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Crispr-Cas9 method and nobel
Since i had my first cell class at university i have heard about Cripsr Cas9 method. But I am quite surprised about one fact.  Why actually wasnt rewarded by Nobel price? Is it something like Einsteins relativity (to early to reward it)?

I'm voting to close this question as off-topic because it is not about biology in the terms of SE Biology.

This question might be on topic on Academia.SE but not on Biology.SE.

i am so sorry but i thought there will be some kind of biological problem with this  method and not only rivarly with money thing.

My guess is that some people (likely Jennifer Doudna, Emmanuelle Charpentier and Feng Zhang) will eventually be awarded a Nobel Prize for the discovery of CRISPR and the development of its applications for genome editing, because it really is a major advance. But for now, the University of California Berkeley and the Broad Institute are still legally fighting over patent conflicts, and the patent situation worldwide is generally complicated. I think this is a possible reason why the Nobel committee decided to wait.


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Is photosynthesis faster in aquatic plants rather than terrestrial plants?
For example : In which of these two plants photosynthesis is faster and why? water hyacinth or sedge?

source: Stack Exchange

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Myelination and time constant
In textbooks, it says that myelination doesn't really affect the time constant as tau=RC where R is the membrane resistance and C is the membrane capacitance. Myelin increases membrane resistance while decreasing membrane capacitance so there isn't really an overall effect on the time constant. However, during active regeneration of the action potential, the current only goes the path with least resistance i.e. the nodes of Ranvier, so wouldn't the R be the resistance of the node of Ranvier instead of the resistance of the entire membrane as stated in the textbooks? If this argument is correct then wouldn't myelination increases decreases time constant? Thanks!

For the saltatory propagation of the action potential the constant of interest is not the membrane tau constant, but the spatial lambda constant. The decrease in membrane resistance due to mielination increases lambda, allowing the current to travel farther to the next Ranvier node.
In the Ranvier node there's a high concentration of ion channels that generates the current necessary to depolarize the next node.

No. When a signal is sent through a myelinated axon, the Nodes of Ranvier act as repeaters in electronics. The signal/action potential will disperse down the axon, the Node of Ranvier will pick up the signal, amplify it, and send it to the subsequent Node of Ranvier. I think you're thinking of the Nodes of Ranvier as cracks in the myelin/axon rather than as mini re-amplification sites.

Welcome to Biology.SE! This looks like it might be a good answer, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best, but textbooks can be OK). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

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Is it possible to make anaerobic media too reducing?
I've been struggling to grow an anaerobe (P. gingivalis), I take every precaution to keep the culture conditions free of oxygen, I was wondering if the conditions can be so reducing that they inhibit microbial growth of an obligate anaerobe.
To make the liquid media I do the following:

TSB supplemented with yeast extract
plus 0.5g/L L-cysteine HCl as a reducing agent
plus resazurin as a redox indicator
heat-sparge with nitrogen until the resazurin goes completely colourless
add hemin (5 mg/L) and vitamin K1 (1 mg/L) from stock solutions (1mL/L hemin in water, 200uL/L vit K1 in ethanol)
filter-inject this media into glass tubes which have had the gas in them removed (this takes place in an anaerobic hood)
all materials (syringes, needles, filters, tubes) had been left in the anaerobic hood before use so that no residual oxygen is left in/on them
swap the headspace for a gas mix of 80:10:10 N2:CO2:H2

I don't get any growth after over 72 hours @ 37oC.
Other protocols I have found are much more vague/lax about removing the oxygen, many just say that the cysteine should be added, and the media should be incubated in an anaerobic hood for 24 hours with the lid loose before being used. This got me thinking that maybe I'm removing too much of the oxygen.
What do you think?

For the record I got the culture growing today, I checked the pH after sparging and noticed it was a bit low (6.6, it should really be 7.4) so I pH balanced it to around 8.0 before sparging and the pH ended up around 7.0. I think I could do better and have media with a final pH of 7.4, but hey, it works!

I notice that you don't specify pH, which might be important.
I don't know if you can put in too much reducing agent (I suspect not), but a large excess is often required as the equilibrium constants for disulfide exchange reactions are typically close to unity (see Cleland, 1963).
I also don't know if any of following has any relevant to your problem (again, I suspect not), but I want to briefly comment on two aspects of using thiols to as reducing agents in general.
Firstly, the oxidized (disulfide) form of thiols may react with a protein sulfhydryl. Using β-mercaptoethanol as an example (Scopes, 1993, p 320), something like the following may occur, where the reducing agent becomes (reversibly) bound to protein. If the reactive sulfhydryl is at an enzyme active site, this may lead to inactivation.
$$\ce{2 HSCH2-CH2OH  +  O2 -> HOCH2CH2-S-S-CH2CH2OH + H2O2\tag{1}}$$
$$\ce{HOCH2CH2-S-S-CH2CH2OH + HS-{Protein} <=>HSCH2-CH2OH + HOCH2CH2-S-S-{Protein}  \tag{2}}$$
As stated, equilibrium constants for thiol exchange reactions are often close to unity (Cleland, 1963).,
 $$\ce{R1-S-S-R2 + R3-SH <=> R1-S-S-R3 + R2-SH \tag{3}}$$
  For this reason, many protein chemists prefer to use dithiol analogs of threitol (dithiothreitol, DTT, or Cleland's reagent) or erythritol as reducing agent, as the oxidized form of these compounds are cyclic disulfides, where the equilibrium constant is displaced to the right  (see Cleland, 1963).
There is also the question of stability.
The half-life of thiols in solution are markedly pH and temperature dependent, as the  table below shows. The half-life of β-mercaptoethanol at pH 6.5 and 20℃ is greater than 100 hours, but at pH 8.5  and 20℃ it is only 4 hours.

The above table was taken from  Stevens, R, Stevens, L & Price, N.C (1983) The stabilities of various thiol compounds used in protein purifications, published in (the now-defunct) Biochemical Education. The full article is freely available as a pdf from the Wiley website

Thanks that's really interesting, I'll look into using DTT as a default reducing agent. I think in the end the problem was pH, I would adjust it to 7.4 before sorting but this would drop to around 6.6 after sparging. I'm not sure why this would be, could be evaporation, or some CO2 might be dissolving. Anyway it seems that Porphyromonas gingivalis prefers a pH more around 7.5

I think I agree with you: that you probably can't have anaerobic media that is to reducing for an obligate anaerobe. So I consider this question answered.

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Is there a system biology approach to compare pathways or famillies of proteins from an evolutionary point of view for the same organism?
I would be interested to know if there is a method/analysis or a set of methods to compare two groups of pathways or families of proteins.
I would specifically be interested by a system biology approach which takes all the components of the pathway or family of proteins. I would like to know if there is a method which can not only compare the similarity, homology, divergence and convergence of a family of proteins (like ribosomal proteins) between species but also between groups in the same organism.
For example I would like to compare the molecular components of vesicular trafficking pathways to the molecular components of non-vesicular pathway in the same organism saccharomyces cerevisiae (yeast).
I would greatly appreciate your suggestions.

I am not sure that I completely understand, it would be a little easier if you described the problem you are trying to solve or what the motivation is.
However, I think that some of what you want to do can be accomplished by inferring gene/protein trees for each gene/protein of interest across different species (including paralogs, maybe?). This will allow you to see discordance or correlation of evolutionary rates of different genes/proteins across species.
THis kind of analysis is built into HyPhy, though I have never used it. There are also somewhat less involved methods for measuring distances between trees.
You might also be interested in protein co-evolution methods, depending on the question at hand.
Your mentioning systems biology methods suggests that you have something rather different in mind, as none of these things I suggest are really systems biology IMO, but I'm not sure what it would be. Possibly you are interested in integrating e.g. protein-protein interaction or metabolic network information as well, but that would probably involve something more homebrewed that might integrate some of these things.
Hope that helps.

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About the definition of ketogenic amino acid
I am studying biochemistry and have been looking at metabolic network diagrams showing the different intermediates of glycolysis and the citric acid cycle that amino acids can be converted to.
I have gone over a list of which amino acids are considered ketogenic and which are considered glucogenic. I was surprised that Serine, Glycine, Cysteine, and Alanine are not considered ketogenic as they can be converted to pyruvate and pyruvate can be turned to acetyl-CoA, so that these 4 amino acids seem like they can then be used for ketogenesis.
I then looked at the definition of ketogenic amino acids on Wikipedia and it says "A ketogenic amino acid is an amino acid that can be degraded directly into acetyl-CoA".
The question is if there's some reason this is the definition of ketogenic amino acids; it seems to make more sense to me to classify Serine, Glycine, Cysteine, and Alanine as ketogenic due to what I said.
Thank you.

The fundamental 'problem' with acetyl-CoA is that it cannot be converted to glucose via the tricarboxylic acid (TCA) cycle: a two-carbon compound (acetyl-CoA) enters the TCA cycle, but two carbons are lost as CO$_2$ during each round of the cycle (in the two decarboxylation steps, ie in the reactions catalyzed by isocitrate dehydrogenase and by the alpha-ketoglutarate dehydrogenase complex).
There is no 'net gain' of carbon when acetyl-CoA is 'burned' in the TCA cycle.
This is why animals cannot convert even-number fatty acids (even-chain fatty acids) to glucose, and a basic principle of animal nutrition is that triglycerides, with the exception of the glycerol backbone, cannot be converted to glucose.
This, is seems to me, is also the key to understanding the difference between 'ketogenic' and 'glucogenic' amino acids.
Amino acids that directly give rise to acetyl-CoA (or acetoacetyl-CoA) cannot be converted to glucose but that can be converted to ketone bodies (such as D-3-hydroxybutyrate)  are referred to as ketogenic amino acids.
Pyruvate can be converted to glucose (via glucneogenesis), and amino acids that may be converted to pyruvate are considered glucogenic. A very good example is alanine which may be converted to pyruvate simply by transamination (alanine aminotransferase).
Alanine is a key protein-derived glucose precursor, especially in times of starvation (Felig, 1975). A commentary on the discovery of this key finding is given in this citation classic
In addition, amino acids that may be converted to TCA intermediates that in turn may be converted to phosphoenolpyruvate (and are thus precursors of glucose) are considered glucogenic (Lehninger, Biochemistry, 2nd Ed, 1975, p629).
We need to be aware that propionate (a three-carbon compound) is glucogenic (and this is particularly important in ruminants): it is even-chain fatty acids (and their CoA derivatives) that are non-glucogenic.
Furthermore, an amino acid may be both ketogenic and glucogenic.

Only leucine and lysine (LK) are exclusively ketogenic
Tryptophan, Isoleucine, Phenylalanine, and Tyrosine (WIFY) are both glucogenic and ketogenic
The other 14 'protein' amino acids are glucogenic

See  D'Mello (2003) for a great ref (it must be good, he's from Scotland).
The catabolism of the branched-chain amino acids (Ile, Leu, Val) provide an example of each type (Harper et al., 1984):

The catabolism of isoleucine gives rise propionyl-CoA and acetyl-CoA and is both glucogenic and ketogenic.
Leucine catabolism yields acetoacetate and acetyl-CoA (ketogenic)
Valine catabolism yields succinyl-CoA (glucogenic)

A quote from Metzler (2001) may help to clarify the origin of the terms.

According to a long-used classification amino acids are ketogenic if (like leucine) they are converted to acetyl-CoA (or acetyl-CoA and acetoacetate).
When fed to a starved animal, ketogenic amino acids cause an increased concentration of acetoacetate and other ketone bodies in the blood and urine.
On the other hand, glucogenic amino acids such as valine, when fed to a starved animal, promote the synthesis of glycogen
... isoleucine is both ketogenic and glucogenic, a fact that was known long before the pathway of metabolism was worked out.

Thus, in feeding experiments, a glucogenic amino acid gives rise
to the synthesis of glycogen, whereas a ketogenic amino acid does not
(but does give rise to an increase in the concentration of ketone bodies)`

We may note that plants can circumvent 'the acetyl-CoA problem' as they have the enzymes of the glyoxylate cycle, where the two decarboxylation steps of the TCA cycle are 'bypassed' (the key enzymes are malate synthase and isocitrate lyase) [and plants can convert acetyl-CoA to glucose].
It is also of interest, maybe, that both arginine and taurine (not one of the 20, of course) are essential in cats (see D'Mello, 2003). Arginine is required because of an inability to synthesis ornithine and a single Arg-free meal may cause a cat to become comatose due to the build-up of NH$_3$ (see D'Mello, 2003; Bequette, 2003) , and taurine is required to prevent retinal degeneration (see D'Mello, 2003; Bequette,2003). In addition, cats need high levels of Phe/Tyr for melanin biosynthesis, otherwise hair color may change from black to red-brown (see Bequette, 2003)
Reference
Some key references given above are from the following book:
Amino Acids in Animal Nutrition (2003) Edited by J.P.F. Mello, CABI Publishing, 2nd Edition

D'Mello, J.P.F (2003) Amino Acids as Multifunctional Molecules by J.P.F. D'Mello (Chapter 1)
List Bequette, B.J. (2003) Amino Acid Metabolism in Animals:an Overview (Chapter 4)

In Addition (Taurine in Cats)

Carnivores Herbivores and Omnivores in Blondes in Venetian Paintings, the Nine-Banded Armadillo, and Other Essays in Biochemistry by Konrad Bloch

“The question is if there’s some reason this is the definition of ketogenic amino acids”

The answer from @user1136 covers the biochemistry of the degradation of ketogenic and glucogenic amino acids. However it doesn’t answer this part of the question directly, which is what I shall use my answer to add. Just as we may classify amino acids as hydrophobic or hydrophilic if we are interested in their function in proteins, this classification as related to a particular context. At least in part, this is:

The provision of glucose, especially for the brain, during starvation
and pathological states such as diabetes

Whether or not so-called glucogenic amino acids could in principle be converted to acetyl CoA, the regulatory mechanisms controlling the pathways ensure that it will be converted to glucose via gluconeogenesis — which is the raison d’être for the breakdown of amino acids during starvation.
Although certain tissues can use other fuels instead of glucose, the brain and the erythrocytes have an absolute requirement for glucose. In the case of the erythrocyte the product of glucose oxidation, lactic acid, can be recycled via the liver. However this is not the case for nervous tissue. So an alternative classification might be glucogenic or non-glucogenic. However the fact that the ketone bodies produced by non-glucogenic amino acids have important positive and negative functions themselves (alternative fuel, but can cause acidosis) presumably led to the use of the term, ketogenic.
Footnote: Context and Experimental Evidence
The experimental evidence for the breakdown products of individual amino acids came from feeding experiments, so that it might be argued that the context of starvation I assert is incorrect, especially given the contemporary fad for ketogenic diets and the like. However as regards evolutionary and clinical importance, I would argue that starvation is what matters.
Further reading
There is more information about gluconeogenesis in starvation in my answer to this SE Question.
There is a useful answer by @Don_S to another SE question concerning the use of glucose and ketone bodies by the brain.
Section 30.3 of Berg et al. 5e (unfortunately no longer available on NCBI Bookshelf)  deals with amino acid breakdown and the use of glucose or ketone bodies during starvation.


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If number of children born were spread more evenly among all parents, would our species' genetics have more variability?
Instead of some parents having lots of kids, if the number of kids were spread more evenly to parents having few kids and people who have no children, would it introduce more genetic variability in our species in general?

Well the obvious answer is of course yes of course it would. That is the essence of natural selection. Variability leads to different phenotypes and selection for and the amplification of beneficial traits. Evolution. Except if there is no selection (everyone has the same amount of kids) no traits are amplified so everything in a large population is static. Until you introduce mutations and that increases variability. Eventually each individual would have such a large degree of variation from the next that I would assume speciation would be a very imminent result of any form of seperation or selection, which is against your original premise.

This is a good answer, and the only thing I would add is that the question does not mention whether all children have an equal chance to grow up and reproduce.  Given that accidents and illnesses might not be entirely random and might have genetic dependencies, natural selection would still be free to operate in a society where fecundity was evenly spread.

To answer this question we need to recourse to the concept of "effective population size" ($N_e$). This is the number of individuals which actually counts in maintaining a population and generally does not coincide with the number of living individuals (the census size $N$). $N_e$ was defined by Sewall Wright as "the number of breeding individuals in an idealized population that would show the same amount of dispersion of allele frequencies under random genetic drift or the same amount of inbreeding as the population under consideration".
In an idealized population with constant size, the chance of generating offspring is the same for all individuals, in such a way that the distribution of the number of offspring per individual is Poisson. In this situation $N_e = N$. In real populations, of course, the number of individuals of the two sexes that actually reproduce may be highly unbalanced, there is a large variation in fertility of different pairs, the number of individuals fluctuates from one generation to another, etc. All these factors lead to deviations such that $N_e < N$ (in most cases $N_e \ll N$).
The effect of variation in progeny size on $N_e$ is modeled by the equation $$N_e = \frac{4N - 2}{V + 2},$$ where $N$ is the total number of individuals (half males half females), and $V$ is the variance in progeny size per mating pair. It may be noted that if $V = 2$, which is the Poisson variance of a population with constant size, $N_e \approx N$ for reasonably large $N$, whereas $N_e$ decreases as $V$ increases.
Therefore, the answer to the question is yes, genetic variability is maintained at a higher level if the number of children is distributed more evenly among pairs.
An interesting point to note is that if the variance in progeny size is less than Poisson, we find $N_e$ > $N$, a result that may appear surprising (if $V = 0$, $N_e \approx 2N$). This suggests a strategy to maximize the effective size of captive populations of species at risk; by sampling a male and a female born from different pairs to mate for sustaining the population, the genetic variability transmitted to the offspring is maximal and the inbreeding is minimized.


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How could be the concentration of airborne pathogens in a specific indoor space be measured?
I wonder if it is possible to measure the concentration of airborne pathogens in a specific indoor space in order to extract a percentage value. This value would be helpful to determine specific infection control strategies that would decrease this percentage and improve the indoor air quality.

I have no idea how practical it would be for your intended application, but people do estimate airborne concentrations of fungi and bacteria by sampling aerosols (i.e., filtering a volume of area to extract dust etc. that can carry the target organisms) and then using quantitative PCR with primers targeted at generic fungal or bacterial DNA sequences to estimate concentrations of particular classes of organisms.
Luhung, Irvan, Yan Wu, Chun Kiat Ng, Dana Miller, Bin Cao, and Victor Wei-Chung Chang. “Protocol Improvements for Low Concentration DNA-Based Bioaerosol Sampling and Analysis.” PLoS ONE 10, no. 11 (November 30, 2015). https://doi.org/10.1371/journal.pone.0141158.

Thank you for your reply, I want to monitor the concentration of airborne pathogens in order to test alternatives of infection control strategies within the built environment and state how these modifications affect the concentration of airborne pathogens. I have searched for several methods such as using tracer gases, using electron capture detectors, or using biosensors, however, I need something which is more practically available and could detect the concentration precisely.

unfortunately, I can't help any more; my answer pretty much says what I know about this topic - I'm an ecologist, not an environmental DNA person. Sounds hard. Hope this points you in a useful direction.


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"Straight" or "linear" helix
If an alpha helix is discontinued for a short while and then continues in a different direction, I prefer to call in "kinked". If the helix is simply uniformly following one direction, I prefer to call it "straight", but I have been corrected, and been told that it is called "linear". Which is right?
Thank you!

Welcome to SE Biology. Please read the Tour and the Help on asking questions. There you will see that you should demonstrate that you have tried to research a question yourself before asking, especially apposite in this case as this sort of terminology is merely a question of convention. In fact there is no right or wrong, just clarity of expression.

OK, let me put you out of your misery. You have a basic misconception. The first image is not of an alpha-helix, but two. It could be a helix-turn-helix. And so the terms straight and linear are superfluous. Anyway, I’d avoid “straight” for the lower one, unless you wish to consider changing “kinked” to…

Okay.. Thanks, but I guess my question is unclear. Yes - it is two helices, it it is not really the helix the is kinked, that is true. It is the conformation I want to describe, a "kinked conformation" vs a "straight conformation" of a protein segment.

Read about protein secondary structure to learn how it is described. You are trying to reinvent the wheel and getting it square.


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What is a Singleton Variant
I'm reading a paper that on a population genetics study where they sequence a number of genomes. The study states that 101 Singleton Variants per individual where found. What does Singleton mean?

A singleton in mathematics is a set with one element.
They are likely referring to variants found in only one individual in their pool. It's possible there are other uses of the word singleton but given the context I think it is most likely.


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Comparion between machine vision & human vision
I hope this is the correct Stackexchange to ask this question.
I am trying to know : What is the current status of knowledge regarding human vision and pattern recognition.
More specifically,

How does the human eye read signals from  the cone cells? Is it row
by row, column by column like a computer? or or there other things
happening ?
When detecting, say, an edge, or a connected component - does the human eye continue searching row by row? or does it jumpimmediately to the next neighbor? Are human cone cells arranged in arectangular gird with 8 neighbors per cone besides for the edges?(my guess is no). Then how are the neighbors addressed? Does somerace condition occur?

As you can see, I am not a biologist, I am a physicist working with computer vision. I have moderate knowledge of anatomy, but I am willing to learn.
Thank you

This is a potentially very very broad question, but I'll try to provide a simple answer that addresses the biggest misconceptions.
First of all, animal vision (and brains more generally) is massively parallel. There may be some serial processing steps, but these are also massively parallel. Computers need to digest information into stereotyped operations that can be executed on a CPU. The brain has separate dedicated machinery to each point in space for early vision, so there is no need to process individual "lines" or points in sequence: it all happens at once.
Photoreceptor inputs are converted into center-surround receptive fields in retinal ganglion cells, where light in the center excites and light in the surround suppresses (ON-center cells), or vice versa (OFF-center cells). These receptive fields are then transmitted to thalamus (the lateral geniculate nucleus), and from there to V1, primary visual cortex.
You can then combine many of these circular receptive fields to detect straight edges, like this:

From https://grey.colorado.edu/CompCogNeuro/index.php/CCNBook/Perception
The cells in V1 that respond to these "edges" are called "simple cells"; there are also "complex cells" that have more complicated receptive fields, and other sensitivity like to motion and color. Some computer vision strategies end up producing receptive fields that look a lot like the ones found in early visual areas, the earliest ones built out of Gaussian-filtered sin waves.
From V1, there are higher order visual areas that respond to things like shapes, motion, optic flow, etc.
Basic neuroscience textbooks tend to contain a lot of information on the early visual system, Purves Neuroscience is a good example, any edition is fine:
Purves, D., Augustine, G. J., Fitzpatrick, D., Hall, W. C., LaMantia, A. S., McNamara, J. O., & White, L. E. (2014). Neuroscience, 2008. De Boeck, Sinauer, Sunderland, Mass.

In this image, the edge has a particular axis. and thus will detect only one particular edge. Are there then many V1 cells responsible for many axes and sizes in different subfields of the frame of vision?
and are the input to the V1 now completely parallel?

i am reading you link - and i will hopefully understand more soon

@Sean Yes. Many orientations, spatial scales, etc. There are lots more in the area responsible for the fovea, peripheral vision is more vague.

Thank you. Do we know anything about the resolution of the orientations and scales?

@Sean The orientations and scales are population coded, it doesn't make much sense to think of their resolution (we aren't coding in binary here). You can look at psychophysics data to get an idea of discrimination thresholds, which will depend on other factors like contrast. Like others interested in machine equivalents of biological perception, I really suggest you start from the ground up and learn about neuroscience if you want to go further.

Okey, thanks. I am specifically interested in vision and perception. Will it be too much to ask you for a few titles and papers?

@Sean I'd recommend starting with a basic neuroscience textbook; vision is often used as a model system in neurobiology and these texts have extensive sections on vision. Purves' "Neuroscience" or Kandel's "Principles of Neural Science" are good choices. Even Wikipedia is okay for background. For the visual processing hierarchy, Felleman & Van Essen 1991 is probably the canonical reference.

The lecture notes I linked above from the University of Colorado are also a good intro.


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Where can I find extensive information on animal blood types and transfusions?
I'm interested in doing research on different animal blood types, including blood transfusion across different species. What are some resources you could recommend for me?

Welcome to SE Biology. Please finish reading the Tour. It's dubious whether book recommendation are on topic here as they are subjective, but you should use the site search facility to find out if there have been similar questions on this topic. You will find one here that may provide some starting points, although I am not an expert in this area.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!


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How does taxonomy work? The case of the Avian Dinosaurs
I recently discovered that the class Aves (or Birds) has been renamed Avian Dinosaurs. My question is when this taxonomic denomination achieved the consensus of the scientific community and through witch process, this change was made.

Freudian slip there. Witchcraft is a reasonable explanation.

There was a taxonomic revolution brought about by cladistics https://en.wikipedia.org/wiki/Cladistics. Willi Hennig wrote about it in 1950, but he was an East German, and his work did not gain traction in the West until it was translated into English in the late 1960s. Then it took a while to become consensus. Since then, all taxonomy is based on phylogenetic relationships. So for 100 years, we talked about "Reptiles" and knew what they were. Under phylogenetic taxonomy however, once we understood that birds were descended from theropod dinosaurs, nomenclatural rules require that birds ARE dinosaurs. This makes sense, because a Robin is more closely related to a Tyrannosaurus than a Tyrannosaurus is to an Iguanodon. Technically, taxonomy changes with the publication of phylogenies that make formal nomenclatural changes. Once a peer-reviewed paper is published, the names change. But sometimes phylogeny papers are sloppy, or wrong. So for something as major as Avian Dinosaurs, it would generally take more than just one sloppy paper to change consensus. Scientists now consider birds to be Dinosaurs. The public will continue thinking of Dinosaurs without birds. This is a difference between common names and scientific names. Birds are a subgroup of Dinosauria. Consensus depends on whether you are a scientist or not. Scientists now are at a consensus that Birds are derived from theropod dinosaurs, and therefore, ARE dinosaurs. The consensus of the public will lag behind.

Some other interesting phylogenies that render old names obsolete: Crustacea is paraphyletic. Crustaceans and Insects now form a group, Pancrustacea. Snakes are closely related to varanid lizards (are part of Lizards), so snakes ARE lizards, and both are in the group Squamata. Call them both squamates. There is no "Kingdom Protista", as protists are wildly polyphyletic.

The tree picture is only (mostly) accurate at the scale of at/above ~1million year separations and within plants or within animals+fungi, OR when considering an individual gene. Closely related species can interbreed (i.e. sapians + neanderthals), and if you try to put animals and plants into the same tree you run into endosymbiosis. Finally, bacteria swap genes so much the tree is significantly not-a-tree.


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Protein A-antibody SDS-PAGE
I wanted to know whether the boiling of Protein A- antibody complex for SDS-PAGE analysis will disrupt the interaction? and result in dissociation of protein A and antibody?
Thank you

Yes. Samples for SDS-PAGE are mixed with a loading buffer containing SDS (final concentration of SDS is usually 2%). Generally, the SDS will disrupt protein-protein interactions, even before boiling. Reducing agent (usually DTT or b-mercaptoethanol) is added to disrupt disulfide bonds.
See diagram here.
There are, however, exceptions. Some protein complexes/multimers are resistant to SDS until boiling, and some even maintain interactions after boiling. Some examples: Xia et al 2007, Kubista et al 2004, Grigorian et al 2009.


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Person-years and relevance to incidence of condition
If the annual incidence (age and sex-adjusted) of a particular condition x is 21.8 cases per 100,000 person-years and this data was determined in one geographic location, then is it correct to say in a city of 1 million people that we may see that same condition, in one year, in approximately 21.8 x 10 = 218 people? I'm just trying to provide some relevance to a group of students on how common some conditions may be. I understand that the exact incidence would vary along with demographic, geographic and environmental features.

I'm voting to close this question as off-topic because it appears to be about statistics rather than biology.

David is there any way to easily get this question into statsexchange?

I'm not a moderator so I can't transfer it for you. You could just  copy and paste it there and then delete it from here as it's your question and nobody has answered yet. (They don't like the same question posted on two SE lists.)


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Does intelligence depend more on environment than on genetic factors?
Many have argued that the test of IQ is simply a test of language. The application of the test consists of asking a number of questions. The person should understand the question presented to them and should be able to answer the questions properly. If a person does not understand the question or do not know to answer or give a wrong answer it results in a negative point.
is there a genetic component in this equation?

Which "equation" are you asking about? ‘When data across all studies are collapsed, genetic influences [on intelligence differences] account for around 50% of the variance’ (Petrill et al. 2004, taken from the Review Genetics of intelligence by Deary et al. 2006).


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Why do cats sleep in a curled up position?
I've noticed that cats will usually sleep curled up like ball, heads down and titled, with tails near their face. Is there any specific reason that cats would have a tendency to sleep this way?

Cats are not the only animal that does this.  Dogs do, as do most small mammals I've seen.  FTM, except for lacking a tail, so do I.  There are a lot of possible reasons: it conserves heat, protects one's belly from attack, is just more comfortable...

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Human femur maximum strength
In this video https://www.youtube.com/watch?v=os98s9kBlOI it is demonstrated that a moose leg bone can support until nearly 10 tonne before break. Is there any similar demonstration on human femurs? How much weight a human femur can support vertically before it is crushed?

that's not a whole bone just a section, there are similar test of other cortical bone. https://www.sciencedirect.com/science/article/pii/B9780128038024000111

It just uses a tiny cube (5mm x 5mm x 5mm) of cortical bone from a femur. Is there any tests that used whole human femurs?

I doubt it, there is not much scientific value to such an act and getting human bone for testing is not easy.

Do you think the midshaft section look stronger than it looks because of its structure (which is shorter with both ends flattened)? I think if it is a whole leg bone, it will break much faster.

That video isn't a scientific test, bone has aligned strength, putting a full femur with curves and rounded ends in a press with flat surfaces doesn't tell you anything useful. Bone is not subjected to force in that way in a living creature, that is why scientific test use small segments.

So that being said, a midshaft section with flattened ends look stronger (can support more load) than it seems because it is more stable compare to a whole leg bone. Isn't it?


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What happens when the conductance of a sodium channel increases?
My intuition is that, since the concentration of sodium within a cell is higher than the extracellular concentration, when conductance increases, this corresponds to the channel being open and means sodium will enter the cell. Is this correct? And what impact will this have on the membrane potential?

No, not quite. You are on the right lines, but incorrect in thinking that intracellular sodium concentration is higher.
At the resting phase of a neuron, there is less sodium inside the cell and more sodium outside the cell. An ATPase sodium potassium pump is constantly pumping 3 sodium ions outside the cell for every 2 potassium cells that enter the cell.
For voltage gated sodium channels to open, there must be a significant change in voltage, which can be triggered by the binding of neurotransmitter to receptors for example. This triggers the sodium channels open and sodium will flood into the cell due to a high concentration gradient (because there are more sodium outside than inside) but also due to an electrical gradient (the neuron is more negative on the inside; positive sodium ions will be attracted to the inside).
Because sodium is flooding into the cell, this will cause the membrane potential to become more positive (depolarised) and will eventually reach an action potential (30mV). After an action potential, the channels will become de-activated and shut. After a period of hyperpolarisation, the neuron will return to a resting state.
Source: https://en.wikipedia.org/wiki/Action_potential


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growth stages of Maize
I am reading about growth stages in Maize and found this image.

I downloaded a brochure of a maize variety grown in Brazil.

On the right column, it says male flowering 63 days after planting (947 degree days) and female flowering 63.5 days after planting (955 degree days).
When stage does the male and female flowering happens in the first image?

In the first image, flowering occurs in the stage labeled "Pollination", which is when the male releases pollen and the female accepts pollen.  It give the time as 56-63 days after emergence, but note the asterisk ("*"); the footnote for it says their given times vary by "growth class" (such as "early" or "late"), indicating that these numbers are just a guide and actual times will vary by the cultivar (breeding strain) selected.


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Could we breed a dog to the size of a thumb?
We've gotten from a wolf to a small breed such as a chihuahua. So the question is: can we go even further and have a dog as small as a thumb (adult dog)?
If not, what are the factors that limit the smallest size of a dog breed? Is it limitations in genetics, or some physiological reasons which would prevent such small dog to survive?

I'm not sure answers to this question would need to be opinion based, so I'm voting to reopen it....It asks for a biological explanation and not conjecture. Even if the answer is "we don't know", the question could still receive a valid, and informed response.

alternatively, I'm assuming you could rephrase your question to ask specifically what genes control dog size or perhaps a question that asks about a specific physiological limitation.

You may be interested in this essay.

How long do you have, and how many individuals?  The problem seems to be that very small dogs (and purebred dogs in general) tend to have lots of health problems, so it would take many generations of many individuals to weed those out.

Whales ans elephants come from small fish, so yes, deffo, itll take 200k years only.

As mentioned above the inbreeding required to select smaller and smaller dogs would be problematic because of the myriad of health problems that would be associated with it (see inbreeding depression).
The question about physiological limitations is interesting. The main reason biological organisms often don't scale is the fact that length, area, and volume don't scale in the same way. E.g. if something is twice as big L to 2L the surface area is L to L^2 and the volume is L to L^3 which means that many systems no longer work or require more energy (see Allometry) . For example in insects the distance for oxygen to diffuse to cells is short enough that simple diffusion is possible, in humans that is no longer the case so we have whole circulatory and respiratory systems to, in effect, help reduce the diffusion distance for oxygen.
I haven't used this kind of analysis in a while so am not very confident applying it here but I would suggest that some issues that could arise due to things scaling with length versus area or volume are:

required heart rate
maintaining body temperature - many small mammals deal with this by falling into periods of cold torpor (sort of like hibernation) where metabolic rate is suppressed
fragility of bones (as Cort Ammon mentions this is actually not a problem: https://jeb.biologists.org/content/207/9/1577)

I believe bones are actually more fragile on large creatures, thanks to the square cubed law.  However, maintaining body temperature is definitely a VERY hard challenge for a small creature.

Inbreeding will defeat the goal of breeding smaller animals because genetic diversity will decrease, which will, in turn, decrease the likelihood of further change. The goal would be to select for smaller size while maintaining genetic diversity.

Compare to the smallest mammals, like bumblebee bats and pygmy shrews.


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Homology modelling of protein with two identical subunits in its quaternary structure
I am using homology modelling to assign the 3D structure of Torpedo acetylcholine receptor (Unwin 2004, 2bg9 in RCSB) to human muscle nAChR. The problem is, both Torpedo receptor, and human receptor have subunit structure A-B-D-A-E: so a same subunit (A) occurs in the model twice. This seems to cause problems for homology modelling software, as it tends to align the second 'A' sequence over the first 'A' sequence, creating a hole in the pentamer, and not filling it up. Any ideas on how to make sure the modelling software acknowledges the quaternary structure? Below please find a link to a file generated using pdb.gz structure data from Unwin model + a set of corresponding FASTA sequences, and attached picture shows the problem (revealed when alignment is set as shown in the picture, by clicking on the same 'boxes' as in the image). Long story short, I need to get the A subunit to complete the alignment in a different spot than it is automatically placed in, as it occurs in the whole structure twice.
https://swissmodel.expasy.org/interactive/JJ5mQf/models/

I don't know a proper solution to this, but maybe you could try 'hack' it by changing  a few amino acids in one of the two A chains?

Thanks for response: was thinking about it, but as I am planning to use it for docking studies with cell-membrane permeating ligand (so can bind both inside and outside): the original Unwin model is quite shabby on its own, homology modelling isn't really optimal either, and docking is notoriously unreliable, so can't quite see how I could justify this 'hacking' (and thus adding another source of unreliability) in a paper. Furthermore, it seems like a type of problem with relatively simple solution: surely, someone must have thought of this before!

For anyone who will struggle with this problem in the future: The trick is in reading WHOLE of the manual, NOT submitting the whole sequence/badly segmented sequence, and in NOT attempting to input the same subunit twice. It is necessary to upload subunit FASTAs separately as a hetero target, and each subunit ONLY ONCE (so A,B,D,E for A-B-D-A-E receptor), and then search for templates: most probably there is a template with your quaternary structure uploaded somewhere already, and if not, you can choose preferred arrangement afterwards.


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Is hydroxyproline an amino acid? (Classification question)
So I know that hydroxyproline is created from proline via hydroxylation as a post-translational modification. I also know that proline is considered an amino acid. However, once you hydroxylize it, you have made a covalent modification to the original amino acid. Can hydroxyproline be correctly considered an amino acid? Or is it simply an amino acid derivative and NOT an amino acid?
Or, a more general question - how much can you change an amino acid and still call it an amino acid?

The other commenter answered correctly that proline is an imminoacid, not an amminoacid. But in biochemistry it is referred to as amminoacid since it basically works like every other amminoacid in any polypeptyde.

how much can you change an amino acid and still call it an amino acid?

Have a look at:

Selenocysteine
Ornitine

As you can see there are some weird modifications of amminoacids in biology. Just like proline/hydroxyproline any amminoacid can be very well modified and be used in proteinogenesis or non-proteinogenesis. Every modification of an amminoacid is allowed, and it will still be considered an amminoacid, even if it doesn't make up a protein. The only parts which can't be changed are the COO- and NH3+ groups, obviosuly, since they give the name of the molecule: "ammino" means that it has a NH group and "acid" means it has a COO- group.


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Examples of plant families that contain species that are safe for human consumption and species that are poisonous to humans?
I am trying to make a point to someone that just because two plants share a family and one plant is safe for human consumption, it does not follow that the other plant also is safe for human consumption. Can anyone provide an example I can use as proof?

Well, given that often enough a plant is considered "edible", while parts of THE SAME PLANT are already poisonous (see the potato), it stands to reason that the definition of "safe for human consumption" is far too lax of a term to even allow for a clear "no there aren't any". [Also there's a ton of counterexamples, like Byans below]

"family" in itself is such a borad term, that even a pure explanation to what a plant family is accidentallly provided an answer to your question:
https://www.maximumyield.com/definition/785/plant-family
[it's the nightshades again though, but this shows how valid your point is]

The most classic example if you want to win this argument would be the family Solanaceae.
Also referred to as the Nightshade family, it includes the deadly nightshade or Atropa belladonna and many other plants not safe to eat.
Other members of the family are tomatoes, peppers, potatoes, and more.
Plant families can be massively diverse, and toxicity doesn't really have much relationship to family. Most of the compounds that are found in plants that are toxic are found in other non-toxic plants as well: dose is crucial.

Potato is also an example of a plant that is considered non-toxic, but parts of the plant are toxic and - even worse - the tubers can become toxic.  The green parts (leaves, stems, etc) contain a poisonous alkaloid.   If a potato in storage starts to sprout, the sprouts and eyes are often toxic.   If the potato itself enlarges while sprouting, it will also typically have elevated toxicity.

@Peter: Another common example is rhubarb.  The stems are edible (at least when cooked), but the leaves are toxic due to concentrations of oxalic acid.

I believe that if the potato tuber is exposed to sunlight as the plant grows, it will also become green and poisonous, like the leaves.

Indeed, not just potatoes - tomatoes are toxic as well (leaves, unripe fruit...), and arguably, so are peppers (not "deadly" toxic, but the capsaicin is definitely another thing "designed" to make mammals avoid eating the fruit; it's not spicy to birds, who are the primary dispersers of pepper seeds) and eggplant (though that one has been pretty effectively domesticated to be safe as long as it's not raw). But it still definitely counts as "safe for human consumption" as long as you avoid the poisonous parts.

Mmmmm...fried green tomatoes! So cooking eliminates the toxicity of unripe tomato fruits, @Luaan?

@DennisWilliamson It doesn't seem to - even deep frying isn't enough to destroy the solanine (and tomatine, while also an alkaloid, doesn't seem to be dangerous to humans); you'd need 10-20 minutes at ~210 °C to decrease the content significantly. Most likely, there simply isn't enough of the toxin to do any significant damage (far less than in potatoes). All I could find is one death from tomato poisoning, from a tea made out of tomato leaves. You'd probably need to make a salad out of tomato leaves to be in significant danger.

The Apiaceae family has many edible plants including carrot, parsley, fennel, celery, and parsnip, and has toxic plants such as poison hemlock, fool's parsley, and giant hogweed.

Both the cashew and poison ivy are members of the Anacardiaceae family.

For what it's worth, part of the cashew plant is actually lethally toxic as well.

@AustinHemmelgarn which parts are toxic? Any sources?

The shell of the nut itself,, which is why they're almost always sold with the shells already removed..  Just like poison ivy, it has oils that cause contact dermatitis, and if ingested can cause potentially lethal internal reactions in the digestive tract.  Also like poison ivy,, the smoke from burning the shells is really dangerous because the oils don't completely combust.

The poison ivy, oak, and sumac all used to be in the genus Rhus alon gwith edible sumac used as a spice.

While all the other answers have described one plant family having both edible species as well as poisonous species, I am compiling all the families in one answer.

Anacardiaceae

Mangos (Mangifera indica) and Cashews (Anacardium occidentale) belong to Anacardiaceae, and also the poisonous Sumacs (Rhus spp.).

Apiaceae

Carrots (Daucus carrota), Parsnips (Pastinica sativa), Dill (Anethum graveolens) and the poisonous Poison Hemlock (Conium maculatum), and Water Hemlock (Cicuta spp.)

Apocynaceae

Milkweed (Asclepias spp.) and the poisonous Dogbane (Apocynum spp.) is commonly known as the poisonous relative of Milkweed.

Ranunculaceae

Marsh Marigold (Caltha palustrus) and the poisonous Buttercups (Ranunculus spp.)

Solanaceae

Food crops like Potatoes and Tomatoes and deadly poisons like Deadly Nightshade (Atropa belladonna), Jimson Weed (Datura spp.) etc.
References

https://survivalcache.com/5-poisonous-plant-families-the-survivalist-should-know/
http://www.botanyeveryday.com/online-classes/2013-plant-talk-8-poisonous-plant-families
http://mentalfloss.com/article/69254/8-edible-plants-potentially-deadly-doppelgangers

This would be better as a community answer.

See Prunus Dulcis: bitter almond vs. sweet almond – contains enough cyanide that "approximately 50 bitter almonds" will kill an adult and "5–10 bitter almonds may be fatal" for children.

Many common names are reused for different plants. This is true for "buttercup" which is also used for daffodils and pink evening primrose. Thanks for including the binomial.

Fungi are not plants and you've tagged this as botany, so this is perhaps off-topic, but I feel like it might help you make your point: the genus Amanita contains extremely toxic species (A. phalloides), highly regarded edible ones (A. caesarea) as well as psychoactive ones (A. muscaria).


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How can protein allergens be passed from mother to baby via breastmilk is proteins are broken down after ingestion?
All over the Internet new mothers are urged to avoid dairy products, a slew of vegetables and even beef if their child displays symptoms of reflux.
In the case of dairy, for instance, it is said that an allergic reaction can be caused by specific proteins that exist in cow's milk.
What I don't get is this: aren't ingested proteins broken up into their constituent amino acids, which are then recombined, presumably somewhere in the milk-producing glands, to create new proteins that are then passed on to the child through the mother's milk?
If that is the case, the original, allergy-inducing proteins should be long gone by then, right? If that is indeed the case, then what is causing the allergy and is there an allergy in the first place or could the cause be something else?

What means "all over the internet"? The usual unscientific websites which claim nonsense? Or are there credible scientific reports?

Well, I try to avoid obviously pseudo-scientific sources, but even the NHS has a web page that states that cow's milk in the mother's diet can "rarely" be passed on to the child through best milk.


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Protein Pathways, Superfamilie, Function database/website?
I'm going trough some old data - but I'm running into this problem that all website we used use is not existing anymore.
What I have is a very long list of proteins with accession number (refSeq from NCBI) and the organism that they are from.
So where do I go to for:
1) Finding information on which pathway they are involved in. It would be great to a visualization of the whole pathway as well.
2) There function.
3) Super-family


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Are there any particular chemicals that initiate either DNA replication or Transcription ?
When does the nucleus of a cell "know" when to bind DNA nucleotides ( for Replication ) or RNA nucleotides ( for Transcription ). From what i read, they're both structurally different and free nucleotides of both are present in the nucleoplasm. So when one's free nucleotides bind ( mRNA nucleotides for transcription for example ) why doesn't the other ( DNA nucleotides in this case )bind, or what keeps the other from doing so?
Are their any chemical prerequisites of some sort that initiate the processes?
TIA

Your question is too broad for this list, where question sof this sort assume some basic familiarity with the topics asked. You need to read about replication and transcription in some introductory book of biochemistry. Berg et al. on NCBI Bookshelf has well written chapters on these topics.

Enzymes, nature’s catalysts, proteins that speed up chemical reactions.  In this case, creating a linear polymer out of deoxribonucleotide monomers, to yield a polynucleotide (DNA).  This reaction also requires a DNA template strand.  Enzymes contain an active site that brings all of the substrates into alignment, and then key amino acid side chain residues that are located in the active site enhance the intended organic chemical reaction, often by stabilizing a transition state in one or more of the substrates.
You are correct that ribonucleotides and deoxyribonucleotides share many structural similarities, but enzyme active sites can indeed distinguish between the two molecules.  Even if the wrong substrate diffuses into the active site it will usually not be able to participate in the reaction.

Oh ok so basically, its the Polymerase enzymes that sort of "filter" out the right nucleotide additions form the wrong ones and the nucleotides connect to the strand all in their due time?


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Are these two same insects?
 These guys are infesting my place. I searched through this site and came to know that they are cloth moths. All these days I used to see the left one type in the image. Recently I started to get the ones looking like the right ones.
As you can see the the right ones have a black border like thing at the end of the casing which the other kind does not have. Also , it looks like it has a different kind of structure from the left one, no ? I don't know..
So, are they the same ones or different kinds ?


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How much shorter is the short arm of a chromosome? And why?
I keep reading that the p arm is shorter than the q arm. But I cannot find an explanation of how much shorter nor an explanation for the difference.

Which chromosome in which species?

Let's say homo sapiens, any chromosomes.

@Remi.b has answered your question. The point to my comment was that "p" just means short, and "q" just means long. Just like you can't say how much shorter a short person is than a tall person, you can't say how much shorter a p arm is than a q arm. It depends on the chromosome (person).

I guess I'm looking for some data on distribution of size differences between the 2 arms. Is the average difference 1%? .00001%? et cetera.

It varies from chromosome to chromosome and from species to species. In some cases, both arms are roughly the same length. In some cases, one arm is so short that it is almost inexistant. For chromosomes with equal length arms, of course the terms p and q do not apply.

p and q are used to describe the relative size of the arms of a chromosome. According to this wikipedia article p stands for petite (french for small) and q is just the next letter in the alphabet.
So p is just defined as the smallest arm in any chromosome. How much smaller is not relevant for this definition. The names are just jargon which make it easy to refer to an arm.


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From what kind of insect might these eggs be
Does anybody know what kind of insect might have laid these eggs:
The photo was taken a few days ago in Limburg, Belgium near a pasture with some goats.

Those are likely moth eggs... moths have a tendency to attach their eggs on metal screens that you might have in your windows or doors.
Here is a video of a moth laying eggs on glass:
https://www.youtube.com/watch?v=L2zf1J8CZdg
Here is a video of a moth laying eggs on a metal screen:
https://www.youtube.com/watch?v=qKHReVNAMYw
Here are photos of eggs on a wire fence, believed to be moth eggs:
https://www.whatsthatbug.com/2013/09/19/possibly-moth-eggs-deer-fence/
And another example of moth eggs on a metal wire:
https://hardtocomebylifestyle.wordpress.com/2014/08/31/moth-eggs/


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How does the brain fake itself into hearing our own sounds even when we are not speaking?
Typically When we are talking to our own selves at any time in the day,the Brain thinks that it's me who's speaking , how does it create illusion of speaking ?

Two points.  First, does it really create the illusion of speech, or is it just processing language?  E.g. my mental "voice" doesn't sound at all like my actual speaking voice, even if it could be said to have a sound.  Second, why limit it to speech?  I can internally "listen" to music, either works I'm familiar with, or things I make up.  (Indeed, sometimes it's hard to get the music out of my head - see "earworm" :-))

That's true :) it isn't just limited to my own voice you're right !

Our brains treat 'talking to ourselves' very similarly to talking to others. There's a small amount of evidence in studies to suggest that when we talk to ourselves, it's like verbalising the speech out loud.
Before you speak out loud, the part of your brain responsible for creating speech copies that information, and moves it the appropriate verbalising areas of the brain. However, at the same time in a process called efference-copy, it also copies it to the area of the brain responsible for listening to sounds. This process overall means that our brains can distinguish sounds that come from ourselves, and sounds that come from other people.
This also partially goes to explain why people with schizophrenia have difficulty recognising their own internal voices as 'own'. It's likely that this process has gone awry in these people, meaning they're not able to recognise their internal voice as themselves.
Here's a link to some research done in Sydney on this matter.


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Why are there inverted repeats in response elements?
The following picture shows an inverted repeat sequence in a response element. Response element sequences for glucocorticoids, estrogen, and thyroid hormone show that they all contain inverse repeats. Why do these inverted repeats exist in so many response sequences? In other words, what advantage do they pose to the function of the response element?

Starting with prokaryotic (i.e., bacterial) transcription factors--which were the first to be characterized in depth, this type of pattern was noted.  Even for the "classic" Type II Restriction Endonucleases used for molecular cloning have palindromic recognition sequences.  In all three cases the answer is that the sequence-specific DNA binding protein binds as a dimer, and so each monomer is recognizing a "half-site" (one of the inverted sequences).

Thanks for your answer. We do encourage links to external sources to support assertions in answers. That way the poster or interested readers can check whether or not they are correct, and learn more about a topic than may be appropriate to include in an answer. You can edit your answer at any time.

@RosieF In that case, is it essential that the repeated sequences be inverted? Wouldn't the DNA binding proteins still be able to bind as a dimer if it were just a sequence repeated without inversion?

I think the most important concept here is that by having multiple binding sites concentrated in small region then this will effectively increase the concentration of the transcription factor.  The more sites, the more specificity, and therefore more biological regulation is possible (e.g., ON vs. OFF).  The location of the dimerization interface on the monomer will change if the recognition sites were direct repeats instead of inverted repeats.  There are probably (?) examples of both.  Certainly the first ones characterized were inverted.


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Why doesn't it feel suffocating when taking a shower?
When one walks into a bathroom where someone is (or just finished) taking a shower it is hard to breathe, because it's filled with steam, yet the person taking a shower can breathe just fine despite being in the area with even more steam.
Why is that?

Can you support that this is a general perception? I've never felt suffocated when entering a steam-filled shower.

@fileunderwater: Nor have I, in an actual steam room.  Seems like an individual idiosyncrasy.

Most likely a matter of relative perception.
For example, if you start with empty hands and pick up a 20 pound weight, you will perceive it as heavier than if you start with a 10 pound weight and then pick up a 20 pound weight.
Likewise, whoever's in the shower had plenty of time to get accustomed to gradually increasing steam, while you walked in and got the full blast immediately.


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Does the deletion of Chromosome 20 cause immunity against prion disease?
I was reading recently about prion disease and it caught my attention that a normal prion protein is coded n chromosome 20, therefore, in order for an infectious prion protein to attack, there must be already normal unsedimented prion proteins, does that mean the deletion of chromosome 20 in meiosis lead to immunity against prion disease, since the protein is not coded, that is if the human survives without chromosome 20

"That is if the human survives without chromosome 20". I suggest you consider the likelihood of that being true or do some investigation to discover how many other genes are encoded on chromosome 20. You may then wish to delete your question.

I read an article that says chromosome 20 deletion occurs so I am quite unsure, I mean why would I ask in the first place

It seems very unlikely to me that a person can survice without chromosome 20. Please cite the article that leads you to think it possible.

Welcome to SE Biology phenolicdeath. Including a link to the article will help other users to answer your question. It sounds interesting.

I see one report of a viable autosomal monosomy,
(https://www.nejm.org/doi/full/10.1056/NEJM196710122771502)
but in general, they are not survivable.
https://www.ncbi.nlm.nih.gov/pubmed/4086989
https://www.biology.iupui.edu/biocourses/N100/2k2humancsomaldisorders.html
https://www.ncbi.nlm.nih.gov/pubmed/29164644
A better question would be if person with a deletion or natural knockout of that gene are susceptible to that prion disease.  Those subjects likely exist in larger numbers, though it's likely that few have been exposed to any particular prion disease.


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Do biologists believe in the existence of an intelligent creator who designed the architecture of life ?
I am referring to the biologists who does not support the theory of evolution or Darwinism .

Are you asking for the specific biologist or a general statement about biologist? because there are about as many biologists  who don't agree with evolution as there is medical doctors who don't agree with germ theory. which is to say a statistically insignificant number who are unable to scientifically defend their position. Basically there are ones who disagree because they are deeply religious but none that are religious becasue they disagree.

I'm voting to close this question as off-topic because this is not a question about biology but about the religious beliefs of biologists.

As the question is phrased, there are almost none.
A 2009 Pew survey concluded that

95% of Americans believe in some form of deity or higher power ... just over half of scientists (51%) believe in some form of deity or higher power; specifically, 33% of scientists say they believe in God, while 18% believe in a universal spirit or higher power.

That's American scientists in general; "biologists and medical" more specifically are in the same range. Americans in general tend to be far more religious than many other nationalities (95% of Americans vs. less than 50% of British, 60% of Germans, 65% of Canadians) and it's likely that scientists from other countries are proportionately less likely to believe in a God. I don't have numbers for those but let's say 60% of the American number, or roughly 20%.
So there is a significant minority of scientists who are religious, but probably 70-80% of biologists worldwide do not believe in God.
Does that mean that 20-30% of biologists reject evolution based on their religious beliefs? Not at all. The idea that evolution conflicts with religious beliefs is a very niche view, mainly held by small (but very noisy) American religious groups. For example, the Pope has stated that there is no conflict between Catholicism and evolution. Francis Collins, the director of the NIH, is famously religious and also argues that there is no conflict between religion and evolution.
So there's no reason to believe that religious scientists should reject evolution, and in fact they don't. Surveys show that around 97% of scientists understand that evolution is real. That survey says that "87% say evolution is due to natural processes, such as natural selection", which leaves 13% as open to the idea that it's guided. That survey doesn't break down different fields, but other surveys and general experience says that few of the 13% are biologists.
The number of biologists who reject evolution based on their religion is tiny.
As a side note, please be aware that "Darwinism" is not a real thing; it's made-up phrase used by people who know little or nothing about biology, who are unaware that Darwin's arguments have been irrelevant to our understand of of modern evolution for close to 100 years, and that modern evolutionary theory has many branches that supplant and extend classical natural selection.

But the question is so clearly off-topic that you are doing a disservice to the list by feeding this troll.

@user1136 IMO, the question is completely and obviously off-topic. Asking about the sociology of religious believes has nothing to do with biology even when the population of interest is "biologists". This question is as off-topic as it gets!


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Chance of cancer as a function of smoking frequency
I was wondering if there is some kind of known relation between the chance of getting cancer and the frequency of smoking cigarettes. A quick Google search did not yield results. Would any of you perchance know of a relation?

There is an approximately linear relationship between the total number of cigarettes a person smokes in their lifetime and the risk of getting lung cancer.
That is, each cigarette someone smokes increases their chance of getting cancer by about the same amount, whether it's their first cigarette or they've been smoking for 40 years.
Pack-years are a way of quantifying someone's total cigarette exposure; it's calculated by the number of packs someone smokes per day times the number of years they've smoked for. So someone who has smoked half a pack per day for 20 years would have a pack-year history of 0.5 * 20 = 10 pack-years.
The following graphs show the linear relationship between the odds of getting lung cancer (relative to non-smokers) versus pack-years smoked.

Source: Lubin and Caporaso (2006), "Cigarette Smoking and Lung Cancer: Modeling Total Exposure and Intensity"


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Does every protein encoding gene necessarily have a transcription factor?
For instance, transcription factor gene A is responsible for activating gene B that encodes protein 1.
However, it is possible for genes like gene B to encode proteins without having transcription factors to activate them?
(Otherwise said, can protein encoding genes have no transcription factors)?


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How to identify whether something is in linkage disequilibrium?

If the following loci indicated the presence of an SNP in flu strains, is Locus 2 and Locus 3, which are located 10 bp apart in linkage disequilibrium?
"When alleles and molecular
markers are associated with each other at a frequency that
is significantly higher than expected by random chance, they
are said to exhibit linkage disequilibrium" Brooker's Genetics
Both loci seem to be linked, but how do I determine if it is significant enough to be considered in disequilibrium or not.

As per the definition you gave, you check whether there is a statistical association between the two. If knowing when allele is present at a locus does not affect the probability of finding a given allele at the other locus, then they are independent (there is no association). Otherwise, there is an association and hence the two loci are in linkage disequilirium.
See wikipedia > Linakge disequilibrium for more info.


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What are the advantages of iTRAQ/TMT technology over electrophoresis?
I'm currently working on the paper regarding proteomics research. I've listed a lot of questions that freshmen may have during their study. Can anyone explain (based on your experience in the lab) the advantages and disadvantages of iTRAQ/TMT technology and electrophoresis? Which technique is better?

I believe this paper can answer your question: Q&As About Proteomics (Q1-Q5). It says that 2-DGE is a protein separation technology developed along with MALDI-TOF technology. In theory, the total protein can be separated one by one with the difference of isoelectric point (IEF) and molecular weight (SDS-PAGE). The actual situation is not that ideal, because the low-abundance protein cannot be successfully stained and seen, and the protein is deviated from the theoretical position after post-translational modification. A 2-DGE can identify a total of 1000–2000 proteins. Compared to electrophoresis-based techniques such as 2-DE and DIGE, iTRAQ/TMT has a high resolution. MtoZ Biolabs found 6,000 proteins at most in the cell samples it has treated, most of which have quantitative and qualitative information. Moreover, its iTRAQ has high flux and can complete up to 8 samples at a time. If TMT technology is used, it can complete up to 10 samples at a time, which is especially suitable for simultaneous comparison between multiple samples and dynamic detection of biological processes.


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Akt phosphorylation at Thr308 and Ser473
I am studying Akt signaling pathway. I know that phosphorylation at both T308 and S473 is prerequisite for full activation of Akt but wonder if phosphorylation/de-phosphorylation of one of them is prerequisite for another. In other words,

wonder if phosphorylation at T308 is required for phosphorylation at S473 or vice versa, or they are phosphorylated independently.
wonder if de-phosphorylation at T308 is required for de-phosphorylation at S473 or vice versa, or they are de-phosphorylated independently (wonder if there is any order of de-phosphorylation by phosphatases such as PP2A between the two sites)

If there is such order, can anyone suggests me some references?


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Why do humpback whales sing songs?
Scientists have documented that it seems to only be male humpback whales who sing structured songs, but do we know what purpose their songs play?

The only way to know in great detail is to translate what they say. Though if they speak in monogrammar, that is only possible if you know a monogrammar language.

There are four hypotheses with varying levels of supporting evidence for why humpback whales sing.
Yes, only males have been shown to sing. It used to be thought that the songs only occurred on breeding grounds and therefore served a reproductive purpose. However, songs have since been recorded on migration routes and feeding grounds, though not as prolifically.
The hypotheses are:

"Mate Attraction" whereby males sing and females approach them to mate. No evidence has ever shown a female humpback whale approach a singing male. Rather, a group of males will swim after a female, vying for position, until she is receptive to mating. Then the closest whale (the primary escort) will be best poised for success. In my opinion, this is the least plausible hypothesis.
"Lekking" whereby a group of males sing to stimulate the females to begin estrus and advertise their body size and health for female mate choice. https://en.wikipedia.org/wiki/Lek_mating This may allow for female selection of choosing a mate later while being pursued as part of competitive group. I am unaware of which articles support this hypothesis and provide evidence. Birds and land mammals are much easier to observe in a lekking behavior than any underwater animal is.
"Territory establishment" whereby males sing to mark their territorial bubble of water. If a male has a larger territory, then it is more likely a female will pass through that larger territory so that the male can respond by pursing her. This could be supported by proving that male humpback whales respect each other's territories and space themselves consistently across their watery world. Refer to http://dx.doi.org/10.1121/1.4962217
"Orientation by echolocation" has recently been put forward by Edward Mercado that song reflects on a broad scale around the whale's environment to provide feedback for navigating the general area. Many researchers argue the plausibility of such low frequencies echoing effectively.

New studies into cultural transmission of parts of songs across ocean basins may suggest the song is not just for reproduction but to fulfill wider communication needs or generate a form of social creativity. See work by Ellen Garland.


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What anatomical structures do baleen whales use to vocalize?
What anatomical structures do baleen whales use to vocalize? How does this differ between species?

Look at there they don't give a definitive answer but it's already something https://en.wikipedia.org/wiki/Whale_vocalization (Baleen whales are called Mysticete whales)

They use larynx and folds in the larynx for underwater vocalizations. Source and details: https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/baleen-whale

Discovery of Sound in the Sea (dosits.org) provides good general information on these topics.
According to DOSITs,
Marine mammals produce vocalizations using mechanisms similar those of land mammals. Pinnipeds (seals and sea lions) have a larynx similar to that of humans. Baleen whales also use a larynx to produce sounds. Toothed whales can produce sounds using their larynx as well as specialized air sacs near their blowhole. The larynx is used to produce whistles, while the air sacs are used to produce high frequency echolocation signals.
See https://dosits.org/animals/sound-production/how-do-marine-mammals-produce-sounds/ for more information and additional citations

The DOSITs website is a great resource with many links to scientific studies, but I believe they made an error in their description of toothed whale sound production. Toothed whales produce both echolocation clicks and communication whistles using the phonic lips in their nasal passages.

Not much is known about the exact method of sound production in baleen whales and current knowledge is mostly based on dissections of dead animals.
Reidenberg and Laitman (2007) examined 6 baleen whale species (37 animals in total) and they identified a structure in the larynx, which they called the "U-fold"1. This U-fold is supported by cartilages and the shape and tension seem to be controlled by skeletal muscles, which might then control the sounds produced. Based on various features, Reidenberg and Laitman suggest that the U-fold is homolog to the laryngeal folds in other mammals. A key difference between the U-fold of baleen whales and the vocal folds of terrestrial mammals is that air flows in parallel with the U-fold, whereas airflow across the vocal folds is perpendicular in terrestrial mammals. Baleen whales also have a laryngeal air sac, which is homolog to the laryngeal ventricles of terrestrial mammals, which captures air as it is used during vocalisations, and allow air to be recycled back to the lungs in-between vocalisations1,2.
To my knowledge, there is no evidence that toothed whales produce any sound in the larynx. Toothed whales produce both echolocation clicks and so-called “whistles” by creating an airflow across phonic lips in their nasal passages, and the resulting tissue vibrations produce the sound, which is then guided into the water via a fatty organ called the melon3. Toothed whales have a pair of phonic lips in each nasal passage, and it seems that echolocation clicks are produced using the phonic lips in the right nasal passage and communication whistles are produced with the phonic lips in the left nasal passage4,5.
References:

Reidenberg, J. S., & Laitman, J. T. (2007). Discovery of a low frequency sound source in Mysticeti (baleen whales): anatomical establishment of a vocal fold homolog. The Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology: Advances in Integrative Anatomy and Evolutionary Biology, 290(6), 745-759. DOI: 10.1002/ar.20544.
Reidenberg, J. S., & Laitman, J. T. (2018). Anatomy of underwater sound production with a focus on ultrasonic vocalization in toothed whales including dolphins and porpoises. In Handbook of behavioral neuroscience (Vol. 25, pp. 509-519). Elsevier. DOI: 10.1016/B978-0-12-809600-0.00047-0.
Madsen, P. T., Jensen, F. H., Carder, D., & Ridgway, S. (2012). Dolphin whistles: a functional misnomer revealed by heliox breathing. Biology letters, 8(2), 211-213. DOI: 10.1098/rsbl.2011.0701.
Madsen, P. T., Wisniewska, D., & Beedholm, K. (2010). Single source sound production and dynamic beam formation in echolocating harbour porpoises (Phocoena phocoena). Journal of Experimental Biology, 213(18), 3105-3110. DOI: 10.1242/jeb.044420.
Madsen, P. T., Lammers, M., Wisniewska, D., & Beedholm, K. (2013). Nasal sound production in echolocating delphinids (Tursiops truncatus and Pseudorca crassidens) is dynamic, but unilateral: clicking on the right side and whistling on the left side. Journal of experimental biology, 216(21), 4091-4102. DOI: 10.1242/jeb.091306.


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Do animals like Seals feel cold on their skin?
Whenever there is a documentary about animals and you get to the colder regions, you will hear about Seals and their layer of blubber keeping them warm.
But the skin is on top of the blubber, in direct contact with the cold water (and air). Do they feel the cold outside the way a human would?

We don't really sense temperature on our skin, we sense heat exchange (see Do humans perceive temperature or heat-flux?. It is for this reason that a 10˚C piece of wooden spatula feels very different than a 10˚C copper pan.

Humans (and other animals) do not feel temperature; when we “feel cold” we actually sense that our body starts to lose heat (we feel the heat transfer). Pinnipeds, notably phocid seals (True seals or earless seals), restrict heat transfer to the environment by reducing skin temperature. To do so, phocids have a thick layer of subcutaneous blubber (or hypodermal adipose tissue) with a low thermal conductivity, which significantly reduces heat transfer via conduction (insulating the skin surface from the body core). On contrary, flippers are the areas of the body with little blubber. Interestingly, in phocids, flipper skin tends to be the least emissive region during cold weather (Kharmas et al. 2012), which could be explained by the presence of counter-current heat exchangers (found in the flippers of pinnipeds). Counter-current heat exchangers (another thermoregulatory strategy) are present in peripheral body parts and help retain heat in the core body by rewarming cold venous blood returning from the periphery as it passes in proximity to outgoing, warm arterial blood. To summary, phocids limit heat transfer with a blubber layer and control heat transfer by using blood flow (see Favilla and Costa, 2020 for a review about Thermoregulatory adaptations in marine mammals).

This doesn't really answer the question. I know heat transfer is limited, but the skin on the outside of the animal is in direct contact with the cold. As far as my knowledge goes at least. Does the heat retained inside the animal warm it enough to not feel the cold from the outside?

FYI: Phocid seals have short hair. Their skin has nerve cells sensitive to temperature (similar to other mammals), so yes they might have the ability to sense temperature. About your question can they "feel the cold", do you mean like experimenting discomfort? It's a difficult question. Those animals are adapted for cold climates.


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Can an importin without any cargo pass through the NPC?
Can an importin (nuclear import receptor) without any cargo pass through the Nuclear Pore Complex (NPC)? If it can, wouldn't it be a waste of energy to have the 'unloaded' importin enter the nucleus and then binding to GTP?


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Skin Colour in "Northern" Regions of The earth
Question: Netflix has recently produced a two-part miniseries, The Evolution of US, that examines the evolution of "man". The topic of of human skin colour was covered and it was stated that 'lighter skin pigmentation was a preferred natural selection for early humans living in the "northern" regions'. The idea being that lighter skin could "absorb" sun-rays; which apparently is necessary for activating vitamin-D. Is this a true statement ? And where might I find good sources of literature to read on this topic ?

Now this particular series does not define "northern" and to be fair neither was the term "lighter skin" . My motivation in asking the question is driven by my own travels in far eastern Russia, Mongolia, Alaska, and parts of Peru and Ecuador. In each of those locations I observed numerous groups of indigenous people with dark brown skin and pitch black straight hair; which seems to contradict the statement in the series.

No "apparently" about sunlight being needed for the formation of Vitamin D. See e.g. [this article]. As regards how much sunlight (UV-B) penetrates the skins of people of different ethnic groups, that I don't know.

@David ; which article are you referring to? Are you sure the link you provided is correct ?

I do apologize — somehow the link never got pasted. Here is is: a review in less-specialized language available from NCBI entitled Vitamin D: The Sunshine Vitamin.

Rather large nitpick here: Equador and Peru are not "northern" (or more accurately, polewards) regions.  In fact (as you might have guessed from the name :-)) the equator passes right through Equador.  As for the indigenous populations of northern Asia & North America, you might ask whether they've lived there long enough to diverge from their ancestral populations.  Evolution takes time.  I might also wonder if the people you saw spent a lot of time outdoors.  Despite a mostly northern European ancestry, I get pretty brown in the summer :-)

Melanin reduces the skin's ability to make Vit D due to reduced UV penetration. This is a disadvantage in northern areas where people get less sun light, and also need to wear heavy cloths to keep warm which adds to the problem. People in Sunny regions have the opposite need as there is more than enough UV light exposure, but they run the risk of developing skin cancer, which is why having melanin provides an evolutionary advantage in these regions.
Interestingly, in the Arabian Gulf region, there is currently an epidemic of Vit D deficiency especially among those with dark skin. Although there is plenty of sun light, people tend to avoid the harsh sun almost completely by commuting strictly in cars and avoiding walking outdoors during the day. Car windows (and glass in general) are opaque to UV rays, therefor reducing the skin's ability to produce Vit D, and forcing many locals who adopt such lifestyle to take oral Vit D supplements.
Here is a link with some references to confirm the medical link between Vit D deficiency and lack of sunlight exposure:
https://www.webmd.com/food-recipes/qa/how-can-dark-skin-lead-to-vitamin-d-deficiency

as a follow up question how might we exlain my observation - the existence of various groups of people living near the arctic regions or at high altitudes and whom have demostrably dark skin colours.

I do not know the specific answer in relation to each of these different groups of people. However I know that in relation to Eskimos, they get their Vit D through diet rather than skin production. Their diet of whale, seal, trout and walrus blubber are all rich in Vit D. I expect you will find the other groups you mentioned have a similar affinity to Vit D rich diets.


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Why are vaccines containing attenuated microorganisms preferable to those containing dead microorganisms instead?
My teacher said it more closely resembles a real infection but I didn't get that.

could you define 'preferable' for your question. There are pros and cons to both, which is why both exist...

It's not necessarily true that attenuated vaccines are "preferable" to killed vaccines. It's a case by case basis. In some cases one or the other simply isn't possible or practical. It may not be possible to make a vaccine that's attenuated enough, for example. Or a killed vaccine may not be effective.
Here are some pros and cons of attenuated vaccines:

more likely to follow the natural path of infection, so there might be more immunity at the specific site of infection. For example, attenuated vaccines against gut pathogens might drive gut-specific immunity.
Might replicate in the host so that the actual amount of antigen seen by the host is greater than the amount delivered -- so you can deliver a much smaller dose to get similar immunity
Might cause more inflammation. Inflammation can drive a much stronger immune response because the body "thinks" it's being attacked by a dangerous pathogen

Cons:

Might cause more inflammation. Inflammation can cause tissue damage or local pain
May be less safe. Replicating in the host may give the opportunity to mutate and become more dangerous
May be more fragile. A killed vaccine could be relatively temperature stable, while an attenuated vaccine might need to be kept in a very narrow temperature range so it doesn't die and become ineffective. That might make it difficult to use in, say, developing countries

There are many more points that could be made but the overall picture is that attenuated vaccines might be more effective but more dangerous. Attenuated vaccines that are used today have been shown to be safe as well as effective, and killed vaccines that are in use have been shown to be effective as well as safe, so these are concerns during development of new vaccines, not in use of present ones.


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Are ligand gated channels saturable?
A major difference between simple diffusion and facilitated diffusion is that facilitated diffusion has a maximum transport and velocity; the rate of diffusion is limited, whereas in simple diffusion, it isn't.
Ligand Gated channels (like any protein 'channel') transports molecules through simple diffusion, so they should not be saturable, but how does that make sense ? The channels open by the binding of a specific ligand/molecule, can't they be saturated by this ligand just like carrier proteins are saturated by the substance/molecule which will pass through ?
If they were in fact saturable, how are they considered to be part of simple diffusion?

Yes, they are saturable, because they have a finite number of 'binding sites', depending on the particular example you are looking at. Then, once they join the substrate to be transported, they need to release it at the other side of the membrane, which takes time (in very short time scales, but time nevertheless). Therefore, the saturation rate and speed of transport depends on the number of transporters on the cell's surface, the gradient differential, and the number of binding sites.
Facilitated diffusion, which needs a transporter as you point out, is a form of passive diffusion, which implies that there is no energy cost to the cell to transport the solute (as opposed to active transport). This is the key difference: energy. It does not mean that it goes as fast as osmosis or any other type of passive diffusion/transport, because, the transport that goes across the membrane (small gas molecules, and other small molecules) will clearly be faster. Also, passive diffusion does not mean that there is no upper limit to diffusion, in fact, diffusion is always limited by the concentration difference of the diffusive molecule across the membrane, no matter if this is passive or active transport.
In short, it is simple/passive diffusion because it does not need energy. Whether is saturable or not is not what matters for this classification. In fact, all diffusion has a limit.

Oh, I was thrown off by the figure in my physiology textbook (Guyton). here's a link to the image :https://imgur.com/a/TMGX9F6 Did I interpret it incorrectly ?


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Is there any case in which excitability increases with lowering the RMP?
My professor says , at a more negative RMP, less sodium ion channels are inactivated, so if you take 2 of the exact same neuron with the same threshold potentials, and try to excite them starting from different membrane potentials, the one you try to excite from a more negative membrane potential excites faster and fires an action potential faster because more sodium ion channels are activated .
I might have missed something from what he said, and I hope I did because this makes no sense to me.
Shouldn't excitability increase with an increasing positive resting membrane potential ? The closer I am to the threshold potential the weaker the stimulus that I need to fire an action potential, isn't that right ?
The only article I found on this is https://www.sciencedirect.com/topics/neuroscience/excitability and its specific to cardiac muscle so perhaps the excitability in cardiac muscle  is an exception ?

A typical voltage-gated sodium channel has 3 gating states: open, closed, and inactivated. The third category is the important one here.
Open channels are open: they let ions through.
Closed channels are closed: they don't let ions through, however, they are available to open and their probability of opening increases as the membrane voltage rises from negative towards positive.
Inactivated channels don't pass ions, but it also cannot be opened by depolarized voltage. Instead, it needs a negative membrane voltage to pass back to the Closed state.
When a sodium channel opens, it only stays that way briefly before going to an inactivated state. Recovery from inactivated back to "closed but openable" requires the
If you depolarize a cell gradually, this will open sodium channels, but it will also increase the number of channels stuck in this "inactivated" state. That means there are fewer channels available to flip from closed to open.
When a cell is hyperpolarized, there are fewer channels stuck in the inactivated state, and so the threshold potential can actually become more negative: it takes a smaller voltage step to open enough channels to trigger an action potential, because there are more channels available to open. You can describe this situation as being "more excitable" despite the hyperpolarized potential.
Some cells, including cardiac cells and other types of pacemaker neurons, will actually depolarize spontaneously from this hyperpolarized potential and reach threshold all on their own without external input.

Oh, I understand but, when does 'a more positive RMP makes the neuron easier to excite' argument apply ?

@LiaAhmed When it is transient. It takes awhile for the population of voltage gated channels to equilibrate; brief depolarization gets you closer to threshold without substantial inactivation. Note that different neurons have different populations of voltage gated sodium channels so they may show different properties.


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Are the alleles that code for the same phenotype all the same exact sequence?
The idea that you can be homozygous for a gene means that there are limited options or alleles , correct ?
My question is, if the mom has the allele b which codes for a blue eye, and the dad has an allele which codes for a blue eye too, are these alleles the exact same ? Do they have the same nucleotide sequence ?
This is probably a basic question but no matter how I phrase it, I can't seem to get an answer off of google.

Most educational texts ignore the nucleotide variations and only look at the gross effect of the gene, and the gene interactions. Like @Cell says, they only care if the gene works or  not. They dont care about the millions of variations that may cause the gene to not work.

No the same phenotypes do not mean the same sequence. For example some phenotypes are associated with alleles that are caused by non-functional gene products (like proteins). But there many ways to alter a gene to produce a non-functional protein.


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How can DNA replication result in hair pin structures?
My professor said that one of the reasons SSB proteins are so important was to prevent the formation of hair pin structures, I can't see how or why DNA would form hairpin structures and there's not much about it on the internet so can anybody explain this hair pin thing and how SSB proteins prevent it from happening ?

DNA Hairpins are formed when two regions in same single stranded DNA are complementary in nucleotide sequence but in the opposite directions (as represented in image below). These two sets of nucleotide sequences base-pair with each other by forming hydrogen bonds between adenine-thymine and guanine-cytosine respectively to form hairpin loop. Same structures can be seen in case of RNA.

(Figure via: https://brilliant.org/problems/dna-zipper/)
Single stranded binding (SSB) proteins bind to single DNA nucleotide sequences and prevent the breakdown of newly synthesized DNA because of nucleases and it also removes the secondary structure of the DNA  strands like hairpin loops so that other enzymes can bind to DNA strand and operate properly. As represented in figure below SSB bind to ssDNA through electrostatic interactions and prevent the bond formation within the nucleotides of single DNA strand, thus preventing formation of hairpin loops in DNA.

(Figure via: http://helicase.pbworks.com/w/page/17605582/Amanda-Kinney)
(via: https://proteopedia.org/wiki/index.php/Single_stranded_binding_protein)

If you have a stretch of single-stranded DNA that is palindromic, that palindromic region can form hydrogen bonds to itself, forming a hairpin. SSB proteins bound to and travelling along ssDNA physically get in the way of and undo hairpin folding.


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How does the cardiac cycle and electrical activity all relate to blood pressure in the heart?
I know how the cardiac cycle works and understand the electrical activity in the heart such as the AV nodes, SA nodes and Bundles, but how do they work together in relation to blood pressure?

Blood pressure is determined by cardiac output and the total peripheral resistance, where, from Ohm's Law (Q= P/R):
Mean Arterial Pressure (MAP)= Blood flow (Q) x Total Peripheral Resistance (R)
The cardiac cycle and heart activity will essentially control the cardiac output through the FORCE and the FREQUENCY of contraction.
Cardiac output is determined by the stroke volume, and the heart rate:
CO= Stroke volume x HR
Changes in HR is linked to changes to the SAN and is controlled by sympathetic and parasympathetic inputs. An increase in HR, will cause cardiac output to increase, causing an increasing in blood pressure (simply put, other physiological changes can also influence blood pressure, such as vasoconstriction and vasodilation).
With regards to the AVN, SAN and bundles of His, this allows electrical conductance which causes the contraction of the heart. The contraction of the heart leads to blood being ejected (i.e. blood flow, which is linked to cardia output). This, together with the peripheral resistance of blood vessels will be linked to blood pressure.