Why are vaccines for polio taken orally while vaccines for TB need to be injected? My thoughts are that maybe the TB antigens necessary to produce an immune response are proteins; therefore they can be digested in the stomach and small intestine. But I may be wrong though. I am confused why I can't say the same for polio vaccine.

There are different polio vaccines - one live (attenuated) vaccine which is given orally and one inactivated, which is injected. The main reason for using the live orally vaccine is that it provides excellent immunity (better than the inactivated) since it uses the natural infection route (oral-faecal) in the body where it enters through cells in the intestine. Besides that, it is also much less expensive than the inactivated form, which is a big thing when doing mass immunisations in developing countries.

The live vaccine, however, may mutate back into a more infectious form as you shed live (attenuated) viruses after the immunisation, so these are not used anymore. Now we are very close to the eradication of the poliovirus. The risk of getting new infections is viewed as being too high these days. See this paper for more information: "Vaccine-derived polioviruses and the endgame strategy for global polio eradication."


How does bath application of KCl depolarize a neuron? Increasing extracellular KCl is often a way to depolarize neurons in experiments.

My understanding is that increasing K+ extracellular concentration changes K+ reversal potential to more positive values and hence depolarises the neuron as the open leaky potassium channels will lead to influx of K+ into the neuron. Is this correct?

However, this explanation does not take into account Cl- ions.

How can this be explained in terms of Goldman equation?

Also, how does intracellular injection of KCl affect neuron membrane potential as compared to extracellular KCl application? In patch clamp experiments, often the pipette is loaded with KCl and injected into neurons that leads to depolarization. How can this be explained?

Membrane potential (measured electrophysiologically, or calculated using the Goldman equation) depends on two things: concentrations and permeabilities. In the Goldman equation you see this directly: concentrations multiplied by permeability, in both the numerator and denominator.

If the membrane is not permeable to an ion (PIon=0), that ion will not affect the reversal potential. In a typical resting neuron, in the absence of any synaptic activity, Chloride conductance is near zero compared to ions like potassium.

I'm not as clear what you are asking about patch clamp experiments, I will try to just describe the process and hopefully that helps.

In a whole-cell patch clamp, the inside of the cell is continuous with the patch pipette solution, which usually contains high concentrations of potassium, like the normal intracellular environment. This is done on purpose, to try to record from cells in the most natural condition that can be replicated simply.

During the process of making a whole-cell recording, however, the experimenter has to first place a patch pipette down near the cell. While doing this, some solution is leaking out of the pipette and increasing extracellular potassium concentrations, which can depolarize surrounding cells. So, patch quickly my friends, you are making it uncomfortable for everybody before you make a good seal.

(the process would be similar for inside-in patches; for on-cell or inside-out patches, one would use different ionic concentrations in the pipette to mimic the extracellular space, or these would vary depending on the exact experiment performed)

edit: Just wanted to note that a statement in your question is mostly wrong; "the pipette is loaded with KCl and injected into neurons that leads to depolarization" - KCl inside a cell would not depolarize that cell, unless the concentration of K+ was lower than the typical K+ concentration of the cell, in which case you would probably have other issues and a dead cell from osmolarity problems.


How to convert enrichment/depletion to frequency for comparing deep sequencing to sequence profile? I have two datasets, from different sources, that I need to compare.

The first set is deep sequencing results of a directed evolution experiment, where I have the naive library and selected library counts, and have calculated enrichment/depletion (positive and negative values with no upper or lower bound).

The second set is a set of protein sequences for which I calculate amino acid frequencies (positive values from 0-1).

The goal is to calculate a similarity between the two datasets. Typically I have two of the second type of set (protein sequences) and I calculate similarity based on the amino acid frequencies... What's the best way to convert enrichment/depletion to frequency so I can compare?

Example deep sequencing data, for position 77 of the protein:

$$\text{enrichment} = \log_2\left(\frac{F_S}{F_N}\right)$$

Where $F_S$ is selected frequency and $F_N$ is naïve frequency.

I came up with a possible solution for frequency equivalent from enrichment ($F_E$) but am open to thoughts if it's good or not:

$$F_E = \frac{\displaystyle\frac{F_S}{F_N}}{\displaystyle\sum_\text{amino acid}\frac{F_S}{F_N}}$$

Although the question is kind of confusing at some places, what I understood is that you are trying to compare the relative amino acid enrichments in the two datasets.

As far as I know, you could construct the protein sequences from directed evolution experiment (presumably a time series data. Please clarify that.) and make a multiple sequence alignment (MSA) of that. In order to construct the sequences, there would be some technical procedures that would depend on the type of deep sequencing data you have. Factors such as the read length, protein length and coverage would need to be taken into consideration.

You could similarly make MSA for second datasets too.

Then using tools such as Rate4site (https://www.ncbi.nlm.nih.gov/m/pubmed/12169533/) you would be able to get evoutionary rates per site from MSAs. Then compare the evolutionary rates per sites for two datasets by correlating them.

If the correlation is high, the enrichments in both datasets are similar, otherwise not.


How does a tiger have stripes? A vague question, but let me try to explain. My friend explained to me that in females, some cells use one X chromosome, while all others use the other X chromosome. This can result in some differences of appearance of certain individuals. The Wikipedia page on X-inactivation shows an example. There is a picture there that shows a cat with fur of two colors, each showing in seemingly random groups. My friend had explained that when one cell "deactivates" its X chromosome, all of its descendants have the same deactivated X chromosome, so it makes sense that the similar colors appear in groups on the cat's coat.

But it seems tigers' coats are much more complicated than that. The pattern on a tiger's coat is not completely random. They make very discernible shapes. There are clear borders inside which only black fur grows, and outside of which only orange fur grows. How is this possible?

I'm not suggesting that the patters on tigers' fur is in any way related to X-inactivation, since I know that only applies to female mammals. But X-inactivation seems like a "natural" phenomenon, while the stripes on a tiger (or other animals with complex patters) seem a bit more bizarre. How do the cells on a tiger's body know which color to show and still follow the pattern?

It turns out that this was a question that was answered by Alan Turing in the 1950s.

Turing hypothesized there would be two morphogens, an inhibitor/ activator pair, each of which would produce a one of two phenotypes by activation or suppression of a trait.  He hypothesized that this would produce a pattern like stripes or other patterns (e.g. black and orange stripes).

This year just such inhibiting/activating pairs produce patterns like ridges in the top of the mouth of mice.

In a broad way, this seems like X-inactivation, where there is an X-inactivation center (XIC) that is inhibited or activated when the cell is created in mitosis.  XIC is still hypothetical and undiscovered, but it can create patterns and is non-random.

So I would say that this tiger stripes and X-inactivation may share Turing's mechanism, but the stripes, found in male and female tigers alike is not linked causally to X-inactivation.


Cleanliness of cast iron never cleaned between meals Cast iron cookware has unique benefits. One difference between cast iron and most other cookware is that many people advocate for not cleaning it with any soap between uses, because the soap can degrade the seasoning which protects it. I wonder, how hygienic is that?

The way I understand it, the seasoning on cast iron cookware is a smoothed layer of polymers that prevents food (and bacteria) from contacting and sticking in the iron cookware. Simply scraping it clean, maybe rinsing with some hot water briefly and drying off immediately after, is generally considered enough to 'clean' the cookware.

How is it that bacterial growth on the cookware is never a problem, given they are not washed with soap for long periods of time? I'm under the impression that most kitchenware - pots, pans, dishes, utensils - are susceptible to bacterial growth that could make you sick or transfer illness if you eat with them and don't properly wash off all the food, oils, etc. that gets on them. Does the layer of polymer on cast iron protect it from such growth? The main question here is: Does other cookware really need soap any more or less than cast iron to be used hygienically, and why or why not?

Soap or detergent does nothing to kill organisms. Instead each detergent molecule has two ends, one being hydrophobic (meaning it's repelled by water) and the other end is hydrophilic  (attaching the end to water). When anything is washed with soap or detergent, the oils and dirt on the object - whether it's a dish or your hands - can combine with water as an emulsion and be rinsed away.

Dishes and utensils are only susceptible to bacterial growth if there's traces of food on them. Washing is meant to remove traces of food and oil so bacteria can't multiple on them. The conditions must be right for bacteria to multiple. If traces of food were to be completely dry and hardened on a dish and someone ate off it, the likelihood of any bacteria present on it is close to nil. They need moisture to grow. If dishes had no oily food on them, washing and rinsing with very warm water would be sufficient. I've seen people from other cultures wash dishes with traces of food that are soluble in water. They come out perfectly clean. (As an aside, using a tea towel can often spread bacteria when they're not used properly.) Towels top kitchen contamination hazards list

Bacteria can't multiple in oil. For example, ordinary cooking oil doesn't need to be refrigerated although it can go rancid. A cast iron frying pan is properly meant for frying foods only. No watery sauces should be cooked in them. Even "scraping it clean" shouldn't be done with a sharp metal object as it can remove some of the polymerized hardened oil layer.

I have several cast iron pans that I don't wash. I wipe them out after each use, then I add a little oil nd roughly a teaspoon of salt. With a paper towel, I rub at any bits of stuck on food. If done within a few hours of being used, it effectively removes any food traces, leaving a smooth surface. I usually rinse off the salt in warm water, dry it and then apply a very thin film of oil. I've been cooking in cast iron pans for decades and have never gotten sick or had mild food poisoning (what many people call a 'stomach flu').

Cast iron pans with a layer of proper seasoning and treated like this will definitely not cause sickness. It can't support bacterial growth and as @jeanquilt mentions, the pan gets very hot - enough to blister your skin if you touch them with a bare hand.


Why is the heart adversely impacted by chronic psychological stress, yet it benefits from routine physical exercise? Chronic psychological stress is commonly said to be deleterious to the heart, and predispose one to cardiovascular disease. Yet the opposite is said about regular aerobic exercise. Physiologically, What is the difference between psychological stress and physical exercise, with respect to their impacts on heart function/health? Both involve an increase in sympathetic cardiac input, and thus more vigorously contracting cardiac muscle; but how is one damaging and the other beneficial?

From the perspective of sympathetic nervous system

Exercise induced adaptations of heart

A common phenomenon in endurance athletes is the athlete's heart /athletic heart syndrome

Once athletes stop training, the heart returns to its normal size.

You must understand why this type of adaptation is happening in them:
Firstly the athletes train to produce work output at near maximal levels/ sub maximal levels of work done which cannot be physiologically achieved in a day.So the increased heart rate generated by the sympathetic stimulation is sufficient to fulfill oxygen demand of the body only at certain levels of work done by raising the heart rate
As the grade of work done nears submaximal level the oxygen demand increases in the body and the increased sympathetic stimulation (which also restricts the cardiac muscle efficiency by decreasing diastolic time,coronary blood flow) is no longer able to suffice it.Such high oxygen demand is responsible for the useful adaptations of the heart in the form of athlete's heart.Athlete's heart reduces the need for sympathetic stimulation to increase cardiac output .

During intensive prolonged endurance or strength training, the body signals the heart to pump more blood through the body to counteract the oxygen deficit building in the skeletal muscles. Enlargement of the heart is a natural physical adaptation of the body to deal with the high pressures and large amounts of blood that can affect the heart during these periods of time.

Comparison with chronic psychological stress

During stress the body may or may not have high oxygen demand (the principal stimulus for adaptation) because the sympathetic stimulation is psychological and not in response to physiological work.So the heart instead of adaptating gets afflicted with detrimental pathophysiological effects of prolonged sympathetic stimulation.

stressors’ contributions to diverse pathophysiological changes including sudden death, myocardial infarction, myocardial ischemia, and wall motion abnormalities, as well as to alterations in cardiac regulation as indexed by changes in sympathetic nervous system activity and hemostasis.

From the perspective of cortisol (stress hormone)

Effect of psychological stress on athletes

When we are talking about the detrimental effects of psychic stress it is important to note that it may override the cardiac adaptations and severely affect performance like,for example high cortisol levels in blood released in response to stress (physical/ psychological).Although cortisol levels in the blood observe a circadian rhythm in normal healthy indivituals, some reports claim that exercise reduces detrimental effects of high cortisol levels on the heart.However,stress may override exercise induced effects in athletes but this is a prospective study, subject to greater research

A prospective study found a clinically significant increase in overnight urinary cortisol:cortisone ratio during a high training load period in triathletes, who subsequently underperformed and reported fatigue

REFERENCE TEXTBOOKS:

Exercise Physiology And Ergonomics (An Introduction) Asis Goswami Academic Publishers.Pg-39 to 57

Essentials Of Exercise Physiology (4th Ed.) Victor L.Katch,William D.McArdle,Frank I.Katch pg-302-333


How big can a colony/society get? I hope this is the appropiate place for this question, asked from a math/physics perspective with little to no training in biology.

Bacteria are very small and live in huge colonies, ants are bigger (but also very small) and live in smaller colonies (but also very big). Ignoring the human species, I can't think of any big animal living in big colonies

Is there any name for this relation? I want to study it from two perspectives: first, why? (this may be easy to explain in terms of resource supply or energy available) and second, what is the precise relation? (clearly inverse, but linear, logarithmic...?)

Thanks!

It is not trivial to define a "colony/society". Sure, you can say "this bacterial blob is a colony", or "this ant nest is a colony", and so on, but these would be your own definitions. These systems you mention don't have definite boundaries (temporal or spatial). Although physicists like to do gross approximations to things in nature (and I'm pretty sure there is already some paper 'answering' your question), I'm not sure anyone can get a "precise relation" for a concept that even biologists struggle with (that of a "colony"). This is because at core, what you are really asking, is what is a biological individual and how can I measure it? (the individual ant, the individual colony, etc); and that's something we have no answer for. For what is worth, I recommend you read about the problem of biological individuality, which will give you no answer to your question but at least can tell you why you can't really answer it: https://link.springer.com/article/10.1162/BIOT_a_00068


Floats of Algae, a house-made conjecture Background

In North of Scotland there are many seaweed types. One is a green algae (chlorophyta).

They are full of 'bubbles'. According to web searches one of those bubbles (there are two types you can notice by sight) are spores; the other ones are called floaters.

According to searches, Kelp (or brown algae) floaters are full of gases. But we find most of the Chlorophyta full of water, some of them contain bubbles but tiny ones.

Conjecture

The water inside could be of a lower density than the sea water, instead of air bubbles.

Question

Any information on this respect?

One consideration is the energetic costs to the organism. It's going to be energetically more favorable for an organism to be in osmotic balanced (isotonic) with its environment than to constantly work to maintain lower internal osmolarity through active transport of water or solutes. Second thing to consider is cell size and density differentials. Air at sealevel is several hundred times less dense than water, so even tiny gas bubbles would create significant buoyancy for a cell. On the other hand, pure water is only about 2.5% less dense than sea water, which means a much (much) larger volume would be needed to generate equivalent buoyancy.

All that said, there seems to be some plausibility to your conjecture, as there are some large marine phytoplankton that use active water transport to maintain vacuoules at lower density than that of seawater (Source).

This paper discusses some other competing mechanisms as well, but as the author of the article states:

  "... most of the cases of positive buoyancy in phytoplankton not
  generated by gas vesicles concern diatoms..."

That's not an incontrovertable refutation of your conjecture, but it seems to me that gas vesicles are a much more efficient means of generating buoyancy, and would probably be energetically favored over other biological means of generating buoyancy.


What animal makes these spherical sand clusters? I encountered these structures on a beach in Hong Kong (the Ham Tin Wan beach in Sai Kung country park). There were many of these structures and I have photographed two of them in detail and attached a larger image which shows the extent to which these were spread on the beach.

It seems these were made by an animal of some sort. All these sand deposits were organised around a single hole in the ground which presumably is the animal's home or hide out. And all such structures had a clear "walking" path which was almost a straight line. These paths had no sand deposits in them.

Am I right in assuming that these structures were made by an animal? If so, then which animal makes them? And what is the purpose of the round(ish) deposits of sand around the main hole? Are they an obstacle for predators?

Image 1: A structure in detail

Image 2: Another structure in detail

Image 3: Overview of structures

Not sure what exact species it is, but those definitely look like crab holes. They create the holes in the sand to get away from the heat and predators. They clean their homes by depositing unwanted ~sand around their door (the hole).

So yes, you're totally right in assuming those were made by an animal.


What animal is this bone from? 10.5 ounces, found laying on ground, central California coast.

This is the cannon bone of an adult artiodactyle.. The size points towards sheep or goat.


Can you tell if a corpse was male or female by only examining its skull? There are articles that says women have more rounded corner faces than men, than women noses are usually shorter, etc.

But are those (and other features) tendencies or deterministic features that makes you really able to tell if a corpse was male or female, by only examining its skull?

According to textbook of forensic medicine and toxicology by Ks Narayan reddy:

Qualitative differences are:

Male mandible has everted ramus, but female have inverted ramus.
Males have chin U shaped, but it's rounded in females

Quantitative differences:

Suparaorbital ridges are prominent in males but often absent in females.
Mastoid process is wider, longer and blunt in males but is narrow and pointed in females.

And there are many more differences, see the pics below:


epigenetic vs. environmental factors I'm trying to understand the difference between epigenetic and environmental factors. For example, if gene A increases the risk of lung cancer by 50% and smoking increases the risk by another 75% when combined with gene A (just throwing out numbers) person X now has a higher chance of developing lung cancer. However, if for example, certain epigenetic factors are inhibiting the expression of gene A than that 50% higher genetic risk has now decreased because those high-risk genes aren't being fully expressed. The environmental risk factor of smoking still plays a role but it too could be decreased because that 75% increased risk was associated with gene A being fully expressed and not inhibited by epigenetic factors. Am I thinking about this correctly?

If I understand you correctly what you are saying is

  There is envrionmental variance and epigenetic variance underlying the phenotypic variance. There can even be a covariance between the envrionment and epigenetics.

Yes, this is true. You might want to have a look at this intro post to quantitative genetics.

Note, there are several definitions of epigenetics. Epigenetic effects are some kind of factors that affect phenotypic variance and that are external to the DNA sequence. Often we think of modification directly on the nucleotides on on the histones (such as a methylation on the histon tail) but we sometimes also extend this context to include all the stuff that is the in the zygote or sometimes even further. In its broadest sense, the term "epigenetics" would be a synonym of "environment".


How are lesions in the RNA corrected? I quite understand why thymine is present in DNA. So we can mark it out where cytosine undergoes a reaction and is converted to uracil. Then we can repair the DNA.

But how can we make that out in RNA ??

RNA is shortlived and need not undergo repair. A "mutated" RNA will degrade and will be replaced by the correct RNA.

Even though RNAs are shortlived compared to DNA (which does not really undergo turnover), some RNAs are stable and have low turnover. Nonetheless RNA would be present in multiple copies it is improbable that all of them would have undergone mutation.

Moreover RNA with certain mutated codons e.g. non-sense mutations are cleared off by the exosome.

Thanks to har-wradim for pointing out about RNA repair mechanisms. There are few reports that say that methylations in the RNA can be corrected by the enzymes AlkB (in E.coli) and its eukaryotic homologue hABH3. These enzymes were known to repair methyl lesions in the DNA (1-methyladenine and 3-methylcytosine), but it was subsequently shown that they can act on RNA as well [1,2].

However there seems to be no mechanism for repairing deamination damage; this study has demonstrated an artificially designed system which is capable of targeted RNA deamination (but there is no system yet that can fix a deaminated base in RNA).

This article comments that AlkB is tightly regulated because if uncontrolled it can demethylate functional methylations too. Overexpression of AlkB is actually toxic to the cells unless they are under alkylation stress by agents such as EMS/MMS (Ethyl/Methyl MethaneSulphonate).

But IMO RNA repair is not as essential as DNA repair because of aforementioned reasons.


What is the purpose of DNA? My very basic understanding is DNA gets transcribed into RNA by effectively replacing thymine with uracil, then RNA is translated to make proteins. Looking at it from an engineering perspective, it would appear that, while the RNA to protein translation is non-trivial, the DNA to RNA transcription process is rather redundant: As it's just a simple replacement, why not start with RNA in the first place? My assumption therefore is that there is something about the RNA molecule (e.g., too reactive, too unstable, etc.) that requires it to be put in "cold storage" as DNA.

I don't have a background in genetics or biology, so could someone ELI5 why DNA is needed?

Imagine you want to produce a widget. You have thousands of worker, but only one blueprint. Each worker needs the blueprint to build a widget (they're really forgetful and can't build from memory). So only one worker at a time can build your widgets.

What you would do is to create copies of your blueprint and distribute them to your workers. That way multiple workers can produce the widget at the same time.

DNA is the blueprint, and RNA is the copy. Your workers are the ribosomes that translate the RNA into proteins.

This is of course grossly simplified, and there are other reasons for the specific arrangement, but this is certainly one of the reasons why the intermediate RNA is used.


No bands show up in gel electrophoresis, not even marker I haven't seen any gel lanes in neither my PCR samples nor the marker itself when photographing them.  This is not my first time performing 1.2% agarose gel electrophoresis.

I see gel lanes when I take the gel out the apparatus, but when I go to photograph them:  nothing shows up.  I only let the samples "run" for 30-40 minutes (when I ran for an hour, the bands almost ran off the gel).

Tried using different markers:  no luck.

Re-added some more EtBr to better stain the gel:  no luck.

I am also keeping the lights off in the dark room, so I do not think I am exposing the film to light early on (errors still a possibility though).

What could I be doing wrong?  Am I taking the film out too early?

What I can quickly think of is that you were running the gel incorrectly: instead of from - to + direction,  You ran it the other way around and your DNA went out of the gel. Another thing might be that the UV light was not turned on or is broken.


Help me understand voltage patch clamping Before I type my question it is important to know that I already tried looking this up on my own and could not find an answer because the answers are all in complicated physics terms and this topic is only half a page in a chapter on Action potential in my 1st year physiology textbook.
My textbook says:

This apparatus is used in the following way: The investigator decides
which voltage to establish inside the nerve fiber. The electronic
portion of the apparatus is then adjusted to the desired voltage,
automatically injecting either positive or negative electricity
through the current electrode at whatever rate is required to hold the
voltage, as measured by the voltage electrode, at the level set by the
operator. When the membrane potential is suddenly increased by this
voltage clamp from −90 millivolts to zero, the voltage-gated sodium
and potassium channels open and sodium and potassium ions begin to
pour through the channels.

1: Does that mean that the change in membrane potential that I did resulted in changes in the conformational states of ion channels which in turn changed the membrane potential that I need to control ?

To counterbalance the effect of these ion movements on the desired
setting of the intracellular voltage, electrical current is injected
automatically through the current electrode of the voltage clamp to
maintain the intracellular voltage at the required steady zero level.

2:Is this all still the step of setting the membrane potential to a certain specific value ?

To achieve this level, the current injected must be equal to but of
opposite polarity to the net current flow through the membrane
channels.

3: I'm not sure I understand this.

Finally, the investigator adjusts the concentrations of the ions to
other than normal levels both inside and outside the nerve fiber and
repeats the study.   When sodium is the only permeant ion in the
solutions inside and outside the squid axon, the voltage clamp
measures current flow only through the sodium channels. When potassium
is the only permeant ion, current flow only through the potassium
channels is measured.

4: do they make sure that the flow is only from sodium channels by setting the membrane potential to the equilibrium potential of other ions or a potential between the equilibrium potential of the other ions (so greater than it) and the equilibrium potential of Na (and also less than it )?

I'll try to answer the sub questions 1-by-1

Does that mean that the change in membrane potential that I did resulted in changes in the conformational states of ion channels which in turn changed the membrane potential that I need to control ?

It's the other way around; your book is right - "When the membrane potential is suddenly increased by this voltage clamp from −90 millivolts to zero, the voltage-gated sodium and potassium channels open and sodium and potassium ions begin to pour through the channels". So the voltage step (depolarization) induced by the apparatus triggers voltage-operated channels to undergo conformational changes, this in turn results in additional current flowing through them. On the other hand, hyperpolarization of the potential from say -40 to -90 causes the neuron to close these channels, blocking current to flow. In other words; the patch clamp apparatus controls the membrane potential, the state of the ion channels has little to do with that, as the apparatus will automatically adjust the current injection.

Is this all still the step of setting the membrane potential to a certain specific value?

Yes.

"To achieve this level, the current injected must be equal to but of opposite polarity to the net current flow through the membrane channels."
I'm not sure I understand this.

To set a certain stable potential across the membrane, the flow of current needs to be stable, otherwise it will fluctuate; Ohm's law tells us U = IxR. The resistance R is set by the channels. Let's consider that R is stable for the moment. In that case, you will set the membrane potential U by tightly controlling the current I. If I fluctuates, i.e., when the apparatus doesn't balance the flow of current through the membrane channels exactly and oppositely, a net current will start flowing and u will change. You don't want that to happen.

do they make sure that the flow is only from sodium channels by setting the membrane potential to the equilibrium potential of other ions or a potential between the equilibrium potential of the other ions (so greater than it) and the equilibrium potential of Na (and also less than it )?

This part has nothing to do with equilibrium potentials. They substitute negative ions simply by ions that are not membrane permeable, and the only positive ion available in the test tube is Na+. In that case, only Na+ can flow and you are sure that it is Na+ that is flowing. At least, this is what I make up of this text.


Proteins that cannot form biofilm? I am trying to build a machine learning training set for bacterial protein sequences that form biofilm, and that cannot. I collected the positive sequences from the GO ontology website but for negative sequences I am not sure which sequences to incorporate into my training set.

Can anyone point me to resources for proteins sequences that are known to be not capable of forming biofilms?

Intracellular proteins cannot form biofilms. Additionally, many (but not all) extracellular proteins contain an N-terminal cleavable signal sequence.

Lory (1992) Determinants of extracellular protein secretion in Gram-negative bacteria. J Bacteriol 174: 3423-3428.
https://www.ncbi.nlm.nih.gov/pubmed/1592799

Schneewind & Missiakas (2012) Protein secretion and surface display in Gram-positive bacteria. Philos Trans R Soc Lond B Biol Sci 367:1123-1139.
https://www.ncbi.nlm.nih.gov/pubmed/22411983


What makes heavy metals toxic? I'm not sure all heavy metals are toxic, but most are.

Some may be present as insoluble compounds, or otherwhise hard to get into an organism, but that's a side aspect.
For example, I would count copper as toxic, even if some salts are triggering to vomit just too quickly to swallow poisonous doses.

So, in this sense, are they all toxic?
Is the toxicity based on the same mechanism?

Heavy metal toxicity is actually due to the inhibition of the body's natural enzymes as well as the denaturing of proteins that it causes.

Here, Tchounwou et. al go into detail about the mechanics of different heavy metals and how they interact with the human body specifically. It even suggests ways that the heavy metals could be introduced.

A short summary on the damage caused by what was studied:

Arsenic inhibits DNA repair.
Cadmium toxicity isn't well known, but they think it causes single
strand DNA damage.
Chromium causes chromosomal abnormalities thought to be caused by
oxidative damage.
Lead prevents the body from interacting with Calcium which is a key
element in many biological processes. It also competes with other
metals for the active sites in different enzymes.
Mercury depletes the body's antioxidants.

So to answer your question, no, the heavy metals are not all working on the same mechanism. It all depends on what dose, how it was introduced, and the particular metal. Also, anything can be toxic in the right amount (people have died from water toxicity in drinking contests).


How does HIV mutate into other strains while keeping their virulent phenotype? How does a virus like HIV mutate into so many strains, and yet all of them are  harmful to our immune system? What gives this virus the ability to mutate so efficiently?

Others have already touched the important points. Consider this as a summary.

  What gives HIV the ability to mutate?

All organisms mutate by two mechanisms:

Replication errors
Mutagenesis by physical/chemical agents that cause a chemical change
(lesion) on DNA

The main enzyme responsible for HIV replication is reverse transcriptase which makes a DNA copy of its RNA genome. All RNA and DNA polymerases make some amount of error but the error rate of reverse transcriptase is much higher than usual DNA-dependent DNA polymerases because it does not have a proofreading mechanism.

  How does a virus like HIV mutate into so many strains, and yet all of
  them are harmful to our immune system?

As indicated in previous answers, the mutations will produce a virions with a spectrum of infectivity/pathogenicity (some can even be non-infective).
However, the immune system acts as a selective barrier which selects only those mutants that can survive (similar to what happens in evolutionary process of natural selection). The selected strains expand their population and that is how these strains get established.


Equation relating probability of fixation and number of generations I am trying to find an equation that relates the variables of probability of fixation and generations. Or, how does number of generations affect the probability a gene will fix, if population size doesn't significantly decrease or increase.

From Hartl and Clark's 'Principles of Population Genetics' Third Edition chapter 7: Kimura and Ohta (1969) showed that the mean time in generations until the allele of frequency p is fixed (ignoring cases where the allele is lost) is:

$$t_1(p) = -4N[(1-p)log(1-p)]/p$$

The mean time to loss of the allele is:

$$t_0(p) = -4N[p \cdot log(p)]/(1-p)$$

Thus the mean persistence time of an allele is:

$$t(p) = -4N[p \cdot log(p)+(1-p)log(1-p)]$$

Hopefully I didn't make any typos there, but I reccommend this book to learn all the ins and outs of popgen. There is a PDF of the third edition online in an archive. For more book recommendations, please have a look at the post Books on population or evolutionary genetics?

You can also find these equations in the original article: Kimura and Otha (1968)


How to characterize stability of a protein from Trp fluorescence vs [denaturant] curves? A colleague of mine has taken Trp fluorescence measurements from a dimer in combination with various ligands, over a range of denaturant concentrations.

The idea is that ligands which bind more tightly to the dimer will stabilize it and delay changes in fluorescence. This is what our data look like:

Total fluorescence decreases, probably due to quenching from the denaturant. Papers I've seen using this method show it's possible to calculate the fraction of denatured protein by analyzing displacement in peak emission wavelength. However, they use monomeric proteins with few Trp, whereas I have a dimer with several Trp plus some additional variability introduced by the different ligands.

Additionally, we have data from a scintillation proximity assay that indicates ligand affinity is ordered as 1<...<5 and 6<...<11. Ideally, we would like to replicate this same ordering through the analysis conducted on the data above. I would appreciate any suggestions of methods that will allow us to carry out such comparisons.

Papers I've seen using this method show it's possible to calculate the fraction of denatured protein by analyzing displacement in peak emission wavelength.

Have you tried doing that with your data? What do you get if you plot peak emission wavelength as a function of denaturing agent concentration? If these look like sigmoidal curves (you might need a log scale on the X axis) with a clear upper plateau, then you can apply the method mentioned by these papers because the signal you observe is correlated to the fraction of denatured protein and saturates (this part is important: the signal must saturate past a certain concentration of denaturing agent, because all protein molecules are fully denatured and therefore adding more denaturing agent won't give further signal change; if your signal doesn't saturate, something is wrong).

  However, they use monomeric proteins with few Trp, whereas I have a dimer with several Trp

Oligomeric state and number of Trp residues should not matter, because peak emission wavelength is only correlated to the fraction of denatured protein. Total intensity will increase with more Trp residues, but you're not using intensity as a measure of the fraction of denatured protein (and if anything, it's good to have more intensity to begin with given the quenching effect you observe with increasing denaturing agent concentration).

  plus some additional variability introduced by the different ligands.

To take care of this concern, you need two controls that:

prove that none of the ligands alters the fluorescence of your protein,
prove that none of the ligands emits fluorescence between 300 and 450 nm, or if they do then you need to measure it to be able to subtract it from your total spectra, in order to recover the protein contribution to the total fluorescence.

For 1, record fluorescence emission spectra of the protein without denaturing agent but as a function of ligand concentration (span a few orders of magnitude) and see if the peak emission wavelength changes with ligand binding (it might change, which means the same assay can yield binding curves and Kd values for your ligands, which could also be useful!). Full ligand titration curves would be the most robust control, but you can simply use the same ligand concentrations as used in the denaturation experiments.

For 2, the simplest case would be that your ligands are not fluorescent, but you cannot simply assume that. Therefore, an important control you also need is to record emission spectra for each of your ligands at the concentrations used in the denaturation experiments, and this at each concentration of denaturing agent (or simply at 0 and max concentration: if there's no difference between these two spectra, you don't need to record one at every concentration in between). If the ligands emit fluorescence between 300 and 450 nm, you need to subtract that from your total spectra to recover the fluorescence arising from the protein only.


Why is chronic lymphocytic leukemia (CLL) most common leukemia in the West but so rare in Asia? In "Advances in Chronic Lymphocytic Leukemia" (2013, Edited by Sami Malek), several times it is stated that CLL is very common in Western countries.

However, it is quite rare in Asia. (I do not have data regarding other regions in the world.)

Why would this be? I am familiar with cancers being related to lifestyle, which varies by country. (The obvious example would be how countries with high rates of smoking have higher rates of lung cancer.)

Do we have any reasons why this is? Thanks for any help.

This paper should help get you started. The exact reason is not yet known, but is most likely related to germline genetic differences between the two ethnic groups, as Asian immigrants to the US continue to have a low incidence of CLL.

References:

KAWAMATA N, MOREILHON C, SAITOH T, et al. Genetic differences between Asian and Caucasian chronic lymphocytic leukemia. International Journal of Oncology. 2013;43(2):561-565. DOI:10.3892/ijo.2013.1966.
American Cancer Society: What are the risk factors for chronic lymphocytic leukemia?


Bodyweight loss vs calorie shortfall I have read that 1g of pure fat has 9 Calories.

If I dieted successfully in a way that did not cause me to loose muscle, and I had a cumulative calorie shortfall of 90,000 calories. Would that correspond to a reduction of bodyweight of 10kg? Or would it actually be a bit more, because presumably each kg of fat in the body is tied to a certain amount of water packaged with it?... and if so, how much more than 10kg?

You hit upon several ideas in your post.  First, you are absolutely correct that body fat is composed both of lipids and water, so a 10kg weight loss does not correspond to 90,000 kcals.  The most commonly accepted figure is 7700 kcals per kg of body fat lost (Hall, 2008), but this is a rule of thumb at best.

The translation from caloric deficit to body fat loss is fairly complex, and is the result of feedbacks between metabolism, weight, and other responses.  The National Institutes of Health researchers built a fairly intricate model estimating the actual responses as a differential equation (simulation and references available here), which would probably be a good place to start.

If you're inquiring not from general curiosity but with an interest in developing your own nutritional plan, keep in mind that nutrition is a lot more than merely calories.  It is critical to get macro and micro nutrients, of course, but other factors such as dietary fiber play an important role in the health outcomes.


Why is 450 nm monochromatic light perceived as blue or violet depending on its intensity? Trying to do some color matching I purchased a 450 nm laser. I expected monochromatic light of this laser to have similar properties to those of all others I've already played with — 808, 640, 520, 405 nm — in that they all cause an unambiguous color sensation.

But when I shined it onto my wall (having removed the lens), I was surprised to see something unusual. In the center, where the intensity is high, it looks as "very blue" — much like those 465 nm blue indicator LEDs we can see everywhere today, only more saturated. But on the sides, where the intensity falls off, the color looks like violet! When I shine this laser on a ceiling obscured by a wall, I see its reflected light as violet. When I move the spot so that the reflected light becomes more intense, I begin to see it as blue again in the intense areas, and still violet in dimmer ones.

I've checked with a spectrometer, and there doesn't appear to be any fluorescence in the light spot to confuse me.

Interestingly, if I increase amount of ambient lighting (white LED lamps + CCFL ones), sensation of blue once again transforms to violet. Also, the "very blue" intense spot looks violet in bright sunlight, although I can make it blue again by focusing into a smaller spot to make it brighter. In a fully dark (apart from the laser) room I still do notice the violet areas on the sides of the spot.

405 nm light also seems a bit silvery-whitish when its intensity is high, unlike at low intensity. Maybe it's the same phenomenon, which I simply didn't notice before because the tint is not that blue in this case.

In both cases of 450 nm and 405 nm the additional color on high intensities is still "shiny" due to the speckles specific to high monochromaticity, so this indeed doesn't look like the result of fluorescence of the objects I shine the light to.

I've asked several people whether they see it the same, and they answered affirmative.

I suppose it's not related to color balance, because I only changed the intensity of ambient light, not the tint to observe the changes in color. Especially it shouldn't be due to color balance since I can simultaneously see different colors in the areas with different intensities.

Interestingly, while I thought the "very blue" color to be the main color of 450 nm, CIE 1931 XYZ value for it, converted to sRGB, appears to be (if we desaturate and normalize to fit in sRGB range) (0.43,0,1), which is purple, not blue.

So, what is going on here? Is it a well-known phenomenon? Could it be due to some fluorescence of the retina itself rather than the objects lit by the laser?

This is a general feature of human perception of blue-white mixtures. It's known as Abney effect. It's not limited to highly monochromatic blue colors (not even to blue colors). We can observe this blue-related phenomenon even with longer wavelength light than 450 nm – e.g. sRGB blue, whose dominant wavelength is about 464 nm. Here's what most people would undoubtedly call blue – in HTML notation #0000ff:

And here's a mixture of 60%† white with 40% blue (in HTML notation #cacaff):

To me, if I haven't stared at shades of truly violet a few moments ago, this mixture seems to have a considerable amount of violet — more than I'd expect looking at the primary blue. Naturally, shorter wavelength light should give even more violet perception, until it becomes violet even in its pure form.

† Percentage is given in linear scale, actual color presented is gamma-corrected to be displayed on sRGB monitors.


The real definition of carbohydrates Carbohydrates are often defined as compounds with only C, H, and O and the H and usually the O atoms are in a 2:1 ratio.

Exceptions like deoxyribose exist, but why is it recognized as a carbohydrate?

What distinguishes a carbohydrate from other compounds?

The definition of carbohydrates as compounds containing $C$, $H$ and $O$ usually with the empirical formula ${C_m(H_2O)_n}$, is outdated.

More rigorous and a accurate definition would be Polyhydroxy Aldehydes and Ketones composed of Carbon, Hydrogen and Oxygen. Moreover, the nomenclature including Mono-, Di-, Oligo- and Poly- "Saccharide" is preferred over the now obsolete and too-general term "carbohydrate", since the etymological origin of the word "carbohydrate" is from the greek words Carbo- for carbon and hydor- for water which indicates that the carbohydrates are "hydrates" of carbon and have the empirical formula ${C_m(H_2O)_n}$, which is not always true. Instead "saccharide" is derived from the greek word for "sugar" and hence is much more accurate as it does not limit the definition to any empirical formula.

Apart from the polyhydroxy aldehyde or ketone characteristic of carbohydrate, they have a marked structural and functional variation from other biomolecules. This includes the absence of $S$ (as in proteins), $P$ and $N$ (as in proteins and nucleic acids), presence of Glycosidic bond (as compared to peptide bond in proteins, phosphodiester bond in nucleic acid, and ester linkages in fats or glycerides) and much greater structural uniformity as compared to other biomolecules.However, these characteristics are not absolute as is evident from the fact that several monosaccharide derivatives do contain $S$ or $N$ atoms. Actually, the entire group of amino-sugars (Hexosamines etc.) are usually classified under carbohydrates since they are primarily monosaccharide derivatives obtained through enzymatic amination.

These characteristics distinguish this class of compounds without having to assign a empirical formula to it.

ADDENDUM
Adding the clause compounds which can, on simple hydrolysis yield polyhydroxy aldehyde or ketones in the definition helps involve certain non-reducing sugars like Sucrose.


How does an embryo know where to grow limbs etc For example you have a cell or already a bunch of cells. Those cell(s) divide and after several week you have a grown organism, for example a human with limbs, several different organs etc.
However, how do cells know where up, down, left, right etc. is?
I know left and right can be defined clearly in physics, for example by the Wu experiment verifying parity violation really occur.

However how do cells define those directions? What are the mechanisms for them to grow into a certain direction and tell other cells to attain a certain property?

You may want to look into "Evolutionary - Developmental Biology", which deals with how an embryo develops into a grown organism.

  Thus, by combinatorial specifying the identity of particular body
  regions, Hox genes determine where limbs and other body segments will
  grow in a developing embryo or larva. A paragon of a toolbox gene is
  Pax6/eyeless, which controls eye formation in all animals. It has been
  found to produce eyes in mice and Drosophila, even if mouse
  Pax6/eyeless was expressed in Drosophila.

In short, there's a sequence of gene activations that progressively map body into different regions. At first, there are just 3 regions (head, body, tail), then these get broken down into more and more finely defined sections.

You can think of these sections as GPS coordinates for the body. A gene combination at a certain point means that a limb will grow there.

You can look into "Sonic Hedgehog" gene, which allowed scientists to produce fuzzy growth on a fruit fly head.

The most interesting thing is that every living creature is mapped/built using the same toolbox of genes. The genes that define where a fruit fly wing is also define where a human arm is.


Fast standing and the heart's insufficient accommodation of the increased venous return Assume you are 45 minutes on the supine position. Furthermore: you stand all of a sudden and fast and without sympaticus activity.
The venous return (smooth musculature of vessels) accommodates faster to the change (decrease of venous return) so returns blood to the heart before the sympaticus has accommodated for increased cardiac output.
This creates a significant increase in the blood volume entering the heart.
In pathological situation where systemic vasoconstriction not occurring normally, the heart is not capable of handling the overdistension; resulting in a pain during the second cardiac cycle.

I am interested in knowing which phase the heart is most vulnerable:

filling,
isovolumetric contraction
ejection
isovelumetric relaxation

or more explicitly (from my answer here)

Atrial systole
Isovolumetric ventricular contraction
Rapid ventricular ejection
Reduced ventricular ejection
Isovolumetric ventricular relaxation
Rapid ventricular filling

I think filling can happen normally, but not with the sudden isovolumetric contraction (most sympathetic innervations here, so therefore I think this is the weak link).
When there is too much blood in the ventricles, some of the blood is reflected back from the ventricles into the atria causing a painful sensation and possibly tachycardia (as well as an possible increased risk of atrial fibrillation if such events happen regularly).

Is the isovolumetric contraction (systole of ventricles) of the cardiac cycle the possible weak link in accommodating a sudden increased venous return?

Raoul's gives sensible comments:

ventricle overloading not sensible
retrosternal pain $\to$ myocardial ischemia
other cause reminding retrosternal pain such as celiac disease:

Posterior 1/3 of the septum is supplied by the following artery where any ischemia can weaken the isovolumetric contraction (TODO this has to be discussed much more carefully):

ischemia coronariaea posterioris created by problem in ramus interventricularis posterior arteriae coronariae dextrae


What is this unusual structure inside this banana? I was eating a banana, and I found this strange biological structure inside of it.

It was a bit tougher than the banana, and ran inside of the body through most of the length. To be clear, I peeled back banana with my fingers to reveal it; it was enveloped inside. It was accompanied by a small void.

No idea what this is, never seen anything like it. It didn't taste good. I'm thinking it might be a mutation. Anyone know what this is?

It looks like some species of Nigrospora genus took over the inside of that banana. According to Wikipedia, N. sphaerica was first isolated from bananas. The other species that you will find referenced online is N. oryzae. In the articles I
cite below the colonies are grown in potato dextrose, though.

Here is a picture of the red fungus inside a banana (from the Canadian Food Inspection Agency):

Googling 'Nigrosporia banana' also returns lots of similar pictures.

To get a better answer, a sample could be taken from the banana and then cross-check what you see under the microscope with the oryzae morphology images seen in the researchgate article.


Electric Shock To Human Body What happens in our body when we get an electric shock?

Ok. So, first of all, it depends on the power of the shock.

This relates to volts (electrical pressure) and amps (amount of electricity)

I strongly suggest you read
this article

That article explains what happens in great detail, but if you're still curious, here are some other things that would obviously happen:

If it is a constant DC Current, negative ions will rush to the anode, and positive ones will rush to the cathode. The negative ions (including oxygen and chlorine) will bleach the cells in the area and kill them.

The positive ones in the cathode area will raise the ph drastically and liquefy the adjacent cells.

If the current is high enough, the cells will heat, which will denature the proteins and enzymes within and kill them.


Meaning of "stripped" in "stripped antibody-depleted sera" From a research paper:

FOLR1 autoantibody detection
The assay for identification of the presence and relative quantification of FOLR1 autoantibodies in serum samples was performed as previously published.41–43 Horseradish peroxidase (HRP) labelled anti IgG antibody (Cat#I8640 Sigma Aldrich) and IgM antibody (Cat#I8260, Sigma Aldrich) were used to detect IgG and IgM. Antibody-depleted sera (Sigma Aldrich) was used as negative control. Serum effect on blocking FA binding to folate binding protein was detected using HRP labelled FA (FA-HRP, Ortho-Clinical Diagnostics, Raritan, New Jersey, USA). FA in serum samples was removed as previously described. Unlabelled FA was spiked (0.01–2000 ng/mL) into stripped antibody depleted sera to generate the standard curve. The SuperSignal ELISA Femto Substrate (Cat#37074, ThermoFisher Scientific) was used as substrate for detection of HRP activity. Images were collected using a 96-well imager (Q-View Imager, Quansys Biosciences). Intensities were extracted from the images using Q-View Software. IgG, IgM and relative FA-blocking amount were calculated based on the standard curves.

What is the meaning of "stripped" in stripped antibody depleted sera? I think that "antibody-depleted sera" stands for "serum samples that contain a reduced concentration of antibodies". But why stripped? Does it mean that the authors applied some additional techniques to ensure an even lower level of antibodies in the serum samples?
I found it odd because the word "stripped" is used only in this particular place, and nowhere else. They mention 'antibody-depleted sera" earlier, without "stripped".

I believe this is a failure of editing, and the meaning in this paper of "stripped" cannot be determined without correspondence with an author.  "Stripped" is an informal term for either removal of some substance or treatment with a material such as charcoal which affects many substances. Normally in papers "stripped" is qualified (at least initially) to indicate the type of treatment.  Here it could plausibly refer to antibodies, folic acid, or any number of other things.  It may be an artifact of draft editing that was meant to replace "stripped" with "antibody depleted" as a more precise term.  I suggest writing the corresponding author.


Where can I find a compendium of microorganisms? I recently bought a microscope hoping to learn more about algae and bacteria and stuff. I've collected a few samples of pond water and found tons of algae and stuff, but I have no idea what to call the things I have found. I am wondering if there is a list of every known algae with a picture and some characteristics that would help me identify what I am looking at. I've looked around on the internet and haven't found much. Thanks

I do not know how complex of a key you want, but this one is a good identification guide for beginners. It contains a lot of common freshwater pond algae, what they look like, and some basic characteristics. From here, you can identify your specimen and then be able to look them up further. Hope this helps!


Does anybody know what kind of snake is this? FYI the snake is dead and currently in my freezer, I got it from a guy and forgot to ask what kind it is.

This is Orthriophis taeniurus ridleyi, a synonym is Elaphe taeniura. It has a few common names,some are  Ridley's beauty snake,Cave beauty and Cave racer.

https://www.biolib.cz/en/taxon/id310150/

https://www.naturepl.com/search?s=orthriophis+taeniurus+ridleyi2581

https://www.zootierliste.de/en/?klasse=3&ordnung=305&familie=30513&art=21102660

https://www.thainationalparks.com/species/orthriophis-taeniurus

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

https://www.reptarium.cz/en/taxonomy/Orthriophis-taeniurus/2581


Any simulations of four-winged dinosaur flight? (microraptors) This week's podcast of the BBC's Science in Action includes a section by Rory Galloway (12:20 to 18:30) covering the Dinosaurs of China exhibit currently hosted by Wollaton Hal at the University of Nottingham, and includes an interview with curator Dr. Adam Smith.
The exhibit is of highly detailed dinosaur fossils from Liaoning, China where detailed feather structures were well preserved and have been analyzed in great detail.
One section caught my attention:

Rory Galloway: "The similarity between dinosaurs and birds was far more than superficial though. Eventually a branch of small, theropod dynosaurs evolved into the birds that fly around today. But curator Adam Smith says, if we concentrate on flight alone, it gets quite difficult to know exactly which branch of the dinosaurs actually became our birds."
Adam Smith: "Flight is really important and that’s why it evolves many times. Some of the earliest flying dinosaurs, such as the microraptor actually had four wings, not two."

The Wikipedia article on the Microraptor is quite long and includes a lengthy, technical discussion on just how these four wings might have been used. It seems that it is (currently) generally believed that these dinosaurs had the capability of powered flight, and that they could actually take off from the ground, rather than climb trees, jump, and simply glide.
This is with four wings.
There are many variety of insects with four wings and the two pair are used in a variety of different ways. But these dinosaurs are much larger, of the order of a kilogram.
Question: Have there been any complete simulations of the mechanics of four-winged dinosaur flight, showing how the wings would have been used to take off from the ground and gain altitude? A movie or animation of the coordinated flapping of the front versus rear pair of wings would be great. These days the numerical models and computing power are within reach, but it would still be a substantial effort, so I'm not sure if this has been done yet or not.
I'm assuming that this is not currently believed to be the branch of dinosaur that eventually evolved into modern birds, but it's a fascinating branch nonetheless.
below: from here.

Note nowhere in the article does it mention the rear wings flapping. The rear wings do not provide lift, they are acting as control surfaces to improve stability and maneuverability. (think of the tail of a plane).earlier/proto flies have far more demand for control surfaces than developed/derived fliers due to lacking more precise control of flight surfaces.

They basically take off just like any other bird, if they could fly. Flight in dinosaurs likely did not even evolve from gliding as we commonly think of it but instead from raptorian pouncing, the sprawled posture of microraptor you sometimes see, with its hind legs spread wide, is anatomically impossible, you literally have to dislocate both legs to do it. Dinosaur hip joints do not allow for much lateral extension unlike mammalian or varanid ones, more like a hinge than a ball and socket.

The animal in flight would have looked like this.

Hall, Justin, et al. "A new model for hindwing function in the four-winged theropod dinosaur Microraptor gui." JOURNAL OF VERTEBRATE PALEONTOLOGY. Vol. 32. 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA: TAYLOR & FRANCIS INC, 2012.


How many cyclic and non-cyclic photo-phosphorylation is required to produce one molecule of glucose? In non-cyclic photophosphorylation 1 ATP and 2 $NADPH_2$ molecules are produced.

In cyclic photophosphorylation 2 ATP molecules are produced.

For production of one molecule of Glucose 18 ATP and 12 $NADPH_2$ molecules are reqiured.

According to my understanding,6 turns of cyclic and non-cyclic photophosphorylation is required to produce one molecule of glucose.

Because 6 turns of non cyclic photophosphorylation will produce 12  $NADPH_2$ and 6 ATP molecules.

And cyclic photophosphorylation will produce 12 ATP molecules.

Total=12 $NADPH_2$ and 18 ATP.

I think Iam missing something , Please answer me if I am correct or not.

In non-cyclic photophosphorylation the stoichiometry of ATP:NADPH is predicted as 3:2, i.e, for every two NADPH formed, a total of three ATP are produced.
Source: Cyclic, pseudocyclic and noncyclic photophosphorylation: New links in
the chain. John F. Allen. TRENDS in Plant Science Vol.8 No.1 January 2003.
Cyclic photophosporylation, does not occur under normal conditions in higher plants. It is believed to occur only when either light intensity is low (lower frequency so as only PS1 can function) or when carbon fixation is not at par with light irradiance (i.e, too much light).
And hence it is not advisable to come to this generalization "Six Turns of non cyclic photophosphorylation will produce 12 NADPH2 and six ATP molecule"


Where does the additional 1 proton cost of oxidative phosphorylation come from? I've been quite confused by the source of the additional 1H+ cost right now. I know it costs the F1Fo-ATP synthase 3H+  to produce an ATP, and it is also stated that:

  ADP3−cytoplasm + ATP4−matrix → ADP3−matrix + ATP4−cytoplasm //
  ADP/ATP exchange is energetically expensive: about 25% of the energy yielded from electron transfer by aerobic respiration, or one hydrogen ion, is consumed to regenerate the membrane potential that is tapped by ADP/ATP translocase.(Wikipedia/ADP/ATP Translocase)

So in some books I find out that they regard the net cost of producing an ATP as 4H+. Here is another statement:

  The phosphate carrier, which works in concert with ATP-ADP translocase, mediates the electroneutral exchange of H2PO4-for OH- (or, indistinguishably, the electroneutral symport of H2PO4- and H+). The combined action of these two transporters leads to the exchange of cytosolic ADP and Pi for matrix ATP at the cost of an influx of one H+. (Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition. New York: W H Freeman; 2002. Section 18.5, Many Shuttles Allow Movement Across the Mitochondrial Membranes.)

And my question comes here. Why do we not consider the effect of the process of ADP + Pi → ATP on the membrane potential? It also produces a net cost of 2e-. Putting these together, this will lead to 0, i.e. no additional net cost. Or should I only consider H+ but not e-?
(This might lead to another problem about H2PO4-'s breakup.)

The energy required for the ATP production by ATP synthase is obtained from movement of ions (H+ or in some cases Na+) downstream of their potential (proton motive force). I guess, there is no exact stoichiometric exchange as in case of ion pumps. The rotation of the motor is generated by the movement of protons through a channel. The H+/ATP ratio is estimated using biophysical/biochemical techniques.

Brand and Lehninger (1977) estimated this ratio to be greater than 3.

Turina et al. (2003) recalculated this ratio using constituted liposomes and their estimate is  3.9 ± 0.2.

This is an excerpt from a more recent study on chloroplast ATP synthase by Hahn et al (2018).

  The symmetry mismatch between the 14-fold Fo rotor and the
  near-threefold F1 head means that the number of c subunits rotating
  past subunit a to generate one ATP is not an integer. cF1Fo requires,
  on average, 4.67 c subunits, or protons, to produce one ATP. The
  nearest integral numbers of c subunits per step would be 4, 5, and 5,
  equivalent to rotation angles of 103°, 129°, and 129°. Surprisingly
  however, the three conformations are separated by rotations of 103°,
  112°, and 145°, or 4, 4.4, and 5.6 c subunits (fig. S5C). This means
  that the position of the c subunits relative to subunit a in the three
  conformations differs.

The structure and efficiency of chloroplast ATP synthase may be a little different but what I want to emphasize is that there is no exact exchange of protons and ATP.


Allamanda blanchetti fertilization mechanism Here is an Allamanda blanchetti flower in my garden.
My question is based on the observation that the flower seems to be devoid of any reproductive structures, i.e., Stamen or Carpel, so how does it set seed? In the picture below it can be seen that the plant isn't sterile and successfully produces seed pods.

As far as the ID goes, this looks like Allamanda blanchetti.  See this question.


How do I interpret SNP nomenclature? I am combing through my 23 & me raw data and I am a little confused on SNP terminology. I am using NCBI's genome browser and SNP database. As an example we can all follow here is a link to a CYP1A1 SNP https://www.ncbi.nlm.nih.gov/snp/rs28399430. When you open this link you will see alleles listed as G>C. Which one of these is the reference genome and which is the pathogenic allele? Is the relationship always constant (like in x>y, x is always the reference and y is the substitution). If you scroll down to the genome browser view, there also doesn't appear to be any way to tell + vs - sense strand (ie making it difficult to tell G for C mutations or vice versa). I would just assume its the top strand? The ultimate goal here is for me to look through 23&me and compare my SNP genotype to the reference genome and see if my genotype exhibits pathogenic SNPs in certain genes.

Quick answer is yeah, the G is the "reference allele" as you put it.  The greater than symbol is acting as an arrow, ie, G goes to C, that is, G is replaced with C.

Actually you get a pretty clear indication of that if you look down a line it two where it mentions the frequency:

  C=0.000419 (104/247982, GnomAD_exome)
  C=0.000494 (62/125568, TOPMED)
  C=0.000538 (62/115296, ExAC)

The C frequency is way too low to be the "normal" allele.  It's rather the substitution which results in a missense variant. You can see more specific stats by clicking on the frequency button.  In this case they basically just say that in all studied populations the G variant is by far the most common.


A question about cancer antigens and their mechanism Can you name the most common antigen that cancer cells in general can't live without?

This is a hard question to answer because each type of cancer is a whole different game at the molecular level, however there is something you might be interested in called "hallmarks of cancer" (image 1) which are key features for cancer to thrive. They were originally described by Hanahan and Weinberg (2000) and have been revisited by Fouad and Aanei (2017) in an updated review. The hallmarks of cancer aren't specific genes themselves, but rather broader categories that englobe certain types of genes.

If you want to look at specific genes, we could talk a bit about what more purely data driven approaches have found. There is a very interesting work by Kandoth and collaborators (2013) that presents data from The Cancer Genome Atlas (TCGA), which is a database of different kinds of genomic features from several different cancer types. Among the results of this work (specifically on figure 2 which I include here as Image 2) you can see a table of 127 significantly mutated genes across 12 different cancer types. One gene that is well known in medical literature for being frequently mutated in almost any cancer type (situation which is also observed in the aformentioned table) is TP53 which encodes a protein that is key for genome maintenance in normal cells by participating in DNA damage and repair (which is a cancer hallmark under the "altered stress response" category). In the table you can also spot tissue-specific cancer genes such as APC in colon/rectum cancer and VHL in renal cell carcinoma.

Just to make sure you can understand the table, the gene names are presented in the right (rows) and the names of the cancer types are presented at the top (columns). The description for the cancer types abbreviations can be found here. To the left of the table there is a functional classification of the genes so you can know more or less what a given gene does in a quick manner. The values presented are simple frequencies (divide the number of samples of a particular cancer type that have the mutation over the total number of samples of that same cancer type) expressed as percentages (so they are already multiplied by 100). The final column (Pan-Cancer) shows the same idea, but taking all samples from all cancer types into consideration for the frequency calculation.

So for answering your question regarding if there is a common feature in all types of cancers: strictly speaking at the gene level no, since even the TP53 mutation which is the most common amongst all cancers might not be present in some cancers; however, looking at it by categories of genes (as one or some of the 7 hallmarks) reveals that all cancers apply similar strategies to thrive (they exhibit different mutated genes, but these genes frequently belong to the same biological pathways and participate in similar functions). I hope you find this useful (:

Image 1: 7 hallmarks of cancer (2017 review).

Image 2: frequency of mutation by gene and cancer type.

References:

Fouad, Y. A., & Aanei, C. (2017). Revisiting the hallmarks of cancer. American journal of cancer research, 7(5), 1016–1036. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5446472/
Kandoth, C., McLellan, M. D., Vandin, F., Ye, K., Niu, B., Lu, C., … Ding, L. (2013). Mutational landscape and significance across 12 major cancer types. Nature, 502(7471), 333–339. doi:10.1038/nature12634
National Cancer Institute. TCGA Study Abbreviations. Retrieved from https://gdc.cancer.gov/resources-tcga-users/tcga-code-tables/tcga-study-abbreviations


How can I search for and find specific biology topics in scientific journals? I looked on google to find "scientific paper on biological explanation of homosexuality" but nothing comes up that appears reliable or from a journal. Then I looked up "scientific journals" and I found a directory for them, and searched through that directory, but of all the journals, I cant seem to find an efficient way to search for topics in these journals over the web.

Is there a way to efficiently search for specific scientific journal papers, specifically for biology?

There are two possibilities for searching for scientific articles:

The first one is to use PubMed, a database which has been set up by the National Institute of Health in the US. It contains about 25 Million journal articles. All articles in this database are coming from peer-reviewed journals.

The other one is to use Google Scholar, which is better when you are unsure about search terms. It will give you more results, but you have to be careful here, since not all hits are from peer-reviewed journals, sometimes you get some quite questionable sources.


Why is it not advisable for humans to drink distilled water? Distilled water is pure and it does not contain any minerals, so may not be advisable for drinking.
Although laboratory made distilled water is completely pure, industry made water may still contain harmful impurities.
Also there is some probability of exosmosis into body tissues which may lead to swelling.

As you said, distilled water is completly out of minerals/ions. The principle of diffusion is that reagents diffuse from high-concentrated to low concentrated places to reach an equilibrium. So normally, ions from the erythrocytes would diffuse into the plasma to reach that equilibrium. However, it is quite difficult for ions to pass the cell membrane which is not the case for water. So what finally happens is that the distilled water wants to dilute the ions in your erythrocytes, passes the cell membrane and the cells explode because they are too full. As consequence, you die because there is no oxygen transport anymore.


Books about human evolution I want to read some books about human evolution and about other extincted types of humans.

The book "Sapiens: A Brief History of Humankind" writes about history of agricultural and scientific revolution too, which is the part that is not interesting to me as it sounds more like history. However, I want a book about humans living millions years ago up to and before agriculture. I want to know how modern human evolved and what there were besides homo sapiens.

The Journey of Man is a great book that really dives into the archaeology but also the genetic history of evolution.


Does chromosome cross occur over male and female or vice versa? My understanding is homologous chromosome pair, which means male and female chromosome inside the DNA. So if that's homologous how does male do with female? Does it flip over and change direction, that could not happen as male chromosome 1 (say) is indistinguishable from female?
And what about the XY chromosome in male,say?
I know some are pseudoautosomal, but most are normal sex chromosome nucleotides.
So what about them?

The question is unclear to me but hopefully that will help a little bit.

  My understanding is homologous chromosome pair, which means male and female chromosome

There is no male and female chromosome. Chromosomes have no sex. In humans, to the exception of chromosome Y all chromosome can be found in individuals of any sex.

There are paternally inherited chromosomes and maternally inherited chromosomes though. As you said the maternally inherited chromosome is indistinguishable from the paternally inherited chromosome when comparing their sequence (they may well differ in terms of epigenetic changes).

  chromosome inside the DNA.

A chromosome is not inside the DNA. DNA is the name of the very long molecule from which a chromosome is (mainly) made of. DNA can be organized in different forms one of which is into chromosomes (another one would be a plasmid for example). While it would still sound funny, it is more correct to talk about DNA inside a chromosome than talking about chromosome inside DNA.

  So if that's homologous how does male do with female?

This is very unclear...do what? Why would the paternally inherited chromosome (assuming this is what you mean by male chromosome) do anything with the maternally inherited chromosome rather than the other way around? While it is clear from the what follows that you would like to talk about recombination, I don't get where you're heading.

  does it flip over and change direction, that could not happen as male chromosome 1(say) is indistinguishable from female?

I don't get what kind of "flip" you are thinking about. You probably should have a look at the wikipedia article for cross-over.

In short, synapsis are formed during prophase I of meiosis and when segregation happen synapsis are resolved with a probability of $\frac{1}{2}$ of causing a recombination event. Synapsis occur as they allow matching pairs of homologous chromosomes together that will ensure their separation during anaphase 1. You should probably take some time to review the meaning of this paragraph.

  And what about the XY chromosome in male,say?

Sorry, that's a bit unclear too.

  I know some are pseudoautosomal, but most are normal sex chromosome nucleotides. So what about them?

Sounds like you misunderstand what a sex chromosome is and what pseudoautosomal mean.

In short, in humans, there is only one pair of sex chromosomes (XX or XY depending on the sex). The other 22 pairs of chromosomes are autosomes. There is no such thing as a pseudo-autosomal chromosome in humans but there is a pseudo-autosomal region on the Y-chromosome.

Most of the Y chromosome never recombine (while the X chromosome recombine in females only) as it is never present with another Y chromosome in the same cell. There is only a short sequence on top of the Y chromosome that recombines with the X chromosome, this region is called the pseudo-autosomal region. This region probably still exist to allow separation of X and Y chromosomes during anaphase I.

Please also note that you seem very focus on humans (without saying it and maybe without realizing it). The diversity of sex-determination is huge. You might want to have a look at Do males of all sexual species have Y chromosomes?


If we sequenced the genome of every species, would all phylogenies agree? The Tree of Life is still up for debate. Most of this debate seems to be due to a lack of genomic information, but that deficiency is decreasing rapidly with advances in technology and sequencing power.

Hypothetically, if we knew the genome of every species, would we resolve all phylogenetic debates? If not, what would still be up for debate?

Horizontal gene transfer

Don't expect to have a tree! Horizontal gene transfer happens and therefore we would end up with a network, not a tree.

Gene trees

Different DNA sequences have different evolutionary histories. See, in particular, the question of incomplete lineage sorting. This means that one may compute a tree for a given DNA sequence that must disagree with the tree of another sequence. So, don't expect a perfect species tree where all sequences will agree on.

Note that the two points "Horizontal gene transfer" and "Gene trees" are highly related. So much so that they could fit together.

Not all individuals have been discovered

If by saying of every organism, you meant "of every organism that we encounter", then we still have the issue of organisms that we have never encountered. If you meant "absolutely every individual that exist", then this is a non-issue. It also matters as to whether you mean every individual of every species or just one individual per species.

Also, it is slightly unclear whether, in your hypothesis, we can sequence all dead individuals! Extinct lineages would still not be resolved if we cannot sequence them.

Massive mutational events

It is possible that very large mutational event could prevent us to see the exact relationship between individuals. But that would only interfere on an extremely fine scale phylogeny (intra-species level).

Methodology

If we really sample all the individuals, the detail of the methodology may not matter much. It will still need to be decided whether we want to consider AATC closer to AA.C or to AGTC (where . indicates a deletion). Again, this will likely only matter on a very fine scale (intra-species level).

Computational power

Of course, if we sequence every nucleotide that exists on earth, we would never have the computational power to even store the data. Not talking about actually processing it. We would not either have the computational power to process the sequencing (nor the necessary amount of products to allow for the sequencing to happen).

If you meant to fully sequence only one individual per species (and then again the arbitrary nature of the concept of species will complicate things up), then we might have the computational power (see @KonradRudolf's comment)

The concept of species can often be misleading. You might want to read the post How could humans have interbred with Neanderthals if we're a different species? for a discussion on the concept of species.


What hair do aquatic mammals have? I'm reading an essay on the creating of the Mammalia zoological classification (Londa Schiebinger, The American Historical Review, Vol. 98, No. 2 (Apr., 1993), pp. 382-411).

It contains the statement (page 386)

  All mammals (including the whale) have hair, and it is still today considered a distinguishing characteristic of mammals.

Is that statement correct? Do all known species of whale and dolphin have hair? If so, where is it? You can't see it on the surface of the animal, is it internal like we have nostril hair?

Well, technically yes, but most adult dolphins do not have hair:

  Unlike most mammals, dolphins do not have hair, except for a few hairs around the tip of their rostrum (beak) which they lose shortly before or after birth. The only exception to this is the Boto river dolphin, which has persistent small hairs on the rostrum.

Whales do, and depending on your definition of "hair" - that includes Baleen - which is composed of fine keratin fibers, much like normal fur/hair, which is the distinguishing characteristic of "Baleen whales" (like the Blue Whale).


What is the structural difference between beta and gamma globin chains of Hb? Hemoglobins are tetramers composed of pairs of two different polypeptide subunits. The subunit composition of the principal hemoglobins are α2β2 (HbA; normal adult hemoglobin), α2γ2 (HbF; fetal hemoglobin) and α2δ2 (HbA2; a minor adult hemoglobin)

The total number of amino acids in beta chain and gamma chain is the same-146. The higher affinity of HbF to oxygen is due to presence of serine(in gamma chain) in place of histidine(in beta chain), which inhibits its binding with 2,3-bisphosphoglyceric acid.

Is this the only difference, or are there more such differences in the amino acid sequence?

Here's a pairwise sequence alignment of the human hemoglobin beta (HBB) and gamma (HBG1) chains:

HBB_HUMAN          1 VHLTPEEKSAVTALWGKVNVDEVGGEALGRLLVVYPWTQRFFESFGDLST     50
                     .|.|.|:|:.:|:|||||||::.|||.|||||||||||||||:|||:||:
HBG1_HUMAN         1 GHFTEEDKATITSLWGKVNVEDAGGETLGRLLVVYPWTQRFFDSFGNLSS     50

HBB_HUMAN         51 PDAVMGNPKVKAHGKKVLGAFSDGLAHLDNLKGTFATLSELHCDKLHVDP    100
                     ..|:||||||||||||||.:..|.:.|||:||||||.|||||||||||||
HBG1_HUMAN        51 ASAIMGNPKVKAHGKKVLTSLGDAIKHLDDLKGTFAQLSELHCDKLHVDP    100

HBB_HUMAN        101 ENFRLLGNVLVCVLAHHFGKEFTPPVQAAYQKVVAGVANALAHKYH    146
                     |||:|||||||.|||.||||||||.|||::||:|..||:||:.:||
HBG1_HUMAN       101 ENFKLLGNVLVTVLAIHFGKEFTPEVQASWQKMVTAVASALSSRYH    146

You can see the H143S (or S143H?) substitution, as well as many more.


Is it safe to work with HeLa cells? Hela cells are infected with HPV. So is it safe to work with them? What are the safety precautions?

Most guidelines for HeLa (and most cells of human origin) say they should be kept at a BSL2 level. For example, from a 2007 publication in Applied Biosafety:

  Work with cell cultures from human or primate origin should generally be performed under BSL2 conditions. Containment level 1 may be considered if all manipulations occur in a Type II biosafety cabinet ...

--Animal Cell Cultures: Risk Assessment and Biosafety Recommendations

ATCC general guidelines recommend BSL2 containment for the broad category covering HeLa:

  Biosafety Level 2

  Cell lines that harbor mycoplasma or any other BSL 2 agent (See: NOTE)
  Cell lines exposed to or transformed by a primate oncogenic virus
  Primate cell lines that contain viruses
  Cell lines carrying a part of certain viral genomes, even if whole virus is not released from the cell

--ATCC® ANIMAL CELL CULTURE GUIDE: tips and techniques for continuous cell lines

Their specific page for HeLa also recommends BSL2, with the note "[Cells contain human papilloma virus]".

That said, HeLa cells have been very widely used, including for decades before modern lab safety practices were agreed on, and I'm not aware of any actual problem ever arising (including such amazing practices as injecting live HeLa cells into convict "volunteers" to see if cancers would appear - They did not).

So the answer to the question is that it is safe to work with HeLa cells, but that proper BSL2 lab practices should be followed.


Are hybrid-species individuals considered to be of the same species as their parents? This question arises given the definition of father and mother as seen in the Spanish dictionary composed by the Royal Spanish Academy. Basically it says that a father/mother is a man/woman or a male/female animal that has engendered/given birth to an individual of the same species (Spanish: "especie").

The Spanish word "especie" could also be translated here as "kind", but let's assume it refers to its zoological definition. That definition would be mostly true, but what about mules or ligers?

In the case of mules, they are the offspring of a male donkey and a female horse. A male donkey is considered to be of the species Equus asinus, while a female horse is an Equus caballus. The mule is an individual of the species Equus asinus♂ × Equus caballus♀, but what is exactly that? It is the set resulting from the addition of the two parent species, or is it a complete, new species? In other words, are mules considered to be of the same species of a donkey or a horse? Or what they all have in common is just the genus?

TL/DR We usually don't give specific names to those hybrids.

This is a fairly complicated question, actually, without an easy answer. Hybridization can have different outcomes, depending on how different the hybridizing species are. The cases you mention (liger, mules) actually do not deserve a specific names, because, first, they don't occur in nature, and, second, they are sterile, so there's no reproduction, hence no progeny. This lack of descendants goes against any defenition of species that we have in biology. There are cases where hybrids might become their own species, for example the butterfly Heliconius heurippa appears to be a species that evolved through hybridization between two closely related Heliconius species. There are also many examples in plants and more are being discovered in animals. These cases do receive a species name, because they occur in nature and populations can be predictably found.

Another case, similar to the cases you mention, involve hybridizations that occur in nature, but are rare and the individual rarely has any significance effect on the population. Sometimes those individuals are fertile, but look so different that might not be able to reproduce. Other times they can only reproduce with one of the parental species and if this happens successfully, new alleles can be introgressed into the parental genome. But for what we know, reproductive barriers between species tend to be successful in nature, tend to be broken down with human intervention (captivity, movement of species, among others) and, in most cases, don't have a significant evolutionary impact, except the cases when they do.


Why is sexual reproduction so much more common than asexual (in macroscopic organisms)? Fundamentally, what makes it better? I'm experimenting with an evolutionary method of creating a neural network. I use an asexual approach, but I've seen others use sexual approaches.

So I'm interesting in learning what's better about sexual reproduction as apposed to asexual, and biology is probably the best way to approach that question. So, why is sexual reproduction so much more common than asexual (in macroscopic organisms)? Fundamentally, what makes it better?

I'm struggling to understand what the combination of two gene sets does that couldn't be achieved by mutations to a child of asexual reproduction.

Genetic diversity is needed to prevent everyone from dying of the same disease. This is the problem with monocultures. Higher organisms are more susceptible to disease and thus reproduce sexually.

Furthermore, basically all organisms exchange DNA so they are effectively sexual.


What makes E. coli yellowish? LB, TB media, and yeast extract are also yellow but at the heart of the question. What chemical(s) make E. coli yellow?

I think of E. coli being more white than yellow.  When you compare E. coli and S. aureus on an agar plate, the Staph colonies have a much more distinctive yellow tint.  The yellow tint in Staph colonies is due to staphyloxanthin, a carotenoid pigment.


Interpretation of graph from evolutionary biology I am studying evolutionary biology, and been presented with this graph:

I am having some difficulties understand its meaning. For a start, why is time measured as a fraction of the population size? Also, what does it mean by allele frequency? Does it mean the frequency of a single allele? But if the first caption it referred to 'frequencies'... Any help? :)

I assume that the figure comes from a section on genetic drift (since this seems likely), and it shows how the allele frequency will change over time under drift in a diploid population. So in short, each line represents the distribution of allele frequencies in different hypothetical populations, that all started with the allele frequencey p=0.5.

As for your specific questions, as the comment from @remi.b says, t is expressed as generation time since this is the relevant time scale for evolutionary changes. The reason why it is a function of population size, N, is that genetic drift acts more stongly in small populations, since it is essentially a sampling effect. You can see it as a repeated application of binomial sampling. So in small populations different populations will quicky drift away from the starting point of p=0.5, while this takes a longer time in larger populations. The effect of population size is clearly shown in this article from Nature education, where you can see the distribution of allele frequencies after one generation in populations of different sizes.

The change in allele frequencies over time under drift has been modelled by a diffussion approximation (see Kimura, 1955 for the original results). His results show that heterozygozity decreases at the rate of $1/(2N)$ per generation, and after 2N generations the distribution of allele frequencies is essentially flat (if you started at p=0.5). The degree of heterozygocity at time t is given by:

$$H_t = H_0*e^{-(\frac{1}{2N})t}$$

However, your graph does not show populations where fixation has occured (only heterozygous populations), and this proportion will increase over time in the absence of new mutations. So what is missing are bars at 0 and 1, and these will become higher as time goes by (more populations will have become fixed for one of the alleles). It should also be mentioned that these results deal with the effective population size, so $N$ is really equal to $N_e$.

As for the confusion of frequency/frequencies; the graph shows the frequency of one allele in different populations (so the allele frequency on the x-axis), but each line shows the distribution of allele frequencies in different populations. This is probably why you found this confusing.

However, your question is a bit unclear since you haven't described from where you got the graph and exactly what it is supposed to represent.


What is this plant from Morocco? The plant was photographed in spring in Morocco. It's an angiosperm. It is about 2 metres high and has feathered fruits. What species is it?

Looks like Nerium oleander based on the leaves and the seeds/pod.  If not that species, certainly in the genus.  This is a common landscape plant in arid environments, and native to your area according to Wikipedia.  It contains extremely toxic substances that affect the heart, called cardiac glycosides.  Consuming these substances, which are found in the white latex, causes the heart to beat itself to death.