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ATP to disassembly of nucleotide ratio
DNA Helicase, the enzyme that is responsible for tearing apart the strands before DNA replication, requires ATP to rip apart nucleotides. I have asked this question to several professors and they couldn't give me a clear answer. My question: What is the ATP:nucleotide bond breakage ratio? In other words, how many nucleotide  bonds can be broken from a single ATP through helicase.

This paper should interest you, though it likely varies between different helicases.

I think requirement of ATP also depends on the arrangement of oligonucleotide that mean bound between A and T(u) or G and C, and it could be calculate but how I cann't say yet.

All helicase is doing is opening up the DNA double helix by disrupting the hydrogen bonds between the nucleotides. The bond in hydrogen bonds is a misnomer as it is a van der Waals interaction and not a bond between atoms, so there are no bonds being broken, which would require significantly more energy to break than disrupting H-bonds. Topoisomerases on the other hand do need to catalyze breaks in the phosphate backbone in order to relieve tension from supercoiling. This is not to say that ATP is not consumed, just that bonds are not broken in the process as you are stating.

The answer to this is perhaps not as simple as you may think, in part because there are many different helicases in the human body. There is also some passive activity of a helicase that does not require ATP.
It is not clear exactly whether ATP is just involved in the translocation of the helicase or the actual unwinding.
For a RecQ helicase in E. coli, one study found that "The determined tight mechanochemical coupling of 1.1 ± 0.2 ATP consumed per nucleotide traveled indicates an inchworm-type mechanism." For more information see Sarlós et al. (2012).
Another study (Donmez and Patel, 2008) notes that "As compared with non-ring-shaped helicases such as PcrA (Dillingham et al, 2000) and UvrD (Tomko et al, 2007) that move on an average 1 nt for every ATP hydrolysed, the ring-shaped T7 helicase is three times more fuel efficient." This shows how there can be quite a bit of variation.
Bottom line - you can count on your fingers the number of nucleotides unwound by a helicase per ATP.


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Fisher's Method to melt p-values for CpG sites annotated to the same gene?
I have some data I am working with, and I am curious if I am able to combine p-values from a paired t-test for CpG sites in the genome using Fisher's Method to get one p-value for each unique gene. Linked here is the Wikipedia page for Fisher's Method. I understand that an assumption of the method used is that each individual p-value being combined must be independent. I'm relatively new to biostatistics, so I'm curious if using CpGs from the same gene would violate this assumption.

Yes, it would very likely to violate the assumption for any two pvalues computed on data coming from the same chromosome. You might want to read this section of the wiki article to understand how violation of these assumptions may affect your results. However, one would need to know how you computed your pvalues in the first place to be definitive. How did you compute your pvalues?

p-values were computed using a paired t-test before and after treatment

You have to explain a bit more in order to understand whether these pvalues may be independent. What is the response and explanatory variable (or the two groups in your t-test if you prefer) and what is your treatment. But you probably have a good intuition of the biology and of the treatment performed yourself without having to explain of whether your data from one site to the next are independent or not.

Ok I will elaborate as much as possible without divulging too much for the sake of confidentiality. The explanatory variable is a drug treatment given to patients. There are many potential response variables, but the one I am interested is an M-value, which is a log2 ratio of methylated to unmethylated probes detecting a single CpG site. Does that make sense?

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How does the measeles virus form?
I would like to understand how (if possible) the measles virus could start to infect a population that was theoretically isolated from any other population group. Put another way, can the measles virus develop within a person without external influence/inputs?

Is the question "Can a measle virus be created anew and not via reproduction from another virus?" (the answer would be 'No').

So it is not possible for an isolated population to have instances of measles unless they are exposed to it from an external source, correct? I understand that it is an endemic disease, but my confusion is on how a population gets the first instance. Is there a better question I can post to get at that idea? I am interested in measles particularly.

You should have a look at an intro course to evolutionary biology such as understanding evolution by UC Berkeley for example. There is no clear first instance. Modern day measle viruses evolved from an ancestor that was not the modern day measles. In any case, there is no spontaneous generation.

@Remi.b, okay, if you want to post this comment as an answer then I can accept it as the answer and close this out. Thanks.

While the question is clearly quite introductory, I think it can be answered in the broad sense and should not be closed as off-topic. I also think that two down votes is a bit harsh.

The question could be rephrased
Can a measle virus be created anew and not via reproduction from another virus?
The answer to which is "no".
The falsified idea that new life forms can jump pop up out of nowhere is called spontaneous generation. Spontaneous generation do not occur.
Note however that sometimes it may look like as if a new epidemic came from nowhere. The reasons is due to natural reservoir.

A natural reservoir  or nidus (the latter from the Latin word for "nest") is the long-term host of a pathogen of an infectious disease.

An asymptotic carrier can be used as a natural reservoir

An asymptomatic carrier (healthy carrier or just carrier) is a person or other organism that has contracted an infectious disease, but who displays no symptoms.

These reservoirs can keep the viruses (or other pathogens) alive in while from the outside it looks like the disease has been eradicated. At some point the virus can spread again making it feel like it came out of nowhere.
[..] my confusion is on how a population gets the first instance
There is no clear first instance. Modern day measle viruses evolved from an ancestor that was not the modern day measles. Just like there was no sudden first human (or any other species). There were just ancestors that evolved to become what we now call modern day humans.
You might want to have a look at an intro course to evolutionary biology such as understanding evolution by UC Berkeley for example.

I'm somewhat regretful of my final close vote and I nominated for reopening based on your comment above. I think you could add to this answer a brief note on reservoir species and asymptomatic carriers, and how either can sometimes contribute to apparent outbreaks of disease from "nothing", though neither is thought to contribute in the specific case of measles.

@BryanKrause Thanks a lot for the helpful comment.

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Cell biology - Resting membrane potentials
Why do we say there is an overall negative charge on the intracellular side of the plasma membrane at rest, and an overall positive charge on the extracellular side when both potassium and sodium are positively charged ions, and they are in relatively equal amounts on either side? It seems to me that both sides should be positively charged, and I can't get my head around it.

great question... with an equally great answer... where have you looked for this answer?

The resting membrane potential is the voltage at which there is no net flow of ions across the membrane.
Every ion will tend to flow down it's concentration gradient (this is just a basic principle of physics/chemistry). So, without considering charge, for a typical cell, potassium will tend to flow out, sodium will tend to flow in, and other ions will also behave according to their concentration gradients.
The other crucial part of the equation is the relative permeability of the membrane to each ion. This comes mainly from the presence of ion channels. At rest, a typical cell has more permeability to potassium than sodium.
That means that if the driving force for sodium and potassium is the same (it's not identical at 0 mV but fairly close), more potassium will move than sodium.
If the definition of resting potential is the potential where net flow of charge is zero, and considering only sodium and potassium, then rest has to be where sodium flowing in equals potassium flowing out. This situation occurs when the inside of the cell is negatively charged compared to the outside: the membrane voltage "holds" potassium in and "pulls" some sodium in, such that their currents are equal and opposite despite the higher permeability to potassium.
Note that the voltages we are talking about in neurons, on the order of 10s of mV, are very small, and electrical forces are very strong. The concentrations of positive and negative ions are almost exactly identical on both sides of the membrane: only a few ions actually have to move to make a (biologically) large membrane voltage. What is actually important is the permeabilities: that's what makes action potentials and other forms of neuronal signaling feasible.

I had the same question and wanted to re state the answer with more steps. This might be helpful as I had no idea what was going on and this will explain some common misunderstandings that I and probably most people have with this.
At resting potential we have Na+ in the exterior and K+ and organic acids in the ctyosol. The membrane potential relies on electrochemistry to propagate a signal from dendrite to distal synpase. To propagate neuron signals it would not be ideal to transport these anions across the membrane given their size and utility inside the cell. It would be slow and require intensive transporters in the membrane. We can however use cations which are relatively abundant, small and with relatively low thermodynamic cost.
The -70mV resting potential describes the relative charge state across the membrane. It describes that the cytoplasm is relatively more negative compared to the extracellular fluid. Since we have organic acids giving the cytosol a slight negative character, we can use the thermodynamics of diffusion to our advantage. This is where our cations come in to use. At rest we balance the concentrations of cation movement across the membrane via the sodium potassium ATPase which maintains the gradients of Na (high on extracellular side) and K (high on cytosol side). We only need the balance the movement of these cations to create the polarised character on either side of the membrane given the organic acids.
When a dendrite receives excitation signals Na+ transporter proteins open and sodium rapidly enters the cytosol across the gradient. The potential falls as the cytosol becomes more positive and we have a change in the potential (action potential).
This doesn't explain why K+ is needed here. Propagation of the signal along the neuron requires the cytosol beside the site of action potential to change potential and become more positive. Diffusion takes time. If we reverse the Na pumps and immediately removed all Na+ from the cytosol this wouldn't create the necessary change in potential along the neuron because the Na+ is being pulled into the extracellular space rather than given the time to move along the cytosol.
K+ plays the role of repolarising instead. While Na+ allows the signal to propagate, K+ is moved out of the cytosol into the extracellular space to move the potential back to -70mV. When the signal is sufficiently distal, Na+ can then be moved to the extracellular space and the resting potential can be restored.

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How does 'phosphorylation of glucose' maintain concentration gradient in membrane transport (facilitated diffusion)?
Our book explains how glucose from the blood plasma gets inside red blood cells via facilitated transport.
It states here in the book that the glucose will be transported inside by a carrier protein. Then the glucose will be phosphorylated by ATP. The phosphorylation of glucose molecules maintains the concentration gradient. This prevents the glucose from diffusing back to the blood plasma.
Based from my current understanding, concentration only change when the number of dissolved molecules changes.
My question is, "How can phosphorylation maintain the concentration gradient if it doesn't change the number of molecules inside the red blood cell?"

Sort of a "magic trick" that biology does.
With facilitated transport, the movement is passive. That is, you have a protein that certain molecules/ions can pass through, but you aren't doing any pumping or using energy to move molecules. That means that the molecules are free to move in either direction, according to concentration (and electrical) gradients.
Therefore, assuming no influence of electrical gradients, the highest concentration a passively transported molecule can reach is equal concentration inside and out.
Chemically, phosphorylated glucose is not glucose. It is phosphorylated glucose. If you phosphorylate every glucose molecule that comes in, your internal concentration of glucose would stay at zero. If phosphorylated glucose can't leave via the same facilitated diffusion pathway, then glucose will effectively only come in via that pathway, it can't go back out. The result is that, although glucose inside can never be higher than glucose outside, the sum total of phosphorylated glucose + glucose inside can continue to rise above the concentration of glucose outside.
Of course, this step isn't exactly free, because it costs the energy of phosphorylation.


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Can plants live forever?
I know that some plants die for old age like a
lettuce. But there are trees like Baobabs or larger Ficus in the tropics of whom we don't know their age. And trees like spruce reaching 9950 years old, which die for environmental factors and not by age.
However, E.g. when we multiply vegetatively an olive or cacao tree, we use a fragment or clone from a unique individual passing the same genetic information, again and again.
Then, can these plants live forever?

See also: http://biology.stackexchange.com/questions/2055/do-trees-age-on-a-microscopic-level/ and http://biology.stackexchange.com/questions/7010/is-there-any-kind-of-immortality-in-plants?rq=1

The answers to these questions often boil down to "what do you mean by live forever?".
You've included vegetative cloning, so I infer that counts as one living organism for your purposes. In that case, the answer is absolutely.
Pando is at least 10 thousand years old and only getting larger. The Cavendish banana is about 150 years old, but produces at least 70 million tons of bananas yearly.
See here for other giant clones. Of particular interest is King's Lomatia, represented as a species by a single, sterile, individual. Fossilized triploid leaves are too old for carbon dating(at least 45 thousand years old), so it's essentially unknown how old it is.
I would be comfortable declaring Pando immortal, since it's way too big to be eaten, too resilient to burn down, and has already survived the middle and end(at least!) of an ice age. That just leaves (ha) disease and basically nothing else as possible threats.

Pando is actually thought to be ~80,000 years old.

Forever no. For thousands of years yes. And not only plants, other organisms have what is called biological immortality. Look here for some examples https://en.m.wikipedia.org/wiki/List_of_long-living_organisms


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Do we have evidence of heritable personality traits in chimpanzees?
I have read that chimpanizees have distinct personalities. Do we have evidence of heritable personality traits in them?

you should add some details such as what all do you include in personality traits. I am not sure if personalities are heritable in humans. Personality has a very large environmental component

Can you add some more background? Where did you read this?

@WYSIWYG the Big Five are considered to have up to 50% heritability in humans, so I don't see a problem with the premise. I don't know if there is sufficient research on personality traits in apes (or how researchers would deal with the distortion which being lab-reared will introduce to a twin study), but I find the question quite interesting.

There has been some research in order to explore this direction, for instance, see this reference:
A. Weiss et al. - "The Heritability of Personality Factors in Chimpanzees", Behavior Genetics, Vol. 30, No. 3, 2000.,
in which the authors study five human-like factors - Surgency,
Dependability, Emotional Stability, Agreeableness, and Openness.
Quoting verbatim their findings:

Only Dominance ... was significantly heritable. Dependability showed evidence that it might be heritable, but the parameter estimates were not statistically significant ... Two other personality traits, Agreeableness and Emotional Stability, showed positive heritability estimates but the parameter
  estimates were nonsignificant and small. Openness and Surgency showed no evidence of heritability.

In fact, the statistical correlation between dominance and heritability makes a strong sense.  Here's what I make out of this - this was a correlation based study, or kind of an experiment, hence the stress on statistical significance. But the question it raises is - is there a causal relationship between the two, i.e. does there exist any proper mechanism for the inheritance of "dominance". Finding such a mechanism was clearly beyond the scope of this study, but I believe the requisite answer for your question is if one stumbles on to such mechanisms, and not statistical correlations, which are mere pointers.
But on the basis of the study at least, all that one can safely conclude is - statistical correlations suggest that inheritance of "dominance" appears plausible, but the exact mechanism of how this implements out in practice, is beyond the scope of this study.


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Why is centriacinar emphysema more common in the upper lobes compared to the lower lobes?
I suspect it's because the upper lobes get less ventilated (the volume of their alveoli change less during respiration, and they receive less new air with each breath) compared to the lower lobes, and this causes air to stagnate there more in comparison. Since centriacinar emphysema is usually smoking related, I assume it's because smoke remains in the upper lobes more. I feel like this doesn't really make sense, could be because it's incorrect or it just needs a change of wording.
Also, an extra question if it's okay, why is panacinar emphysema more predominant in the lower lobes? Is it because the lower lobes get better perfusion?

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What are the differences between the margins of the lateral and medial condyles of the tibia?
During an osteology lecture about the bones of the leg, the professor mentioned that the posterior (i think it was the posterior at least, I didn't write my notes down very well) margins of the lateral and tibial platues at the articular surface are different; the medial one's is sharper, and the lateral one's is smoother, rounder, or, as he put it, "sloppier", and this helps give more motility to the lateral meniscus and makes its injuries less likely. It also apparently helps the motion range of the knee joint.
I can't seem to be able to find any article or book that talks about this (I've checked Snell's, Gray's and Grant's anatomy books), so I was wondering if this is really a thing.

The proximal end of the tibia is broad and flat known as tibial plateau. The intercondylar region crosses through the midline of this plateau, separating the medial and lateral condyles of the tibia.
The two condyles are in form of flat and broad surface for articulation with the medial and lateral condyles. The medial surface  is convex and subcutaneous. The lateral surface, also known as articular surface is smooth surface and somewhat concave, and articulates with the talus.
[Sources:
https://www.physio-pedia.com/Tibia
http://en.wikipedia.org/w/index.php?title=Medial_malleolus&oldid=240146811
http://www.bartleby.com/107/61.html ]

This doesn't really answer my question; my question was about the two proximal condyles, more specifically, their posterior margins. The bartleby article does mention the fact that the posterior of the lateral plateau is slightly convex, but makes no mention of what that's good for.


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Is glutamate always involved in the deamination and amination of the other amino acids?
For example, are there pathways for the deamination of phenylalanine that simply produce ammonia or pathways for it to be synthesized from phenylpyruvate with ammonia being utilized to form the amine group?
Preferably, I want to know how it is with human metabolism mainly.

What research of your own have you done to answer this question? Amino acid synthesis and degradation are covered on numerous internet sites and in texts on NCBI Bookshelf. Please consult the Help on asking good questions to find out what is expected from posters of questions. (And also include the question in the main body so that it is complete in itself.)

I'm not going to give you the answer, but Berg et al. Biochemistry on NCBI Bookshelf is a good starting point for any biochemical questions. Search for deamination and read the whole section. Tell us what you find — you could even make it an answer to help others and get yourself some credit.

For most amino acids, the removal of the α-amino group involves α-ketoglutarate and glutamate. The amino group is first transferred to a-ketoglutarate by transaminases, and the resulting glutamate is then deaminated (via glutamate dehydrogenase) to yield ammonia.

The same is true for amination. Glutamate and glutamine are the two major amino group-donors. Most ketoacids are converted to their respective amino acids by transamination involving glutamate or glutamine. Glutamine can be synthesized by amination of glutamate with ammonia without transamination (via a synthetase enzyme) and glutamate can be aminated with ammonia too.
Exceptions do exist, of course. For example, Not all transaminations involve glutamate/glutamine (as this user has replied), and serine and threonine can be directly deaminated (via dehydratase enzymes, as opposed to the dehydrogenase used for glutamate).


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Why are superantigens not "MHC-restricted", and what's the significance?
MHC restriction is the requirement to recognize an antigen in association with a self-MHC molecule; CD4+ cells can only respond to an antigen if it's presented with a self-MHC II molecule, and the same goes for CD8+ cells and self-MHC I.
Various sources say that super antigens require an MHCII+ antigen presenting cell to activate a T-cell, but they're not MHC-restricted. I've found one "clarification" on what this could mean, and it's that various MHC II molecules can present a superantigen. Does this mean that MHC II from different hosts can activate a clone of T-cells if a superantigen is involved? What's the significance of that in a single host, e.g., someone infected by a microbe that produces one of these things?

It means they bind outside the groove, and so bind nonspecifically. This is why they cause such a massive immune response. They activate indiscriminately (i.e., not a clone). I may have time to write this up in full later.

By “non-specifically” do you mean in regards to the paratope the T-cell possesses or the MHC haplotypes/alleles that can present it? I think it can do both, but it’s not very clear to me yet.

What's your understanding of how a T cell clone is activated by a normal antigen? What binds to what?

A normal antigen must first get engulfed by an APC, processes then presented on the surface of the APC. To activate a T cell clone, TCR must bind to an antigen-MHC II complex, and some co-stimulation is also needed: CD4 and MHC II, CD28 and B7, LFA-1 and ICAM1. What I understand from superantigens is that they skip the whole engulfment thing (engulfment and processing makes them lose their "super", rather) and bind to the V-beta part of the TCR and the MHC II outside it's peptide-binding groove, so TCR antigen-specificity is rendered irrelevant.

I think different MHC II isoforms bind different peptides, so you need a variety of those to bind a good number of peptides, and conversely, a particular peptide WONT get presented by every MHC II isoform. Superantigens also skip this particular restriction too, right? Is that what the whole "Not MHC-restricted" thing is about? @DeNovo

Yep, you got it. I would suggest you convert to an answer and I'll upvote.

Dope. Thanks for the help, I'll do that now.

Normal, "non-super" antigens activate T-cells in the following manner: they are first engulfed and processed by a professional antigen presenting cell (APC), e.g., a macrophage. The processed antigen is then presented along with an MHC class II molecule on the surface of this cell. The T-cell's T Cell Receptor (TCR) then binds this complex; it must be able to recognize both the MHC class II and the antigen, and in addition to this "main signal" other co-simulatory signals are also needed. The important thing to remember is that a T-cell will only react to a specific antigen it's specific with when it's present with an MHC class II molecule it can recognize. This is known as MHC restriction
A person has 3 genes (each having 2 alleles,for a total of 6 alleles) for MHC class I: HLA A, B and C, and 3 genes for MHC class II: HLA DR, DQ and DP. These alleles are highly polymorphic, i.e., varied, with each of these 6 genes having hundreds or thousands of different alleles, and the combination of alleles differs from individual to individual; it's very unlikely that two people who aren't identical twins would have the same combination of HLA alleles.
MHC molecules can only bind peptides, and in addition, they cant bind ALL peptides; of all the peptides that can possibly be bound by an MHC molecule, a particular MHC molecule can only bind a select number of those peptides. Different MHC molecular forms, be they class I or II, can bind, and thus present, a different set of peptides. Having different HLA alleles at your immune system's disposal means there's a larger pool of possible peptides your APCs can present with the different MHC class II isoforms they have, allowing defense against a larger pool of antigens.
A normal antigen has 2 "restrictions" on its ability to activate a T-cell clone: it must be presented by an MHC class II isoform that can bind it, and it must be recognized by a T-cell with a compatible TCR.
Superantigens activate T-cells in an unconventional manner: They have a domain that binds to the TCR, though not at the usual antigen binding site, and a domain that binds to the MHC class II molecule, but not in the usual peptide-binding site these molecules possess. Since it binds outside of these regions that are specific to particular molecules, they're not restricted by the antigen specificity of the TCR nor are they restricted by the MHC class II isoform they're utilizing. Hence why, even if they do need MHC class II-positive cells to be able to activate a T-cell clone, they're not MHC-restricted.
Readings:

Immunobiology by Charles Janeway, Sections 5-13, 5-15 and 5-16.

Just add references and you're done! A general textbook level reference will suffice.

Refering to "MHC class II isoform": does every cell, or, every cell type have a different MHC complex (are the proteins homologues)?


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What happens to intrinsic factor exactly at the terminal ileum, where B12 is absorbed?
IF is very important for IF-dependent B12 absorption in the terminal ileum, the mechanism by which most of dietary B12 is absorbed. The B12-IF complex bind to IF receptors on enterocytes, but does the complex in its entirety get absorbed, or does B12 alone get absorbed and the IF is left outside?
The latter mechanism I came across in source 1 (see below), which stated the following:

IF-B12 complex binds to specific receptors. Following this, the vitamin B12 is absorbed into the cytosol of the enterocyte by endocytosis, leaving behind the IF at the brush border.

However, several other books and articles (like 2-4) rather vaguely state that the IF-B12 complex is absorbed into the enterocyte. I've found two articles that discuss the existence of these two viewpoints, (5 and 6), but they are kind of old (from 1965 and 1989 respectively) and I don't know if the "mystery's been solved" as it were.
Sources:

Concise Textbook of Human Physiology (this specific page)
The Mechanism of Absorption of Vitamin B12 (cobalamin) in the GI Tract
Marks' Essential Medical Biochemistry (this specific page)
Textbook of Pharmacology (this page)
Intrinsic Factor
Vitamin B12 absorption and malabsorption

After reversible attachment of intrinsic factor-cobalamin complex to its ileal surface receptor, an energy-dependent
process prevents removal of the complex from the cell surface by EDTA or acid; cobalamin dissociates
from intrinsic factor and, as suggested by previous
workers, binds to a molecule antigenically similar to
transcobalamin II; and  intrinsic factor is slowly(after some hours)degraded and forms breakdown products that are detectable in ileal extracts.
References
Textbook of Pathology Page 318
One article
Intrinsic factor mediated absorption of cobalamin
Recent articles-
Physiology of absorption of vitamin b12

This article is also quite old, newer articles than it suggest that the issue was still controversial at the time

@Dahen yes I agree. Though I have added one recent article proving the degradation of IF. However upon more research I found some articles stating the controversial fate of IF.

Thanks for going out of your way to look for so many sources, I appreciate it.

@Dahen thanks. I too got to know about this. It is a good question.


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How are steroid hormones secreted?
Peptide hormones for example tend to be secreted by Ca2+ mediated exocytosis following depolarisation and are secreted in vesicles. How are steroid hormones secreted and what stimulates their secretion? Please leave references if possible.

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Is it possible to stimulate the EPOC process?
On Wikipedia, EPOC is defined as:

Excess post-exercise oxygen consumption (EPOC, informally called afterburn) is a measurably increased rate of oxygen intake following strenuous activity intended to erase the body's "oxygen deficit".

My question is what influence has post exercise habits on the efficiency of this process?
For example, after an intense exercise, a person rests in bed during this process, consuming a very low amount of oxygen.
Would this process be stimulated if this person would ride the bike for 30 minutes, very slow, but enough to put the cardio-respiratory system at work?


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Potential homogeneity across cell membrane
During respiration, individual bacteria (and mitocondria)  produce a relatively large potential difference (∼100 mV) between the inside and outside, using energy to pump $H^+$ out of the cell to the liquid environment (a proton motive force is created). Together with proton pumps, or sources, also sinks of protons are present, channels which reuse the voltage difference for other goals.
Imagine a cell like a bag, with only very few and sparse sources and sinks of protons. At the limit, take only 1 source and 1 sink, diametrically opposed, which continuously work. Is it reasonable to assume that the voltage difference created is homogeneous in space (it has same value everywhere along the surface)? How would this depend on the size of the cell?
My guess is that the homogeneity of the voltage should depend on the speed of diffusion of protons in water, which I imagine is extremely fast (but how fast?). So all variations around the mean value would be washed out on very short time scales (shorter than the shortest times of μs−ms
which are biologically relevant). But I may miss something. Any insight will be appreciated.

what is the question exactly?

The main question is Is it reasonable to assume that the voltage difference created is homogeneous in space (it has same value everywhere along the surface)?

it depends on the process you are looking for http://www.ncbi.nlm.nih.gov/pubmed/20566861 for example. Look for images in bacteria using voltage-sensitive dyes/proteins. Problem to do it is resolution


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conduction in unmyelinated axons
(Not a specialist here) Several questions touch the voltage propagation along an unmyelinated axon, but I'd like to focus on the following.
How fast does the voltage of a sub-threshold perturbation propagate?
More specifically, as in the picture, consider two positions $x_0$ and $x_1$ along an unmyelinated axon. At time $t_0$, a current step is injected at $x_0$.
My understanding is that, at every position $x$ the voltage will charge up with a characteristic time given by the (local) RC value, up to a value that will build, in space, an exponentially decaying profile, with characteristic length given by the resistances of the system.
At position $x_0$ the charging starts at time $t_0$, and at position $x_1$ it starts at time $t_1$.
How much is $t_1$? Is $t_1=t_0$, as suggested here, and probably by cable theory? Does the voltage propagate at, or close to, the speed of light? Doesn't diffusion of ions enter into the picture at all?
And, importantly, can you give me references where I can learn more about this aspect?


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Plasmid copy number and Rop protein
If i want to transform a bacteria (E. coli) with a particular plasmid (in my case pBR322) will the presence of the Rop gene affect the production of it ?
Is it desirable to use a plasmid without that gene to increase plasmid copy number ?
I found some informations about the protein cited on these links:
https://en.wikipedia.org/wiki/Rop_protein
http://www.proteopedia.org/wiki/index.php/Rop_protein

Since the pBR322 is derived from the pMB1 plasmid (which is closely related to the ColE1 plasmid, it does indeed contain the coding information for the rop gene. It's expression will limit the copy numbers from the plasmid, so if you are looking for high copy numbers, the usage of a plasmid without the rop gene should be preferred.
If it is only for the yield in a plasmid preparation, you could also simply scale up your production and make a midi prep instead of a mini or a maxi instead of a midi. It also depends, what you are planning with the plasmid. For cloning purposes mini preps with pBR322 have always given enough yield for me.


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Definitions of common and rare disease
Is there an epidimiological way to define rare and common diseases ?

How about doing it by the case numbers?

Could you please explain me better your suggestion ? I'm not sure to understand it correctly.

A rare disease has very low case numbers, while common diseases occur in much higher numbers.

Thanks for the clarification ! Do you know if there is a threshold between the two cases ?

To those who voted to close: This question is great, multiple countries build their Health systems budget according to their definitions of "rare" disease. In addition, the issue of these definitions is of great importance for the community health as well.

Thanks for the positive feedback about my question; i found this site very interesting but i need time to properly use it !

While "common disease" has obscure incidence and prevalence definitions, "Rare" or "orphan disease" is more defined.
In the US, the rare disease defined as a condition which affect one (or less) of 200,000 people in population. However, this definition can be different in other countries, p.e. in Japan 1:50,000 or less.
We can assume that "common" disease is much frequent than "rare" one, thus the incidence and prevalence are much greater than per "rare disease" definition. However, again, there is no agreement of clear cut of "common disease" incidence and prevalence.

Thanks for the answer !! I think to have read something similar years ago, but not in detail... i would vote your answer but i still have a low reputation so i can't.


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Is hypoxia/anoxia the ultimate cause of death?
I know there are different causes of death for humans like heart disease, cancer, stroke, injury and so on, but i was thinking if in every case in the last instance death is due to hypoxia/anoxia.
Am i missing other mechanisms ?
What i'm searching are the last mechanism that cause the organism to collapse and die.
E.g. (non detailed just an example)
In the case of heart disease, a plaque could lead to the block of a myocardial artery followed by local hypoxia/anoxya that kills the heart tissue followed by cardiac arrest and death by general anoxia.

Copy of this http://biology.stackexchange.com/questions/41207/why-do-you-die-if-you-cannot-breathe ?

There is no one ultimate cause of death. For instance, there are neurotoxins which kill brain cells while oxygen remains plentiful, and there is complete disruption of the brain, as with a suicide-bomber.

You will first need to define death, Mauro. Good luck. You might say, when the organism stops moving for good, but I have shot deer that keep moving well after I shot them. Like 15mins after. You could say when the heart stops, but I know people whos hearts have stopped at one point and they are still alive today. So our first task would be to define death, so that you may later classify an organism as dead or not dead. Let us know what you come up with.

@Nathan Thanks for pointing that out, i would check it later to deepen my knowledge about hypoxia... there are indeed common parts in the two question, but the one that you linked is focused only on hypoxia while my question is more broad in the sense that i'm searching for other mechanism different from hypoxia that cause the death of a person.

@mgkrebbs Thanks for the comment, could you gently suggest me some reading about one of these neurotoxyns ? But if a neurotoxin badly damage the brain is there a chance this in the end lead to the failure of lung function (by poisoning of the respiration centre) and consequently general hypoxia ?

@DonJulian When i thought about this question i remember an MD (i was young and not really into science so i'm sorry to bring this without reference) that said something like: In the end we all die of heart failure. I think he was referring to the fact that independently from the primary cause of damage (a trauma, a pathology, a poison etc) in the last instance the collapse of the organism was caused by failure of heart function and blod flow to the entire body.

Having the head removed by an axe or sword is fairly ultimate...


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What are the molecular/cellular basis of pruritus ?
Could someone please explain the cells and molecules involved in the clinical phenomenon of pruritus ?
I'm interested in a general view about the subject, but detailed answers will be appreciated.

Molecular basis:  histamine.


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Patterns/Motifs Repository
I am new to this area. I am a researcher working on fast pattern searching in general scenarios (e.g., regex in string matching).
I am curious about the "regular expression (regex)" (pattern/motif) in bioinformatics. Can anyone help point out some repository where I can see some "regex" instances (used by people in real cases)?
So that I can get a sense how complex they are and the possibility to apply our techniques.
Thank you!

There are only a fixed types of characters for DNA or protein sequence. For inexact matches you can use a regex. People do it quite often for general stuff. I don't understand what you mean by a repository.

Prosite (http://prosite.expasy.org/) uses regular expressions to search for protein domains, in contrast with Pfam. If you look at an entry, such as http://prosite.expasy.org/cgi-bin/prosite/prosite-search-ac?PDOC00022, you can see the consensus pattern under the PATTERN section towards the bottom. Prosite does not have the same coverage as Pfam, but the ease of searching means it is updated much more frequently and has tighter integration with UniProt.

Regular expressions are not commonly used for DNA or Protein analysis, but many people use Hidden-Markov-Models (HMMs).
If you are looking at protein domains, you can find many HMMs here:
http://pfam.xfam.org/

You will probably want to read up on Position Frequency Matrices (PFMs) and Position Weight Matrices (PWMs).  These tend to be much more sensitive and useful for pattern recognition in nuclei acid sequences. Two examples of databases with these patterns are TRANSFAC and JASPAR. Regex patterns can be useful in protein sequences sometimes, although PWM have application there as well.


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How does an electrical impulse spread in a muscle fiber spread from the motor end plate?
Does this impulse in skeletal muscle spread much in the same way it does in neurons, with an initial potential change that spreads to its immediate surroundings and is then re-amplified or is it the case that in muscle fibers, the initially produced end plate potential must be "enough" to depolarize the whole muscle fiber?
My issue is with this bit in a lecture about NMJs I took:

Because the ACh-gated ion channels are localized to the end plate membrane, the End Plate Potential (EPP) is generated at and confined to the end plate region only and, therefore, the amplitude of EPP declines progressively with increasing distance from the end plate region.

I only found this site which talked about something similar, and there it talked about it in the context of a muscle fiber that's been blocked by a non-depolarizing neuromuscular blocker, i.e., no contraction occurs, it's just a measurement of how the EPP changes by itself, so perhaps the lecture was talking about something similar?
So, to put it simply, do electrical signals in skeletal muscles get re-amplified as they travel along the fiber, like they do with neuronal action potentials, or is the initial membrane potential sufficient and it just "spreads around"?

Skeletal muscle cells are excitable, like neurons. Enough summation of end-plate potentials causes the cell to reach threshold and fire an action potential (which then spreads throughout the cell membrane through positive feedback, just like a neuronal action potential).
There are some differences between skeletal muscle and typical neurons, like greater importance of chloride in setting resting potential in muscles, but otherwise their action potentials are driven by voltage-gated sodium channels, just like typical neurons.
You quote:

the amplitude of EPP declines progressively with increasing distance from the end plate region.

which is true as long as the threshold potential isn't reached, and would also be true for subthreshold receptor potentials or post-synaptic potentials in neurons.
In the reference you link to, I assume you are referring to the mention of curare. Curare blocks the nicotinic acetylcholine receptor, so it is interfering with the end-plate potentials themselves, rather than the intrinsic excitability of the muscle.

See:
Philip M Hopkins, Skeletal muscle physiology, Continuing Education in Anaesthesia Critical Care & Pain, Volume 6, Issue 1, February 2006, Pages 1–6, https://doi.org/10.1093/bjaceaccp/mki062


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Why is angiotensin converting enzyme localized in the lungs
I understand that it's also found elsewhere, such as in renal capillaries, but I can't see logic behind it being located in the lungs. Isn't ACE's function, through making more angiotensin II, causing increased fluid and sodium retention and increasing peripheral resistance? What benefit does that purpose get from ACE being mainly in the lungs?

I guess you do mean ACE, i.e you do not mean ACE2.
It looks like some  coincidence that you started your question when "Corona" began.  ACE2 (in spite of homology: not ACE)  is target receptor of CoV and COV-2  in lung: Pneumocytes type II. - Your question makes me re-research on ACE not ACE2 in lung epithelia.  In fact, as answered: ACE2 but not ACE in lung epithelia.
Highly interesting: in evolution, ACE2 might have mutated from ACE as both receptors are almost identical. ACE might be  the more ubiquitious protein in the sense of answer given.

ACE is present on the luminal surface of vascular endothelia throughout the body and is abundantly present in the endothelium-rich lungs.
ACE in the kidney—particularly in the endothelial cells of the afferent and efferent arterioles—
can produce enough ANG II to exert local vascular effects.
Thus, the kidney receives ANG II from two sources:
✓ Systemic ANG II comes from the general circulation and originates largely from the pulmonary region, and
✓ Local ANG II forms from the renal conversion of systemic ANG I.
• In addition, the proximal tubule secretes ANG II into its lumen and thus achieves intraluminal concentrations in excess of
those in the general circulation. ANG II in the circulation has a short half-life (~2 min).

Oh, so the reason ACE is abundant in the lungs is simply a product of the fact that the lung has a lot of endothelium?

Yes, you are right.


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Is breathing a reflex action or is it an intrinsic process?
The process of breathing is controlled by respiratory centers in the brain stem. Do these centers have an innate activity, i.e., just send out signals to breathing muscles intrinsically, and have the rate and manner in which they do so modified by various regulatory factors?
Or are they driven by imbalances (in levels of oxygen, carbon dioxide, hydrogen ions) like a reflex? Let's say that hypothetically these levels remain static in an acceptable state such that this reflex is no longer needed, would breathing stop since there's no longer a driving motive or would it continue because the respiratory centers have an intrinsic activity?

While the ultimate purpose of breathing could be considered to be the maintainance of a balance of the substances you are referring to (such as blood oxygen, carbon dioxide, and hydrogen ions), the blood levels of these substances do not directly control the production of action potentials within the motor neurons that promote the contraction of the diaphragm and intercostal muscles.
The propagation of these action potentials is initiated by signals from the medullary respiratory center, specifically the neurons in the dorsal respiratory group (DRG) and the ventral respiratory group (VRG). In the VRG, a complex of neurons known pre-Bötzinger complex is responsible for generating the signals that cause the rhythmic muscle contractions involved in breathing:

The respiratory rhythm generator is located in the pre-Bötzinger complex of neurons in the upper part of the VRG. This rhythm generator appears to be composed of pacemaker cells and a complex neural network that, acting together, set the basal respiratory rate.

Vanders Physiology, p473, 15th ed.
So breathing is indeed, as you mention, a process that is controlled by innate neuronal activity but regulated by the concentrations of PO2, PCO2, and H+ concentrations. I recommend you read pages 473 to 477 of Vanders Physiology, which explains these controls in detail, some of which do involve reflexes, say, if O2 concentration in the blood strays too low.
Interestingly, expiration, which is typically a result of actions potentials ceasing and respiratory muscles relaxing, can be controlled by a reflex, known as the Hering-Breuer reflex, during strenuous exercise when the lung is inflated by a large tidal volume. Stretch receptors in the airway in this case are activated, causing the inhibition of inspiratory neurons in the DRG.
Source: Vanders Physiology, 15th ed, section 13.9: "Control of Respiration"

That makes much more sense than the whole reflex response. The lecture our college had was using three different sources, each with a different explanation for the driving motive of respiration. Two of those were behind the innate activity idea, but for different origins interestingly enough: one source (Tortora’s Principles of Anatomy and Physiology) said the activity originates in the pre-Botzinger complex like you said, and the other one (Guyton and Hall) said it originated in the DRG, so I suppose Guyton and Hall is the odd one out here (wouldn’t be the first time it is tbh)


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How much electrical energy is required for intracellular stimulation of a neuron?
How much electrical energy is required for intracellular stimulation (firing) of a human neuron? Electrical energy is measured in joules, and equal to voltage multiplied by current. If you don't know energy,  you may specify voltage applied and current. Just for example, to capture heart, a pacemaker must discharge 0.1 microjoule of electrical energy.
There might be more parameters involved like pulse width,  phase etc.  Energy combines all the parameters in one single value. In case you don't know energy level,  please specify the defining parameters as well.

I think this question is somewhat ill-posed, but I'll try to answer it:
None.
All you have to do is to short the inside of the cell to the outside/ground. Of course in reality this means expending some energy somewhere, but at that point it's an engineering problem, not one of biology, and it has nothing to do with the neuron itself.
Action potential firing is a completely passive process. The only part that requires energy (besides protein synthesis) is for the sodium-potassium ATPase that maintains sodium and potassium gradients.

I agree that this is an ill-posed question. (OP is probably trying to ask the engineering question...) Na/K-pump spends enormous amount of energy to ready that state though. Each AP does have an associated energy cost that way.

Yeah, that cost is necessarily driven by things like the size of the neuron, how branched the axons are, myelination, etc, and the cost is still a fraction compared to the cost of synaptic transmission in most cells: action potentials are really incredibly efficient. Synaptic transmission is really only costly because you have excitation and inhibition that cancel each other out in terms of voltages but create large currents that require pumping. All that said, I read the OP's post to be mostly about triggering, rather than propagating an AP.


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Does soap kill human cells?
I see many products, particularly hand soap and cleaning products, that claim to kill 99.9% or more of bacteria.
This makes me wonder, if the chemicals are potent enough to break down bacterial cell membranes, can they also break down human cells? If not, why not?

salamander is right about triclosan being the active ingredient in antibacterial soap, but the reason why it doesn't kill human cells doesn't have anything to do with the skin. From salamander's same source:

Once they are in microbes cells, triclosan poisons a specific enzyme (enzymes are proteins that have particular functions, think of them as cellular machinery) that is used in making microbes cell membranes. Humans dont have this enzyme, so triclosan doesnt poison us.

The enzyme in question is called Enoyl-acyl carrier protein reductase (ENR), and is used by bacteria as part of their fatty acid synthesis. Eukaryotes use a different set of enzymes for fatty acid synthesis, so we aren't effected by this activity of triclosan.
For some more specifics about the interaction of triclosan and ENR, we can turn a study about the antibacterial mechanism of triclosan that was done soon after triclosan was first crystalized in situ with its target enzyme.
From Heath, et al (1999):

Triclosan is a broad-spectrum antibacterial agent that inhibits bacterial fatty acid synthesis at the enoyl-acyl carrier protein reductase (FabI) step... The ubiquitous occurrence of type II fatty acid synthase systems in bacteria and the essential nature of the FabI reaction make this enzyme an attractive target for antibacterial drugs. Accordingly, triclosan is effective against a broad spectrum of bacteria, including multi-drug-resistant Staphylococcus aureus.

Your answer is correct. Thank you for clearing that up. +1

During the current coronavirus lockdown, there's much discussion that regular ole non-antibacterial soap will tear apart the lipid membrane of the virus. I'm fairly certain that human cells have a bi-lipid membrane, so it would seem that regular soap should also kill human cells like it does the virus. Any insight into this non-antibacterial case?

Yes, soap will absolutely kill human cells, under the right conditions. This is why if you wash your hands over and over again, they will become red, chapped, and damaged

The longer answer is that human skin is a complex, many-layered structure that is made up of both (highly specialized) cells and other non-cellular components. The barrier formed by the outer layers of your epidermis is what keep soap from doing you any real harm, so long as you don't overdo it. Some refs: Interactions Between Surfactants and the Skin... and Effect of Surfactant Mixtures on Skin...

Antibacterial soap commonly uses triclosan, which can pass through the phospholipid bilayer of bacteria and disrupt the production of essential enzymes, killing the bacteria (source). This triclosan
 would kill human body cells in the same way as it does bacteria, however we have a 1-1.5mm thick layer of dead skin cells(called the Stratum corneum) that exists to protect our epidermis from chemicals like antibacterial soap.
EDIT: I was absolutely wrong about triclosan killing human cells. In fact, it is impossible for triclosan to kill human cells, because the enzyme that is destroyed in bacteria by the triclosan does not exist in the human body.

Can you please add a specific citation for the stuff about the Stratum corneum blocking triclosan? I can't find it anywhere

Forgive my blatancy, but this is incorrect. Triclosan WOULDN'T kill human cells even if it did come into direct contact with them because it binds enoyl-acyl carrier protein reductase (ENR) used in fatty acid synthesis in bacteria. Human cells lack ENR and are thus unaffected.

@CDB No, I appreciate the frankness. According to the European Union's Scientific Committee on Consumer Safety's Opinion on triclosan  you are absolutely correct. I'll edit my post to reflect this.

Excellent! Your edit is perfect. +1 for a great answer.


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How many ancestral generations do I have?
Following on from this question: How many humans have been in my lineage? Is it almost the same for every human currently living?
How many generations back do my ancestors go? Not just human ancestors, but all ancestors, right back to the first lifeform.
I recognise that there are some impossible unknowns here, so I’m looking for some kind of Fermi estimate.

sexual reproduction changed the generational thing so you have perhaps 1 - 4  billion sexually reproductive generations since your precambrian times, if you have an average 1 to 4 generations per year, seasonally, on average. since 4 billion years, zircons from australia have isotopes of oxygen that suggest life, and stromatolites date from <3.7, so we are talking about 4-400 billion prokariote and eurkariote zygote meioses.


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compute contact mixing matrix from partnership degree data
In a discussion of sexual partnering, we are given the following information on a momentary degree distribution (as percentages):
degree    0       1       2      3
men      32.3    53.2    12.4    2.
women    26.7    71.9     1.1    0.2

From this, the authors construct a "proportional mixing model", treating the data as providing the marginal effects.  (The rounding error is small, so I'm going to ignore it.)  I want to understand what this means.  I'll try to get started.
To begin, since this is heterosexual mixing, there cannot be the same number of men and women participating, since men and women must be in the same number of partnerships.  So if there are say 10000 individuals, we must have about 4707 men and 5923 women. From this (and the above percentages) we know the number men and women of each degree, and thereby how many total partnerships (3954).
degree    0          1         2        3
men    1520.36    2504.12    583.67    94.1399
women  1413.23    3805.67     58.22    10.586

I think (?) the challenge is first to find the number of partnerships of each type.  Obviously there are no partnerships with individuals of degree 0, so we are looking to fill a 3 x 3 matrix of partnership counts, so that each deflated row sums to a male total and each deflated column sums to a female total (as given by the table).  (By deflated, I mean divided by the degree.)  This does not seem too bad on the face of it: 9 variables with 6 equations looks to leave solutions to spare.  But the system appears to be inconsistent.  So, I must misunderstand.
I get the impression that this is very standard stuff, but I'm not finding it in the textbook I have at hand.  I'm happy to work through the math if pointed to a careful discussion.


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single units vs ensemble recording for signal detection
I would like to know, when looking (in vivo electrophysiology) at response properties (latency, magnitude) in response to sensory stimuli, is there any advantage to looking at single units over ensembles of neurons? My ensemble data is really good, while my single units are only ok.
Any advice or resources regarding this would be helpful. I've talked to members of my lab, and looked for answers elsewhere, but havent really found what Im looking for.
Best!

The answer is going to depend a ton on your research question; there can be advantages and disadvantages to each approach.

Can you elaborate please? I am measuring chances in latency of primary visual response to light flashes due to pharmacological manipulations.

First spike latency or similar measures when looking at ensembles only tells you about the latency of the least affected unit when you are talking about latency increases, or the most affected unit when you are talking about decreases.
For example, if you record from 30 cells on a multiunit cluster and the latencies of 29 of them increase but 1 does not change, you might conclude no effect on latency.
Also, changes in detection probability can be harder to recognize in multiunit recordings. If a pharmacological manipulation increases or reduces activity overall, including at distant sites, this might change your threshold of which cells' spikes you can accurately detect as spikes by increasing or decreasing the noise floor.
For example, if your threshold decreases, you might be recording spikes from ~20 cells in your control condition, but then sample from ~50 in your pharmacological manipulation. Note that in this circumstance the total number of spikes you record might actually go down, but you would underestimate the affect because you don't know how many cells you are actually sampling from.
Of course there are problems with single cell recordings too. Sometimes it's really the ensemble activity that matters more, in that case the single units aren't as informative. You also have the problem of tracking accurately a single unit throughout a pharmacological intervention, which can be problematic depending on the time course of the manipulation (electrodes drift, cells die) or if the manipulation itself affects spiking properties (it may be more difficult to ensure you have the same cell if spike widths or amplitudes change).

Thanks a lot for your explaination. I think I'm going to collect single units from the channels I can isolate them on, and ensemble data from the channels I cant isolate single units on. then ill run seperate single unit and ensemble statistics.


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evolution of advanced math ability
I am trying to convince a friend that human beings evolved from primates, and he challenged me that advanced mathematical ability couldn't have been the product of mutation and natural selection because this ability wouldn't have conferred any reproductive advantage until the last few hundred years, and the process of mutation and natural selection would have taken much longer than this to produce the extensive genetic basis of advanced mathematical ability. How do we refute this?

What is his definition of advanced mathematical ability?

I think, advanced mathematical ability is more an effect of the social evolution, that is a consequence of the brain evolution anyway.

Your question may be valid, but give up on thinking that you will convince your friend of anything. Believe me, it's a waste of time. In cases like this people believe what they want to believe — rationality or logic doesn't come in to it.

@David How come you voted to close if you think the question is valid?

@Remi.b  — I didn't say it was valid I said it may be (or may not be — understood). I voted to close because it was a request for debating ammunition which I do not consider appropriate to SE or ultimately useful for the OP. A pity, as your answer was interesting.

Mathematics is the queen of all sciences, of engineering roofs, of counting arrows, geometry of tools, counting days and reserves for travel, trading pelts, so all those survival skills benefit from increased maths and geometry. maths reasoning is qualitatively the same as geometry planning. not all humans are equal at programming, or have the same brain size, ask him why dolphins swim like dogs and breathe air and have milk, and treat him like a child with too many questions. maybe he will rationalize clearly one day.

Just to avoid misunderstandings
Just to avoid potential misunderstandings on your side, I wanted to talk about the saying that

human [are] evolved from primates

Humans are primates, so did our common ancestor with other primates.
Our ancestors are different from modern day primates. Chimps for example (which are great apes, like us) are not our ancestor more than we are their ancestors. We just share a common ancestor (who lived about 13 millions years ago).

Spandrel, exaptation and panselectionist arguments
Your are doing two mistakes. 1) The mistake of the spandrel (named after the title of the famous and old paper Gould and Lewontin (1979)) and the exaptation and 2) a panselectionist mistake.
1. Spandrel and exaptation
Spandrel

In evolutionary biology, a spandrel is a phenotypic characteristic that is a byproduct of the evolution of some other characteristic, rather than a direct product of adaptive selection

See also What is the “Spandrels” debate about?.
Exaptation

Exaptation [..] describe[s] a shift in the function of a trait during evolution.

While the existence of a spandrel in an evolutionary process does not necessarily cause the existence of an exaptation, but I will not go into these semantics details for simplicity.
Consider for example the two following wrong statements.

Birds have feathers to fly. It is impossible that birds evolved feather to fly because early feathers would have served no purpose to flight.

Bird feather actually probably first evolved for temperature regulation. Once this was done feathers were an exaptation for early flying tools.

Humans have nose to wear glasses. It is impossible that nose would have evolved because there was no glasses before

Noses evolved for another purpose and happen to be an exaptation for wearing glasses.

Humans have a big brain for advanced mathematical skills. It is impossible that humans evolved such big brains as such mathematical skills were useless in a time where we did not invent/discover much of the most basic math concept yet.

Humans evolved a big brain, mainly for social reasons incl. social hunting and social communication and probably because it was/is under sexual selection (see wikipedia > evolution of human intelligence). It just happen that logical reasoning, abstract thinking and other cognitive skills are an exaptation for advanced math skills.
2. Panselectionist view of evolution
I just want to highlight that there is much more to evolution than just mutations and natural selection. Not every trait has been selected for (otherwise we would not have any genetic disease).
On this subject, you might want to have a look at the paragraph Did you say Natural Selection? of this answer to Why don't mammals have more than 4 limbs? and to Why do some bad traits evolve, and good ones don't?

There is no such thing as "advanced mathematical ability" as a separate ability of the human brain. Advanced mathematical ability is formed by aspects of the general human intelligence. Given that not everyone is able to do advanced maths, it's a moniker for the high end of these aspects of human intelligence.
I can't give you a perfect description of all the aspects of human intelligence that are important for "advanced mathematical ability", but maybe a few examples will suffice:

The ability to abstract.
Reasoning by analogy.
Logical reasoning.
Spatial or geometric imagination.

All these abilities are pretty obviously useful, even in our far evolutionary past. Especially the first two abilities underly pretty much all our thinking.

Why did humans become increasingly intelligent long past what they needed to hunt prey? A large part of it is the intelligence needed to outfox other humans without being manipulated themselves. After language developed, we were our own greatest selective pressure. Indeed, no matter how smart we became because of this mechanism, it would continue to select for greater intelligence still to out-think the brains of the present. Going back to the spandrel point, the reasoning in mathematics may be a side-effect of this.

Thanks to B for posting this question -- I asked him to post it to biology.stackexchange, so that our interaction might be useful to others. My answer is a quickly-typed email but might be useful anyway.
My answer follows:
Hi B -- briefly, advanced mathematical ability WASN'T the product of mutation and natural selection.  Neither was writing, poetry, symphonic music, representative democracy, genius comedy, etc. etc. yadda yadda.
All of these cultural achievements are the product of a very long line of causes, very roughly,
A. general human physical and mental traits
B. hundreds of thousands of years of co-evolution of human brains, societies, and fundamental human technologies like the making of spearpoints, fishing hooks, clothes, rock art, etc. in stone-age, hunter-gatherer societies
C. farming and subsequent large, high-densities human societies
D. writing
E. well-organized governments, nation-states, and subsequent "space" for "high arts" (science, math, opera, whatever)
F. substantial economic and technological progress (better ship-building, international trade, the Mediterranean mercantile revolution before/during the Renaissance)
G. A long history of cultural development within each of the specialities in (E). Each of these began seriously building and expanding, generation on generation.  E.g. for math specifically, we only really got going seriously with the introduction of Arabic numerals, the idea of the numeral "0", etc., into the context of the European economic and academic structure, and their linkage to the general Scientific Revolution (e.g. the massive success of Kepler, Galileo, Newton etc. in applying math to physics and astronomy)
H. A concurrent massive expansion of organized, formalized educational system, ranging from childhood education through to university and postgraduate education
I. Massive growth in the human population, and generation of a huge leisure class, creating a relatively large number of people that can do advanced math.  Most of us still can't!
I suspect that advanced mathematical ability is roughly on a bell-curve.  Most of us have the aptitude/ability/focus to do things like counting, which would have been useful even in stone-age times, and which clearly exist even in animals.  It is relevant to know that you have better odds getting by 1 lion, instead of 10 lions.
The rest of the explanation of math ability is mostly due to the cultural factors above, which, through massive training (20 years plus for advanced math), take human's general counting abilities, language ability, good memory, etc., and produce mathematicians ranging from OK (like me) through to amazing (Einstein or someone).
Natural selection only has a role in explaining A and B.  The rest is culture, which (very slowly) built on humans' general intelligence, language ability, sociality, etc.
Repeat this explanation for any other remarkable cultural achievement.
And, anyone else wondering about evolution and some major cultural achievement, should ask themselves the following:

Can I myself produce a similar cultural achievement in the same area? Is everyone as good as Mozart and Einstein were in their specialties?  If not, why not?
For humans, language is easy, but any non-trivial math is hard.  But for computers, math is easy and language is hard.  Why is that?  Hmm, which one was useful back in the Stone Age?
Similar question: Why is math hard for most people?  Why is producing new advances in math basically always hard, even for extreme experts?

Cheers!
Nick Matzke
nick.matzkeATanu.edu.au


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EM Brainwaves VS Brain Wave (EEG)
The brain purportedly produces very weak EM waves.
EEG is a method of measuring electrical brain activity, it has classifications for the types of brain wave it can detect: Theta, Alpha, Beta, Gamma etc.
Are these the weak EM waves the brain produces?
If not what is the frequency range of the EM waves that the brain produces and does it vary depending on mental state?

I assume with EM you refer to electromagnetic?
You are right that the EEG (electroencephalogram) is a tiny signal. When about 50.000 neurons fire simultaneously, it possible to see a change in the measured signal. Typical EEG amplitudes are in the microvolt range.
Now, when the EEG is recorded, it is a function of time. You could for example collect data from 64 sensors, using a typical sampling frequency of 1000 Hz, and obtain 100000 samples from each sensor during a 100 second measurement.
So, what are alpha, beta, gamma, etc? When the recorded EEG signals are transformed into the frequency-domain (using the discrete Fourier transform), the signals become represented as a function of frequency. The obtained frequency range is half of the sampling frequency (according to the sampling theorem). So, with $f_s = 1 $ kHz you may observe frequencies from $0$ to $500$ Hz. Now, to make it easier to discuss about specific parts of the frequency range, they have been given names: delta refers to frequencies from 0-4 Hz, alpha to frequencies 7-15 Hz etc. So, these are just arbitrary names for different frequency ranges. (And yes, some processes do occur in quite exact ranges.)
So what effects what the EEG spectra will look like? Just about everything. From a short segment of data, it is rather impossible to say anything. This is why many paradigms do averaging: for example, you are presented a sound 100 times, and the repetitions are averaged to cancel uncorrelated noise. Have a look at the so called oddball paradigm, for example. Single-trial and continuous recording are also done today, but they are more difficult to analyse.
(Side note: since you asked about electromagnetic brain waves, have a look at magnetoencephalography too..)
For reference, see e.g. Luck (2005), An Introduction to the Event-related Potential Technique. Fourier transforms, sampling theorem, and signal averaging are well covered in Wikipedia.

It would be great if you added some references to your response!

It's important to clarify what an EEG machine measures. Electromagnetic waves are photons. An EEG does does not detect radiation. It detects magnetic fields by measuring an electrical current induced in the measuring device by the brain.
Electricity is the movement of electrons. Electromagnetic waves are photons of light. Magnetism a force which fills space from energy and matter with electrical charge.
EEG machines detect magnetism induced by action potentials. Magnetism is not a wave. It's a field.
Brain waves are an observation that action potentials may fire in a pattern which resembles a wave. There are also neurons which do not fire in wave like patterns. The wave here is an emergent property only.


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Null distribution of Blomberg's K
I've noticed different functions in different R libraries have different ways of assessing significance for Blomberg's K. For instance, picante's phylosignal looks at a distribution of PIC variance values from shuffled trait values to assess significance; when phytool's phylosig calculates a null distribution of Blomberg K values for shuffled traits.
What is the interpretative difference between the two and when should one approach be used over another? And what does it mean if the observed Blomberg's K is greater than 1 (traits less similar than expected under Brownian Motion model of evolution), but significantly greater (or less) than the null distribution of Blomberg's K-values?

The methods should be equivalent, given the same data. Using phylosignal's demo:
library("picante")
library("phytools")

set.seed(5)
randtree <- rcoal(20)
randtraits <- rTraitCont(randtree)

phylosignal(randtraits[randtree$tip.label],randtree)

phylosig(randtree, randtraits[randtree$tip.label], method="K",test=TRUE)

phylosignal returns:
         K PIC.variance.obs PIC.variance.rnd.mean PIC.variance.P PIC.variance.Z
1 1.430635          0.01147             0.4631411          0.001      -2.662701

and phylosig:
$K
[1] 1.430635

$P
[1] 0.001

Both give K = 1.430635 and an identical P-value.
Mathematically, it shouldn't matter if you shuffle the trait values or generate a null distribution of K. To get a null distribution for K, you have to shuffle something, and the tip values are probably being shuffled. You could check the code to be sure. An analogy is that, when doing a randomization for an ANOVA-like test, you can either shuffle the observed values or the group membership. Either way will give the same answer.
As for interpretation, Brownian motion is the simplest model for trait evolution, implying no direction, optima, rate changes, etc. K = 1 when the observed variation equals the expected variation. If K is greater than 1 then neighboring tips tend to resemble each other more than you would expect, suggesting a deviation from Brownian motion.


text:
Blomberg's K and branch length
Do different values of the smoothing parameter lambda for estimating the divergence times (in situ Sanderson 2002) will affect trait conservatism (e.g., Blomberg's K)?

I don't know if lambda for estimating divergence times works in the same way as it does for scaling internal tree nodes, but I'm going to assume it does given the context of your question.
My gut reaction was: of course it must because K is the ratio of observed to expected variance and tip variance is moderated in part by branch lengths. So if you change the node positions, the expected tip variance should also change.
A quick simulation shows that this appears to be true.
library("ape")
library("picante")
library("geiger")

set.seed(5)

tree <- rtree(30)
y <- rTraitCont(tree)

lambdas <- seq(1.0, 0.05, by = -0.05)
M <- data.frame(lambda = lambdas, k = numeric(length(lambdas)))

for (lambda in lambdas){
  tree_trans <- rescale(x = tree,
                        model = "lambda", lambda = lambda)
  M$k[M$lambda == lambda] <- phylosignal(y, tree_trans)$K
}

plot(k ~ lambda, data = M)

Generate a tree with 30 tips and generate random data along the branches. Then rescale the tree for a series of lambda values and calculate k for each lambda scaling.


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Sansevieria species specification needed
What are the botanical differences between the species S. parva and S. senegambica? Please highlight the main ones.
I have 2 groups of plants. One with label "Sansevieria dooneri" (a synonym of S. parva) and one with label "Sansevieria senegambica" and sadly both groups look awfully the same at first sight.

You could use this key to the genus. The differences between both species should become obvious when tracing back the decision tree. It seems that they can be distinguished mainly by the leaf size/shape of adult plants.

Thank you! I've searched in BHL, but didn't found this key. It would be useful. :)

authors: Атанас Танев


text:
Microsatellite shifts (peak calling) GeneMapper! Thesis help!
I'm a masters student attempting to conduct a parentage analysis on a population of fish for my thesis. My advisor and post-docs haven't been very helpful, so I need some help! I have dinucleotide microsatellite markers that I've run on a set of individuals.
I'm using GeneMapper 4.0 to score the alleles of said markers but something isn't making sense. My alleles are shifted to where they are not evenly distributed in their sizes. For example, at a given locus for one individual I have one allele peak at 152 while the other allele peak is at 161 (It's an obvious heterozygote).
This "shift" doesn't make sense considering my markers are dinucleotide and should be spaced 2 bp apart, right? So either 152 is actually 151/153 or 161 is actually 162/160. How can I score these and resolve this issue while keeping consistency for my analysis later? I see this shift everywhere and I've already ruled out contamination and I'm positive these peaks are real. Any pop gen people out there that have a clue what to do?
I've been stuck on this for weeks, no amount of web searching/paper reading helped.
Thanks!

@MikeTaylor
Thanks so much! I'm really glad to hear that. My peaks are beautful, but there are so many shifts that I'm not sure which way to score either allele. Should I make the odd even or the even odd? I'm using GeneMapper if you have any experience with that, I'd really appreciate some advice!
Thanks again!

You don't need to change the allele size. Is there a reason why you can't use the sizes as they are called by the software, regardless of odd or even size?

Here's another way to think about it. Assume the ancestral alleles all had even sizes but you don't know what the sizes were. An indel occurs after the repeat region. If a deletion, the size will decrease by one. If an insertion, the size will increase by one. In general, you can't tell whether the change was due to an insertion or deletion. That's why you shouldn't change allele size. You're changing data based on unverifiable (and unnecessary) assumptions.

@MikeTaylor Thank you SO much for your replies! I don't trust the automatic binning and calling of the peaks on the software only because the same allele is inconsistently called different sizes if it's shifted ever so slightly. I know I have to keep the same peak across all my samples called the same throughout, but the odd/even thing worried me for the sake of inconsistency. I'm not as hesitant now to call an even peak even when the rest are odd, so long as I call that peak that size consistently, I guess. Thank you for all your help Mike!

Your markers are probably fine, especially because you keep seeing the same allele in multiple individuals. Dinucleotide repeats do not always copy perfectly. More likely, remember that the primers you use to amplify your microsatellites bind outside of the actual repeat region. You could have an insertion/deletion in the region between the primers and the repeat region, changing your allele sizes from to even to odd (or vice versa).


text:
Focusing your attention on an area within your body, what effect does it make?
When I focus on tactile signals from a certain part of my body for a while (e.g. for one minute), this part of the body will usually become warmer. For example I can do that with a certain finger or with my palm, or with a certain spot on my forearm or on my leg, etc. Basically any part of the body.
From what I heard, when you focus on a spot within your body, the blood flow increases there. But what is the mechanism exactly? How does it happen? From what I found in neuroscience, sensory system only sends signals in one direction, from receptors to the brain. Attention is something happening within the cortex. What processes exactly take place when you focus on a certain body area? Is there a "response" signal from the brain to the area? How does it increase the blood flow?
My interest actually comes from my discovery that using my attention I can do surprising things within my body. I can relieve pain in most cases, it only takes 5-15 minutes of deep focusing. Once I successfully used this technique to relieve itching sensation from a minor skin inflammation on my leg, and after that the inflammation has gone away completely by the next morning. So I assume that focusing attention initiates certain processes in the body. I'm researching to find out what exactly these processes are.

Welcome to Biology.SE. Are you sure it is getting warmer? Did you rigorously measure it with a surface thermometer and comparing before and after focus? If not, then it is possible/likely that the question "why" is based on a false belief that the focus increase the temperature. Without an evidence for the claim, the question should be closed as based on a potentially false belief.

Hmmm ok I'll have to get a precision surface thermometer to make sure the temperature actually increases and not only my feeling of temperature.
Another my suggestion is that the blood flow increases because of deep relaxation of the muscles in the area.
If the temperature doesn't change though (which is still a subject to test), there is still a way to relieve pain by concentrating on the source of pain. How is that working at all? And does it only turn off the pain or also helps healing? Has there been any research on this subject?

You are all in the field of subjective experience here. If you are already convinced that concentrating on a wound helps reduce the uncomfortable feeling, then it probably will work for you (via the placebo effect). Most of the time people rather attempt to divert their mind from the pain to reduce the uncomfortable feeling. You might get better answers to your questions from a psychologist (see CognitiveScience.SE) than from a biologist.

Remi.b, psychologists focus on non-bodily aspects, I'd rather focus on the biology of the process here. Actually that's one of the main reasons I started studying neuroscience half a year ago.
So from your answers I would assume that your opinion on the subject is that nothing is happening in the body in response to the person's attention, right? Or at least nothing like this has been reliably observed/researched/proved.


text:
How do transitional forms survive without the full adaptation?
This may be an odd question, but this is one thing I've always wondered. How does a dragonfly ancestor with early structures that will one day become wings gain any benefit from these useless limbs that don't work?
It seems in an intermediary context like this, that the adaptation would almost fall under a category more along the lines of something vestigial--something defunct.
I understand the creature adapts with no understanding or control of the process, and it takes extremely long periods of time to see any significant changes from one anatomy to another, but it would seem that statistically that would work against the animal, not for it. It's not like the dragonfly goes from the land and water to having fancy new fully operational wings.
The longer a species is stuck with an unhelpful adaptation, the longer they would be exposed and at a disadvantage. There is one way in which I could see this happening, and that is a prolonged series of random mutation in favor a winged route for the insect with no real input from their environment.
We all know that mutation and variation drift (all of which are relatively random) are part of the evolutionary process, but it is often described in more concrete terms, and the creatures in between an ancestor and a descendant have been discovered and described, but often not very well to the public.
The mutant albino bear ancestor being better suited for arctic stealth and eventually becoming the polar bear and diverging from the brown bear is an example given in the new Cosmos that actually could happen overnight. The bear is born with the full adaptation.
Even if the bear weren't instantly white, fur slowly becoming lighter leading to better hiding capability, or having a thicker coat to help it keep warm makes more sense than the precursor to an entire limb like wings or a tail though.
I suppose that it's possible to say the that random mutation is the primary method of evolution, and the apparent improbability of plants and animals surviving with incomplete, underdeveloped adaptations can be answered by realizing that the plants and animals alive today are the cousins of countless species that actually weren't helped by the wings, and some of that is random too.
And with that in mind, it's slightly more obvious, but I'm wondering if there's more to it or something I'm overlooking.
I've struggled to find any discussion about this topic in the literature, which I may have simply missed because it often goes over my head. I'm hoping my conclusion is helpful.

It is always a little disturbing that some high rep users can close questions as duplicate without the opinion of other users! It surprises me when the question closes while I just wanted to cast a vote. Anyway, @RealisticWuxia, please have a look at the ost marked as duplicate and if it did not answer your question, please try to explain why the other post did not answer your question.


text:
Which method of seed dispersal is the most common among the seed plants?
The five most common methods of seed dispersal in the plant kingdom are:

wind (anemochory): tumbleweeds, dandelions, maples
animals:(epizoochory) externally - burs / (endozoochory) internally - fruits
water (hydrochory): aquatic-water lily/terrestrial-mangrove trees
gravity (barochory): apples, coconuts
ballistic (ballochory): impatiens, geraniums

source: https://en.wikipedia.org/wiki/Seed_dispersal
As far as which one of these five is the most common, this site says that animal dispersal is more common than wind but nothing in relation to the other methods listed above.  Each method likely is most common in it's most well suited niche, but which one is the most common (in the widest range of species) overall?

Clarification: When you say most common, do you mean: 1. Common to the widest range of species or 2. Common to the greatest number of individual plants? Say hypothetically you could have a billion different species with only ten individual plants each present, or you could have ten different species each with a billion individual plants.

Widest range of species.  Good catch.


text:
Is the Opah a warm blooded fish?
In 2015 many sources, including USA TODAY, Discover Magazine, and National Geographic, ran stories about the Opah fish (Lampris guttatus) being warm blooded.

Image Source: http://discovermagazine.com/2016/janfeb/58-meet-the-first-warmblooded-fish
Headline from USA TODAY 5/14/2015:  First warm-blooded fish identified

In a discovery that defies conventional biology, a big fish that lives
  deep in the Pacific Ocean has been found to be warm blooded, like
  humans, other mammals and birds.

Article from National Geographic 5/14/2015: Meet the Comical Opah, the Only Truly Warm-Blooded Fish

The opah’s wonderful nets are in its gills, and that makes all the
  difference. The blood vessels carrying warm blood from heart to gills
  flows next to those carrying cold blood from the gills to the rest of
  the body, warming them up. So, while a tuna or shark might isolate its
  warm muscles from the rest of its cold body, the opah flips this
  arrangement. It isolates the cold bits—the gills—from everything else.
This allows its huge pectoral muscles, which generate most of its
  heat, to continuously warm the rest of its body. It also keeps that
  heat with the help of thick layers of fat, which insulate the heart
  from the gills, and the pectoral muscles (which produce most of the
  animal’s heat) from the surrounding water.

According to the Merriam-Webster Dictionary warm blooded is defined as:

having warm blood; specifically : having a relatively high and
  constant internally regulated body temperature relatively independent
  of the surroundings

This definition seems to agree with the stories about the Opah fish being warm-blooded.  However, it seems different from humans, mammals, and birds which generate and maintain body heat when muscles are at rest too.  Are there different definitions of warm-bloodedness that would fit the Opah fish that is different from humans, mammals, and birds?

Did you say warm-blooded?
Despite the definition you cite from Merriam-Webstre Dictionnary, the term warm-blood is very unclear. The correct terms are endo-, exo-, poikilo- and homeo- therm. In short…
Source of heat

endo = inside
exo = outside

Variation in inside temperature

Poikilo = varies
homeo = does not vary

Please note, that these terms refer to extreme cases. There are organism which temperature are extremely constant (homeotherm), organisms which temperature are extremely variable (poikilotherm) and anything in between.
Any combination of these two axes exist. For example: If the temperature in the environment never varies you can be homeotherm without needing to be endotherm. Also, some organisms manage to keep a quasi constant body temperature via behavioural actions (moving to the sun when cold, going into the water when it's hot). A fun example (although debated to what I've heard) are the large dinosaurs that are thought to be homeotherms because their metabolism produce some heat and they are so large that they remain warm thanks to this heat source. However, they were probably not able to regulate actively their temperature. Therefore, I would tend to qualify dinosaurs as homeo-exo-therm but I wouldn't be surprised if someone prefers to call large dinosaur homeo-endo-therm individuals.
Opah fish
From what your second quote, it sounds like the Opah fish is endotherm. It is unclear from the quotes whether Opah fish are homeothermic.
Wegner et al. (2015) is a great read on the subject. Below is their abstract but I recommend reading the whole paper, it is easy to read and is very short (3 pages).

Endothermy (the metabolic production and retention of heat to warm body temperature above ambient) enhances physiological function, and whole-body endothermy generally sets mammals and birds apart from other animals. Here, we describe a whole-body form of endothermy in a fish, the opah (Lampris guttatus), that produces heat through the constant “flapping” of wing-like pectoral fins and minimizes heat loss through a series of counter-current heat exchangers within its gills. Unlike other fish, opah distribute warmed blood throughout the body, including to the heart, enhancing physiological performance and buffering internal organ function while foraging in the cold, nutrient-rich waters below the ocean thermocline.

In the whole, paper, I could not find a mention of how much variation in body temperature there is. They highlight however that the point of such adaptation is for foraging in cold waters suggesting that they would just make a boost of temperature in extreme cases but not necessarily actively maintained a constant temperature otherwise. I would tend to think that Opah fish are much more variable than birds or mammals. To reinforce my believes, in the wikipedia > Opah fish it is written (without reference unfortunately) "The opah is not homeothermic like birds and mammals".

FYI, this answer was written by partially recycling this other answer of mine.

IIRC, the opah is not unique.  Other large fish like tuna and swordfish also have various temperature-regulating mechanisms for keeping parts of their bodies (like eyes & brains) above ambient temperature: https://www.ncbi.nlm.nih.gov/pubmed/7079766

@jamesqf: That is correct.  However, from how I'm reading these articles, the opah is set apart because it heats it's entire body instead of just parts of its body.


text:
Does applying sugar to the tongue taste buds releave sugar withdrawal symptoms?
I found several online articles discussing sugar withdrawal symptoms that people experience after cutting back on large sugar intake.
http://healthyeating.sfgate.com/refined-sugar-withdrawal-symptoms-9911.html
http://www.growyouthful.com/remedy/sugar-addiction-recovery.php
One question that came to mind, was the following: If one experiences a sugar withdrawal, what happens if they apply sugar to the tongue, but do not digest it? Does that trick the brain into stopping the sugar withdrawal, or is it far more complicated than that?

It's not clear to me that "sugar withdrawal" is a real medical condition, despite what a newspaper and a site pushing low-carb diets might say.

Theoretically if you could somehow activate the G-protein-coupled receptors (GPCRs) corresponding to sweet stimuli without absorption of the sugar into the bloodstream than it may be possible to "trick" the brain. (See this review to learn more about how taste signaling works). However, the process of absorbing sugars into the blood stream begins in the mouth (see this question), so testing your idea would be nearly impossible.


text:
Why does DNA need to be pure for restriction enzymes to act on it?
My textbook states: “In order to cut the DNA with restriction enzymes, it needs to be in pure form, free from other macromolecules. Therefore DNA isolated from other chemicals of the protoplasm like carbohydrates, lipids and proteins via techniques of DNA isolation.”
My question is, why does DNA need to be alone? Won’t restriction enzymes work if there were a DNA molecule in a sugar solution? I understand that the DNA has to be freed from cell membranes and walls for restriction enzymes reach the DNA but how does the presence of other macromolecules hinder DNA’s digestion of a restriction enzyme?

AFAIK its not that other macromolecules hinder the activity of restriction enzymes, its just that we don't want other macromolecules in the solution, we want pure DNA for our job. I might be wrong though...

Some other macromolecules or other solutes may be present that could interfere with the affinity of the restriction enzyme. For example, there could be salts that denature or modify the conformation of the enzyme or inhibitors present that may interfere with the enzyme. Hope this helps.

Welcome to Biology.SE! Could you please add some references?

No Problem! https://www.promega.com/-/media/files/resources/protocols/technical-manuals/101/restriction-enzymes-protocol.pdf


text:
Help identify this Caribbean plant
Could you please help me identify this plant. I think it grew from some seeds we brought from Cuba (I might be mistaken though).
The plant in the picture is about 1.5 years old; it stands about 50 cm/20 in. tall. The leaf shown seems pretty large compared to the plant height, it's about 20 cm/8 in. long.
Leafs though appear shiny are rough to the touch on both sides, like very fine sandpaper.

The leafs remind me be a bit to a cocoa tree, but I am no expert on identification.

@Marzipanherz Thanks for the comment, I agree there is some similarity, but my tree's leaves seem wider and have those little teeth, while cocoa leaves don't seem to have teeth.

Finally I think I can answer my own question. Having spent the summer outside in full sun, the tree has produced flowers that helped us identify it.

It appears to be Cordia sebestena


text:
Can anyone help confirm this tiny insect larvae?
Can anyone help identify this insect larvae?
Found: UK, autumn, in a bed.
Size: less than 2mm

The bed was searched thoroughly and no others were found, but is there likely to be more of them?
Thanks!

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