unknown viruses could appear once again.
As for SARS-CoV-2, it seems that melted ice sheets are unlikely to be the source of such a virus considering (among other reasons) that the virus was first noticed in Wuhan China, a place lacking permafrost.


What would happen if there were no more spiders?

Spiders are extremely important predators, both in "natural" ecosystems and in agriculture. They therefore function as biocontrol agents, and without them we would suffer larger crop damage from pest insects (or would require much higher levels of pesticide use). Loosing them from all natural ecosystems would also cause enormous effects, due to cascading effects through the foodwebs. The effects would differ between different ecosystems though (with the largest effects probably in forests and grasslands, see links 3 and 4 below), and nobody can really overview or predict the full implications.

  A new study reveals some stunning estimates about just how much the world’s spiders eat annually: between 400 and 800 million tons of insects, springtails, and other invertebrates. In the process, these eight-legged carnivores play an important role to keep countless insect pests, especially in forests and grassland areas, in check.

(from third link below)

For more, see e.g.:

Rusch & Bommarco. 2016. Agricultural landscape simplification reduces natural pest control: A quantitative synthesis. Agriculture, Ecosystems & Environment
Öberg & Ekbom. 2006. Recolonisation and distribution of spiders and carabids in cereal fields after spring sowing. Annals of applied biology. DOI: 10.1016/j.agee.2016.01.039
Spiders eat astronomical numbers of Insects (popular overview of paper below)
Nyffeler, M. & Birkhofer, K. (2017). An estimated 400-800 million tons of prey are annually killed by the global spider community. The Science of Nature


Can a gene be inactivated using CRISPR if it is not in the interspace of short palindromic repeats?

When people talk about genome editing with CRISPR, they are really talking about using CRISPR associated nucleases like Cas9 and Cpf1. These nucleases are useful since their sequence specificity is determined by a guide RNA and they can therefore be used to cut at specific sites in the genome. This actually has nothing to do with the repeats themselves.

See this answer for a brief overview of how genome editing with Cas9 works.


why do marine organisms orient with their bellies facing downwards?

I'll address fish here. It's hard to tell which way is up with many sea-dwelling invertebrates, e.g. sea cucumbers. Sea urchins often are oriented "sideways" if you count their mouths as "down".

All animals normally orient themselves in the most advantageous manner dependent on their situation. Probably the most important determiners are field of vision and the inner ears, which work much like those of humans (who walk upright even if blind.) Unlike land vertebrates, the ear of fish is thought to have evolved as a vestibular organ for balance and orientation in space rather than as an auditory organ. Fish (and other sea creatures) also have other sensory apparatus which orient them, such as lateral lines.

Pipe fish swim in a horizontal manner like other fish, but rest vertically, swaying with the sea grass around it. Flatfish start "normal" but as the eye shifts position to the other side of the head, it will assume a bottom dwelling "sideways" position, with a contorted mouth and a fin squashed against the sand.

  “Flatfish are the most asymmetrically-shaped vertebrate to ever live on earth,” says Alexander Schreiber, a flatfish expert at St. Lawrence University. “It sounds likes a really dramatic thing to say, but as far as vertebrates go, it’s true.”

Apparently flatfish brains start to receive stronger signals from one inner ear than the other.

  Two organs — the eyes and inner ears — work together to keep typical fish in an upright swimming posture... If the eyes are not receiving the same amount of light on each retina... retinal neurons trigger the brain to tilt the entire animal and set it straight. ...As a fish’s vertical orientation in water changes, the brain combines information from the eyes and ears to figure out which way is up. ...[f]latfish larvae that are deliberately blinded adopt a sideways swimming posture.

When snorkeling, it is not at all uncommon to see any of a number of fish flip to their sides side to get a good look at you (floating above) with one eye, as opposed to maneuvering itself to face you. I imaging they assess the threat; since I wasn't a threat, they would just reorient themselves normally and go about their business.

Whatever aids survival within the parameters they are confined to (were born with) in that niche will be what you see.

The Improbable—but True—Evolutionary Tale of Flatfishes
The Vestibular System and Sense of Equilibrium in Fish


Does crossover happen between chromosomes from grandparents?

Your question and your rephrased question aren't asking the same thing, so you may want to edit your question.

Crossover occurs during meiosis, which is a type of cell division that occurs in the generation of gametes, during which of course only the chromosomes from one of the eventual parents would be present. Meiosis doesn't occur in the fetus, except eventually in the germ line cells.


Amino acids in human cancer cells expose dextrorotation?

I took a 30 second look at the book you mentioned. The authors just made this up, just like 95% of the book.

The authors are not wrong, they didn't want to write something useful and made a mistake, they're just bullshitting: They're making stuff up, letting it sound a tiny bit scientific and try to sell a lot of books.

If you want to know more about something, usually Wikipedia is a good place to start, and if you're not sure how to distinguish between science and pseudoscience it might be a good idea to read a bit about recognizing pseudoscience.

Now to answer your question: cancer cells are almost the same as normal cells, and they contain mostly levorotatory amino acids. The main difference between a cancer cell and a normal cell is that the cancer cell has one or more mutations that cause it to divide a lot more than normal cells. The DNA, proteins and small molecules in the cells are mostly the same as in normal cells, that's why it's so hard to specifically kill cancer cells.


How does SDS-PAGE separate based on mass?

You are correct that molecule mobility depends on the mass-to-charge ratio, and this means that different sized molecules with the same $\frac{m}{q}$ will have the same acceleration.  However, the velocity of a molecule moving through a gel matrix depends on the point at which the force exerted by the electric field is in equilibrium with the frictional forces acting on the molecule.  Modeling different sized molecules as spheres of different sizes, we can apply Stokes' Law

$F = 6\pi \mu Rv$

where $\mu$ is viscosity of the matrix (constant), $R$ is the radius of our molecule, and $v$ is the flow velocity.

Rewriting your equation, we see that

$F = qE = ma = 6\pi \mu Rv$

and

$v = \frac {ma}{6\pi \mu R}$

For constant $a$ and $\mu$, we see that velocity varies with the ratio of mass to radius

$v \sim \frac{m}{R}$

For our model spheres, assuming uniform density, radius scales cubically with mass, meaning that $\frac{m}{R}$ decreases as molecule size increases.

($d = \frac{m}{V}$ and $V = \frac{4}{3}\pi R^3$ where $d$ is density and $V$ is volume)

So, larger molecules will reach force equilibrium with the opposing frictional resistance at a lower velocity compared to smaller molecules, thus explaining how different sized molecules with the same $\frac{m}{q}$ will separate on a gel.  One caveat to this explanation is that polypeptides and nucleic acids are poorly modeled by spheres, and that the mass of such molecules scales linearly with length.


CD (circular dichroism) spectrum of porin will look like CD spectra of most beta-sheet-reach proteins. You can look, for example, paper on PorB protein (Minetti et al, JBC, 1998) where authors present CD spectra of one of porines:

Circular dichroism spectra of recombinant PorB class 3 protein as a function of SDS. Standard solutions of PorB rclass 3 protein (1.0 mg/ml) dialyzed against a buffer comprised of 10 mM sodium phosphate and 0.05% zwittergent 3-14 and incubated with varying concentrations of SDS (0-1%) at 25.0 °C for 24 h prior to spectroscopic analysis. Far UV CD spectra are recorded for rclass 3 in the absence of SDS (solid circles) and at the following SDS concentrations: 0.15% (open triangles), 0.25% (solid squares), 0.30% (open diamonds), 0.40% (solid triangles), 0.45% (open circles), 0.50% (solid diamonds), and 1.0% (open squares).


How are lysosome membranes protected from the attack of hydrolases?

Early histochemical work indicated that the internal surface of the lysosomal membrane has a glycocalyx - a layer of polysaccharide, presumed to have a protective role.

  Neiss, W. F. (1984) A coat of glycoconjugates on the inner surface of the lysosomal membrane in the rat kidney. Histochemistry 80, 603–608

Subsequently it was found that major membrane proteins of the lysosomal membrane are protected from proteolysis by glycosylation:

  Kundra, R. and Kornfeld, S. (1999) Asparagine-linked oligosaccharides protect Lamp-1 and Lamp-2 from intracellular proteolysis. J. Biol. Chem. 274, 31039–31046

See this paper for a more recent study of another lysosomal membrane protein:

  Schieweck O. et al. (2009) NCU-G1 is a highly glycosylated integral membrane protein of the lysosome. Biochem. J. 422: 83-90

NCU-G1 is the mouse orthologue of the human C1orf85 protein. The NCU-G1 gene encodes a 404 amino acid protein. This is a Type 1 transmembrane protein - i.e. the N terminal domain is directed to the extracytoplasmic surface of the membrane. In vivo the protein is detected in 70 kDa and 80 kDa forms. The discrepancy between the polypeptide size and the molecular mass is shown to be due to extensive glycosylation. The protein sequence includes 9 potential glycosylation sites.


Why does ampicillin in solution turn yellow?

Why is NADH the first thing to come to mind? Time for some physical chemistry.

Beta-lactams has a shorter ring structure which give it a different absorbance (around 322 nm apparently (source needed)) which gives it a blueish hue. Typically Penicillin and Ampicillin start off as an off-white. As hinted by @Mad Scientist, the beta-lactam rings are unstable and will undergo acid-catalyzed hydrolysis which breaks the 4-membered ring.

The Penicillin core also near a ketone which can attack the ketone in the lactam (I'm pretty sure this qualifies as enol chemistry but it has been awhile). The cyclization will form a 5-membered oxazole ring. Based on my experience, unsaturated 5-membered rings will absorb at a higher wavelength tending to result in a yellowish color (570-590 nM) so I am going to suggest that is the source of your color.

Ampicillin degradation


Regarding the apoptosis mechanisms in cells and cancer

The processes of apoptosis is not so simple, there is a lot of genes and proteins that participate in it. In cancer cells some of them mutate and not working properly.
Lack of apoptosis is the main problem in cancer. If cell not working properly, it dies. But not in cancer.
So theoretically, yes. If we will fix the apoptosis, the cell probably will die.
It's gene engineering direction. You need to target the cancer cell, and to change problem genes. It's really difficult processes. And every type of cancer has different mutations ...

Read this for example http://www.jeccr.com/content/30/1/87
(Journal of Experimental & Clinical Cancer Research )


To start with, CLARITY is a whole-brain imaging technique , there is no need for sectioning which destroys connections and can cause the brain slices to warp as they are being cut. The costs for setting up CLARITY are much lower because all that is needed is chemicals to get the prep ready for imaging whereas in the Nat Methods paper you have to set up an automated slicing and imaging system,not an easy task by any means. Therefore an investigator is more likely to use CLARITY due to its easy of setting up and low start up costs. Also, as with any brain slice technique , you lose patterns of connectivity among neurons that are more than the slice distance apart(i.e in the next slice) and you don't look at the "whole picture". Thus due to the complexity,high start-up costs and specialized machinery STP is a poorer method than CLARITY for whole-brain imaging.As for resolution, I agree with you on principle that CLARITY has worse resolution(I looked through the paper but couldn't find exact figures) although you have to consider this in terms of all the trade-offs.


Can anyone identify this spider? Found in Italy

Judging by the photo and the web it may be an orb-weaver spider of the family Araneidae.  Orb-weaver spiders get their name from the circular webs they spin.  It's possibly an Araniella cucurbitina, also known as a Cucumber spider, which are commonly observed hanging head down in it's web.  Several photos can be found at eurospiders.com.


Can a cancerous cell from outside cause cancer in a healthy person?

Can a cancer cells from someone else's body cause cancer in a healthy person?

No. Cancer cells from another person cannot cause cancer in a healthy person. The rare cases of transmissible tumors all involve unhealthy or not yet developed persons.

Transmission of tumor cells from one individual to another happens, but is quite rare, and in all cases involves some compromise or reduced development of the immune system. Though tumor cells do metastasize in an individual, when this occurs, tumor seeds must be able to evade the immune system and find an environment suitable for adhesion and replication. Tumor associated cells (non cancerous cells that regulate the microenvironment to make it favorable for growth and replication) are discussed in this seminal paper on cancer biology by Hannahan and Weinberg.  There are similarities to infectious processes, but cancer is not measles. Tumor cells don't shed in comparable numbers, aren't adapted for immune escape in a separate host, and don't express appropriate adhesion proteins for portals of entry on a new host or readily induce tumor associated niches in a new host. The cases where person-to-person transmission of cancer via tumor cell inoculation does occur seem to demonstrate more how cancer cells are not infectious agents.

Donor-related tumors in transplant patients occur in immunosuppressed patients, but are still rare. The low frequency of transmission seems to be due, in part, to screening. The fact that we see this at all demonstrates the significance of transmission route and immune escape.
Maternal-fetal, and in utero twin-twin seem to be exceedingly rare, but have occurred, again, demonstrating the existence, but poor efficiency of transmission. Here, the fetus has an undeveloped immune system. I would not consider this case to be cancer cells causing cancer in a healthy person.
Inoculation of volunteers with tumor cells in a problematic series of experiments at Sloan Kettering in the 50s, transplantation of tumor cells into patients with other cancers, resulted in growth, recurrence after excision, and death in some cases. Transplantation into healthy volunteers (yes, they did this) resulted in nodules that spontaneously regressed. This experiment has since been interpreted as evidence for immune system control of transplanted tumor system in healthy individuals, as compared to growth and progression in a receptive niche in a cancer patient.

So person-to-person transmission of cancer cells is rare and requires an immunosuppressed or undeveloped host, or a host who already has cancer. There are no documented cases of person-to-person transmission to a healthy individual, and documented cases of failed transmission despite a surgical attempt. This is because, unlike an infectious microbe, in a healthy individual, there is not a suitable receptor for adhesion at an exposed or accessible site, a suitable environment for replication, and adaptations for immune escape by tumor cells in the original host are not effective in a new host.

As a side note, there are contagious cancers in other species, but this doesn't seem to be particularly relevant to a question about whether cancer can be transmitted between two humans. Many cancers have transmissible risk factors (e.g., human herpesvirus-8, hepatitis B and C viruses, human papilloma virus 16 and 18, and others)


Overexpression by integration of an additional copy vs promoter exchange

Modifying promoters can give finer, more targeted control of expression than changing copy numbers. In the paper you referenced, for the ddh gene, it sounds like they just wanted to boost production of that protein, so making a second copy made sense. But with some of the other genes, they wanted to alter metabolite fluxes through a more complex pathway. Copying a whole operon would not achieve this, because then you would just get two pathways doing the exact same thing. But even copying the one or two genes in the operon that you want to investigate might change their relation to the other genes in the operon. Bacterial operons are generally organized such that the genes for the transcriptional regulators are located adjacent to the genes they regulate. This proximity is necessary for the proper functioning of the operon, and if you copy a gene, depending on where you put the copy, it may not function as it usually does. In these cases, it's better to mess with the promoters because you can leave the organization of the operon largely intact.


How the size of ribosomes are calculated?

Because Svedberg is not a measure of weight, but it is a measure of a relative sedimentation after centrifugation.
"It is defined as the ratio of a particle's sedimentation velocity to the acceleration that is applied to it (causing the sedimentation)."
The high number of S are correlated to the shape of the particles as well.

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


Does anyone know what type of Cocoon this is?

I think I may have found your cocoon: it appears to be a Magpie Moth (Abraxas grossulariata) cocoon:

According to UK Moths, it's common in the UK.


Is the eukaryotic nucleus composed of a single or double membrane?

The nucleus is topologically single membrane but functionally, and as visualized, double membrane.  Naturally, this is a bit confusing.

First consider the mitochondria and plastids.  One of these organelles has two entirely separate lipid bilayers, one of which is nested inside the other.  If you start inside the organelle and draw a line to an external point, the line will pass through two lipid bilayers (assume there are no membrane folds to be encountered), first through the nested one and then through the entirely separate outer bilayer.

The nucleus at a gross level appears to be structured similarly.  A line from the interior to the exterior will usually pass through two lipid bilayers, one that is the inner wall of the nucleus, then through the outer wall.  This may seem like the inner wall is separate from, and nested inside, the outer wall, but it is not.  As nicely illustrated in your reference (Martin 2005), the two walls are continuous with each other and not nested.  Because of this, a line from nuclear interior to exterior may in fact not pass through any lipid bilayers; it may pass though a nuclear pore.  Topologically (mathematically) speaking, the two walls are one surface, and the "inside" of the nucleus is on the same side of the surface as the outside.  (The topological interior is perinuclear space and the interior of the endoplasmic reticulum.)  Functionally though, the structure acts as a double membrane since it physically constrains its contents.

The distinction is not very important for most biological contexts, but for a few purposes needs to be considered.  The main reason to pay attention to the distinction is that it probably is related to the evolutionary history of the nucleus: it is likely to have evolved from a single bilayer somehow.  In contrast, the mitochondria and plastids, with nested bilayers, evolved from two bilayers, one from a separate cell and one from an enveloping piece of a host cell.  This is why the distinction is important in the cited paper, which concerns the evolution of the nucleus.


Why do different bacteria have different shapes?

Reasons for Bacteria with different shapes as given in Wikipedia/Bacteria:

  The wide variety of shapes is determined by the bacterial cell wall and cytoskeleton, and is important because it can influence the
  ability of bacteria to acquire nutrients, attach to surfaces, swim
  through liquids and escape predators.

There is an article based on research by Kevin D. Young Bacterial morphology: Why have different shapes? which highlights 3 main points which defines the shape of Bacteria:

Nutrient uptake: Cell shape, in and of itself, affects nutrient acquisition and argues that other nutritional situations may create conditions that favor one bacterial shape over another.
Motility: Motility imposes a heavy selective pressure on cell shape. Fast cells are better off as rods with a certain length-to-width ratio, chemotactic cells must adopt shape ratios in line with their environments, and cells that forage near surfaces or navigate viscous environments may do best if they are slightly curved or spiral.
Predation: In their struggle against being eaten, bacteria have adopted morphological defenses that may have produced the wealth of shapes we now observe.

These factors play a role in shaping bacteria. Further he explains what in general gives the shape to bacteria:

  Bacterial morphology is affected by a combination of selective pressures - access to nutrients, cell division, attachment/dispersal, predation and motility (among others). Among these different factors, our understanding of the relationship between motility and cell shape is most complete; for example, highly motile bacteria are usually rods with a specific (optimal) shape and size, and movement through viscous fluids seems to a favor spiral shape. But since multiple selective forces are always in play, there is at the moment no way to predict cell shape based on the environment or vice versa.

Shape Matters: Why bacteria care how they look - This article highlights Kevin's work explaining why shapes matter for bacteria and they take it seriously for survival.

So adaptations to various environments could be possible but depending upon the environment we can not predict the shape of bacteria because some other factor might have played major role in giving shape to it. But the above mentioned 3 main factors gives some explanation.


biologically speaking, what's the difference between sleeping and just resting?

Difference between rest and sleep

There are many factors which describe the difference between rest and sleep.

Rest

Rest occurs with conscious breathing. This allows the autonomic nervous system (ANS) to rest. The autonomic nervous system belongs to the peripheral nervous system. ANS controls many organs and muscles in the body.

In most situations, people do not know about the workings of the ANS since it functions in an involuntary, reflexive manner. For instance, we hardly notice if blood vessels change size.

This is the same case when our heart beats faster. There are some people who can control some of the functions in the body and can know the heart rate or blood pressure.

Sleep

Sleep it is a natural state of rest for mind and body. It happens in cyclic pattern. This can be one of the reasons to describe the difference between rest and sleep. There are four stages of sleep.

In the first stage of sleep, there is low-frequency, low-amplitude $\theta$ waves. This stage last several minutes before you enters into the next stage of sleep. In stage 2 of sleep, you brain moves into low frequency. In the third stage of sleep, you receive more high-amplitude $\delta$ waves.

During stage 4, the delta waves account for more of your brain activity and then they return back to stage 1.

Resting is more like being couch potatoes.

Rest is important for health and sleep is a necessary factor. You need both for your physical and mental activity to create energy. When the energy level goes down and wastes increase, there is tiredness and body needs rest. When you take rest, energy is restored. All the waste in the body gets extinguished. Rest and sleep are dependent upon each individual’s ability to relax. If an individual is tensed, he cannot be in the state of rest. Rest is taken to counteract fatigue.

Source:

[1] http://www.theatlantic.com/health/archive/2012/09/when-you-cant-sleep-how-good-is-lying-in-bed-with-your-eyes-closed/262484/

[2] http://insomnia.ygoy.com/difference-between-rest-and-sleep/


Which human body hormonal systems exhibit 24 hour diurnal cyclical activity?

The real answer is probably more than you want, but its easy to do better than the list above.

I took a look through GEO for human circadian expression data and surprisingly I only found 2.

Looking at GSE2703 - the rhesus circadian expression experiment, they have shown 355 genes that are rhythmically expressed.  This is not a great experiment because they only looked over a single 24 hour period.  Its only the adrenal gland.  Nonetheless they found 355 genes which seemed to be circadian.  the table is supplemental data to the article,  listed below.

I see a fibroblast growth factor receptor, some hydrocarbon nuclear receptor components, sterol regulatory factors, bone morphogenic protein 2, glutamate receptor, thrombonspondin receptor, ryanodine receptor 3 (what is that?) , lysophosphatidic acid G-protein-coupled receptor 2, purinergic receptor P2Y, G-protein coupled.  You might find more if you know what you are looking for.

The other circadian study was on human muscle, which will no doubt give different answers.  I imagine circadian behavior is highly tissue dependent.

Reference: Lemos DR, Downs JL, Urbanski HF. Twenty-four-hour rhythmic gene expression in the rhesus macaque adrenal gland. Mol Endocrinol 2006 May;20(5):1164-76


Change Genbank entry date with Biopython

So, the problem is that you are probably using wrong class for your record. Compare Bio.SeqRecord class with Bio.GenBank.Record class. Reason why in your GenBank format you have this reference date (01-JAN-1980) is because your record has intrinsically no date attribute, so SeqRecord.format set undefined fields to default (look through the source code to see where this happens).

What you want to do for creating GenBank record is following:

$ python
Python 2.7.10 |Anaconda 2.3.0 (x86_64)| (default, May 28 2015, 17:04:42)
[GCC 4.2.1 (Apple Inc. build 5577)] on darwin
Type "help", "copyright", "credits" or "license" for more information.
Anaconda is brought to you by Continuum Analytics.
>>> from Bio import GenBank
>>> from Bio.GenBank import Record
>>> my_rec = Record.Record()
>>> my_rec
<Bio.GenBank.Record.Record object at 0x1030b1890>
>>> my_rec.sequence = Seq(my_sequence)
>>> my_rec.sequence
Seq('ATAGGGACUCATAGATA', Alphabet())
>>> print(my_rec)
LOCUS                         bp
DEFINITION  .
KEYWORDS    .
SOURCE      .
  ORGANISM  .
            .
ORIGIN
        1 atagggacuc atagata
//
>>> my_rec.date = '13-JUL-2015'
>>> my_rec.features.append(my_feature)
>>> my_rec.data_file_division = "ROD"
>>> print(my_rec)
LOCUS                         bp                    ROD       13-JUL-2015
DEFINITION  .
KEYWORDS    .
SOURCE      .
  ORGANISM  .
            .
FEATURES             Location/Qualifiers
type: CDS
location: [2:5](+)
id: Cre
qualifiers:
    Key: foo, Value: bar
ORIGIN
        1 atagggacuc atagata
//

Notice, how print(my_seq) outputs data in GenBank format by default (since that is a GenBank record after all). I am sorry I cannot really talk on differences between GenBank.Record and Bio.SeqRecord and why/when use one object or another.

Anyways, looking up reference documentation is always a good habit: http://biopython.org/DIST/docs/api/Bio.GenBank.Record.Record-class.html


According to "Wile, Dr. Jay L. Exploring Creation With Biology. Apologia Educational Ministries, Inc. 1998" and reported here,

  In alternation of generations, the dominant generation is the generation that occupies the largest portion of the life cycle

I guess that it has to be understood in terms of "time". I am not quite sure though if it has to be understood in terms of generation time of life span. Intuitively, I would say that generation time would make much more sense. Therefore, I'd say that, the dominant generation is the generation which have the longest mean generation time (=mean time from the birth to reproduction).

As @Shigeta said in the comments: For example, in Homo sapiens, the dominant generation is the diploid phase (sporophyte, you and me) and the non-dominant generation is the haploid phase  (gametophyte, sperm/ovule).


Will neurons die if they are inactive for a long time?

Short answer
Yes.

Background
Postsynaptic neuronal degeneration after deafferentation are notorious in the peripheral sensory systems. There, marked degenerative processes are present when input to the secondary neurons is lost due to degeneration of the primary sensory neurons. In other words

When the hair cells are lost in the cochlea, the auditory nerve degenerates (e.g., Kuyama, 2010);
When the retinal photoreceptors are lost, for example due to degenerative diseases like retinitis pigmentosa, bipolar and horizontal cells in the retina degenerate due to a loss of efferent input (Mazzoni et al., 2008). For more information see the works of Marc & Jones, e.g.., Jones & Marc (2005).

Note that in the central nervous system these effects play less of a role, as neurons have ample opportunity to reconnect to other neurons, for the better or worse; e.g., in the hearing impaired and visually impaired, spontaneous sensations of sound and visuals may develop and lead to tinnitus and photopsias, respectively. These symptoms are caused by cortical sensory neurons desperately and randomly looking for sensory input after being deafferented due to peripheral loss of hearing or vision. When they cannot obtain useful input any longer, they gather irrelevant, non-useful input and start generating spontaneous 'illusionary' perceptions instead.

References
- Jones & Marc, Exp Eye Res (2005); 81(2): 123-37
- Kuyama, J Neurosci (2009); 29(45): 14077–085)
- Mazzoni et al., J Neurosci (2008); 28(52): 14282–92


It appears to be a noni fruit (Morinda Citrifolia).


Explanation of universal model of energy flow

If you were to take a snapshot of the biomass present for a species at an instant of time, that would be its standing biomass. So, in a way you are correct with "the organisms not eaten up". But this can be quite misleading when used to attempt to explain pyramids of production up trophic levels. For example, in some aquatic ecosystems the standing biomass of primary consumers is greater than that of primary producers. On study in the English Channel showed 21 g/m3 of zooplankton but only 4 g/m3 of phytoplankton. This is due to the rapid proliferation of the phytoplankton and the rapid consumption by the zooplankton.

Typically it is preferable to describe the energy flow through ecosystems in terms of energy units, Joules for example. However, you could do this with biomass if you summed the biomass produced over time. When done like this, the English Channel example would look like a proper pyramid with the producers out-massing the consumers over a meaningful period of time.

Energy storage is simply the energy stored in the chemical bonds of the molecules created during growth that add to biomass.

My example, and context, is from Biology, Campbell & Reece, 7th edition.


Bed bugs (wiki)! However, you will definitely be able to notice when they are around by bite marks and blood residues.


How can omnivores be in more than one trophic level?

I am not sure I fully understand where is your misunderstanding. I think your whole misunderstanding boils down to the representation of food chain. Actually, let's talk about food web as the name gives an intuition of what is happening that is more correct than the term food chain.

The conceptual view of the food web in a pyramid is super misleading. This is not how ecosystem work. But anyway, if one might want to make some ugly approximations and represent food web into a pyramid, then this person is totally free to represent one species twice, at two different levels. It makes sense that a species can eat things at several level in the same time. Just like you. You probably eat vegetables, salads, fruits, rice, corn, bread, etc... but also eventually fish and meat. Note also as indicated by @fileunderwater in the comments, that some species have different relationship with their ecosystem (typically eat different things) at different life stages.

Here are few examples of more or less realistic food webs. As you can see, one can roughly make category of trophic level but it is not all that clear.


What is the biological reason for a burst appendix being potentially lethal?

Necessary conditions

In order for the process culminating in appendiceal rupture to begin, there must first be proximal obstruction of the lumen (the inside cavity of the appendix) that prevents normal communication with the bowel.

  Obstruction is most commonly caused by a fecalith, which results from accumulation and inspissation of fecal matter around vegetable fibers.
  The bowel wall inside the (now closed) appendix continues to secrete muscous, and bacteria continue to multiply, producing the distention that is often perceived as nausea, vomiting, and poorly localized abdominal pain.1

The process leading to rupture

As the pressure in the appendix increases, venous pressure is exceeded. This means blood can no longer exit the venules of the appendix normally. In the presence of ongoing arterial flow, this leads to vascular engorgement, worsening the distention and increasing pressure further. The inflammatory process spreads from the lumen (inside) of the appendix to the serosa (outside) and then to the parietal peritoneum (lining of the abdominal cavity). This last step is what causes the characteristic shift in pain from poorly localized visceral pain to focal right lower quadrant pain.

As distention worsens, arterial pressure is eventually exceeded, and the most poorly vascularized areas of the appendix (generally just beyond the point of obstruction on the antimesenteric border) infarct first. Dead tissue has very little structural integrity, and once infarction happens perforation is likely to follow quickly.

Why this is (sometimes) lethal

There are several possible mechanisms, more than one of which is probably operative in most cases.

The three I have listed below all converge on the same final common pathway: In the absence of adequate systemic blood pressure (shock), the heart is not able to pump normally and will eventually deteriorate into a non-perfusing rhythm (a.k.a death).

Bacteria in the peritoneal cavity:
As in bowel perforation of any cause (e.g. perforated peptic ulcer, perforated diverticulum, traumatic perforation), bacteria in the peritoneal cavity (the “free space” outside the bowel within the abdomen) triggers an intense inflammatory reaction and fluid sequestration. Fluid pulled from the circulation into the peritoneal space causes hypotension and (hypovolemic) shock.
Infarcted bowel: Dead tissue connected to the body is never a good situation. Intracellular contents are released into the bloodstream – electrolyte release can cause hyperkalemia and other electrolyte imbalances; reactive oxygen species can lead to hypotension and (distributive) shock.
Sepsis: Bacteria (generally gram negative rods from among normal gut flora – most commonly Escherichia coli or Bacteroides fragilis)
may enter the bloodstream due to compromised vessels during the process of infarction and rupture. Lipopolysaccharides in the cell wall of gram-negative bacterial organisms lead to activation of monocytes and macrophages. This results in increased levels of interleukin-1 and tumor necrosis factor and eventually of IL-6 and IL-8. These cause widespread endothelial injury leading to diffuse alveolar damage in the lungs and activation of the coagulation system leading to disseminated intravascular coagulation. These cytokines also lead to systemic vasodilation and (distributive, septic) shock.

References

1. Silen W. Chapter 300. Acute Appendicitis and Peritonitis. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. eds. Harrison's Principles of Internal Medicine, 18e. New York, NY: McGraw-Hill; 2012.

2. Kemp WL, Burns DK, Brown TG. Chapter 8. Hemodynamics. Pathology: The Big Picture. New York, NY: McGraw-Hill; 2008.

3. Charles Brunicardi, F. Acute Appendicitis. Schwartz's Manual of Surgery; 2006.


What happens in the synapse when cocaine administration occurs in the human brain

You are correct that cocaine "fills the tunnel" (the pharmacology terminology is that it "blocks the transporter").  But it is not an autoreceptor, so the reuptake transporter does not send a stop signal, it just removed neurotransmitter from the cleft.  But once you've blocked it with cocaine, neurotransmitter is not being removed from the cleft so it has a much longer and stronger signaling effect on the post-synaptic neuron.

But cocaine can also block sodium channels, which assist in action potential propagation and that has more of a local anesthetic effect.

The effect you are thinking of would pertain to auto-receptors, not reuptake transporters.  Autoreceptors tend to be more like the post-synaptic targets of the neurotransmitter.