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Restriction enzyme digestion
A circular plasmid of 10,000 base pairs (bp) is digested with two restriction enzymes, A and B.  This produces a 3000 bp and a 2000 bp bands when visualized on an agarose gel. When digested with one enzyme at a time, only one band is visible at 5000 bp.
If the first site for enzyme A (A1) is present at the 100th base, the order in which the remaining sites (A2, B1 and B2) are present is -
(A) 3100, 5100, 8100
(B) 8100, 3100, 5100
(C) 5100, 3100, 8100
(D) 8100, 5100,. 3100
NOTE: This is a Kishore Vaigyanik Protsahan Yojana 2014 exam (stream SX) Question. I really couldn't understand the diagram shown in the solution, and my teachers were of no help either. The diagram in the solution is:

Examine the effects of Enzyme A on its own.
Enzyme A performs two cuts that result in 2 fragments that are 5000bp long.
We know that the first cut is made at the 100th bp.  Therefore the second cut is made at the 5100th bp (A2).
You can stop there and determine that the answer is C.  C is the only answer that states A2 = 5100.


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How to get the average number of pairwise differences among populations?
I have genetic data in .structure and .vcf format (and can easily reach other formats with PGDSpider). The population of interest is structured and I would like to calculate the average number of pairwise differences (over a given window) between any pair of populations.
Is there an existing tool that would do it?

With relation to the other bioconductor question I would point you towards these packages;

VariantAnnotation: Provides functionality for reading and manipulating vcf files.
GenomicRanges: Provides functionality for creating genome intervals. Also provides overlap functions for calculating overlaps between various ranges.
rtracklayer: Allows you to easily change formats between different biological file formats.
AnnotationHub: Makes many common and uncommon annotation files available in the R terminal in various formats such as TxDb, OrgDb etc. etc.

Here's a tutorial very similar to what you are asking for. It utilises some of the packages mentioned above. Principally, AnnotationHub, GenomicRanges and VariantAnnotation.
If you want the manual of these packages, they are available on the linked pages.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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How well understood are the long-term effects of nuclear radiation?
Sometimes, when people are concerned about radiation, it is not because it is precisely quantified how dangerous it is, but because we don't know how dangerous it is.
How well understood are the long-term effects of nuclear radiation, for example on cancer? (As opposed to short-term effects such as acute radiation sickness, which is easy to quantify)
I assume this can be researched from an epidemiological approach (Wikipedia mentions an epidemiological study on the atomic bombing of Hiroshima and Nagasaki, for example), and also from an experimental approach.
Also, is the effects of radiation easy to understand, or difficult? My assumption is that something physical, like radioactivity, would be easier to understand than the effects of more complicated things, like complicated organic chemicals or obesity.

Related question, but not quite what I'm asking: http://biology.stackexchange.com/questions/14377/radiation-and-safe-dose

The three major nuclear incidents I can think of are the Japanese atomic bomb attacks, the Chernobyl disaster, and Fukushima disaster. Of course other nuclear incidents have occurred, but usually give much higher doses to far fewer people.
Many studies have been done on the survivors from the atomic bomb attacks, and increased rates of cancer have been the strongest conclusion. This review article looks at those studies for both cancer and non-cancer effects. Leukemia is the most well known cancer to be caused by radiation, and excess leukemia was discovered in bomb survivors within 5 years of the attacks. Rates of most solid tumors had increased by 10 years after the attacks. However "Even 55 years after the
bombings over 40% of the Life Span Study cohort remain alive", indicating that the amount of radiation most people were exposed to wasn't enough to kill them. Here is another article on atomic bomb survivors.
The Chernobyl accident was a very different type of exposure, but many people were exposed to radioactive materials. Immediately after the disaster, the "liquidators" received high doses of radiation while cleaning up the site and building the containment structures, but very few have died from radiation exposure. While the environment around the power plant did suffer in the years after the accident, after the humans moved away the environment has greatly improved. Thyroid cancer rates increased due to Iodine-131 exposure, especially among those exposed as children, but rates were still low.
 Yellow = adults Blue = Adolescents Red = Children.
It is too soon to draw many conclusions about the Fukushima accident, but some studies (7, 8) have tried to predict the number of cancer cases that will be caused by it. In general the rates are expected to be low, with far fewer deaths than were caused by the earthquake and tsunami that caused the accident.
A few instances exposed small numbers of people to very high doses, and are interesting from a radiation safety veiwpoint. The infamous "Demon Core" killed 2 scientists in separate accidents while handling the core. The Goiania incident involved men breaking into an old hospital and stealing a radiation source without realizing what it was. They broke the source open and passed the radioactive material around because it looked cool, resulting in several deaths due to acute radiation sickness.
While radiation can be dangerous, with proper precautions we can avoid accidents and disasters. Remember that Chernobyl was a poorly designed Soviet reactor, and that Fukushima was a 50 year old plant that needed both a magnitude 9 earthquake and a 30 foot wave to disable it. Modern nuclear plants can be built safely and provide clean electricity for many decades, and if they are breeder reactors can recycle the used fuel to reduce both the amount and half-life of the material, making storage easier.

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With humans, is being transgender innate, or caused by social factors?
In humans, is being transgender something that is innate, or is it caused (or made more likely) by social factors such as their political beliefs, their religious views or their social environment?

Something interesting  http://www.ncbi.nlm.nih.gov/m/pubmed/25667367

Transgender is a collective name for a wide variety of cases, the hormonal changes occurs in embryonic stage result in transgender case at birth time itself, for most other cases it is occurred in the puberty period.


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Why is GTP, rather than ATP, used in nuclear transport?
Why is GTP used for nuclear transport and not ATP, given that ATP hydrolysis is used to drive most cellular energonic reactions?

Welcome to Biology SE! This appears to be a homework question. Homework questions are off-topic on our site unless you have shown your attempt at an answer. For more information see our homework policy.

Would be very interesting to know, if there was some systems-biology reason (that would extend beyond a superficial answer such as the most prominent nuclear transport proteins using using GTP). (note: ATP can be required for some aspects of nuclear transport, in particular for RNA)

@vkehayas  I think this is an open question in biochemistry, and as such not likely homework (or else a very tricky assignment :)  To my knowledge at least, it is not understood why different nucleotides are preferred as energy source by different systems -- if indeed there is any advantage to this scheme at all.  Protein synthesis and gluconeogenesis (PEPCK) also uses GTP, btw.

@Roland I am aware that this is not a resolved issue. I was attempting to nudge the OP to give us some background on why this question is interesting to them and what research they have done already.

I have edited the question slightly and removed the homework tag as I don't think it relevant. (I have gone on to provide an answer of sorts.)

Disclaimer
Although this question appears to be either unclear or unanswerable (or both), and shows no evidence of research on the poster’s part, I have chosen to address one aspect of it to emphasize a general concept. This, despite the fact that my knowledge of nuclear transport processes is minimal.
Brief Answer
GTP, rather than ATP, is used for nuclear–cytoplasmic transport via importins and exportins, because this process involves one of a large family of ‘G proteins’ that — as their name implies — operate through the use of GTP. Whereas ATP is generally used to drive endergonic molecular reactions, the hydrolysis of GTP in G-protein cycles can be thought as a device to terminate a molecular process. Whether G proteins adopted GTP rather than ATP merely by chance or for a biological reason is a matter of speculation.
NTP hydrolysis — for fun or profit?
It would appear that the question relates to protein-transporting ‘importins and exportins’, which I learn from the Wikipedia article on nuclear transport are regulated by the small G protein, Ran. When complexed to GTP, Ran facilitates the export of proteins by exportins, a process that is terminated by hydrolysis of GTP to GDP. The GDP-bound form facilitates the import of proteins by importins, a process that is terminated by GTP displacing the GDP.
So if we consider the role of the hydrolysis of the nucleotide triphosphate — here GTP — it is clearly not to supply thermodynamic energy for an endergonic process such as muscle contraction, light generation or a chemical reaction with a +ve ΔG:

Rather, it is to produce a conformational change in a protein which allows the termination of a process. This termination is generally through the GDP-bound form of the G protein (grey) interacting with some other protein (black):

This diagram is deliberately simplistic so that the general features of G-protein action can be seen. However, I think it illustrates the same point made in Berg et al. Section 15.6. Other examples are signal transduction of hormone action via cyclic AMP and binding of aminoacyl-tRNA to the ribosome.
Why do G proteins use GTP?
This ‘choice’ of GTP in the original ancestral G protein could have been mere chance, that was subsequently reflected in other G proteins that arose through gene duplication and divergence. That would imply that, at least, it was not disadvantageous. Or as the oldest G proteins are perhaps those involved in protein biosynthesis — a process still catalysed by a ribozyme — the choice of GTP might have reflected an RNA base-pairing interaction in the ‘RNA world’.
Alternatively one might suggest a biological rationale for separating two types of energy-requiring processes — perhaps by regulation of the enzyme that catalyses the conversion of ATP to GTP, dinucleoside-phosphate kinase. However I am not aware of any evidence to support this idea.
Hydrolysis of GTP in other contexts
As mentioned in a comment by @Roland, there are instances where GTP is used to drive endergonic reactions (phosphoenolpyruvate carboxykinase) in a manner analogous to the use of ATP, but this is quite different from hydrolysis of GTP in G proteins. I do not believe that any convincing rationale for this has been propounded, nor for the similar exceptional use of UTP in glycogen synthesis and CTP in phospholipid synthesis. This question has been discussed in another post.


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The reproduction patterns of fungi: what’s the difference between them?
I am going to take TOEFL, and am getting perplexed by the difference between cell division and budding and fragmentation of fungi.
Those three terms seem like all the same all to me, so could anyone teach me fundamentally how they differ from each other?

Cell division
Cell division is the process by which one cell becomes two. If we consider multicellular fungi, cell division happens whenever the fungi grows by one more cell. Cell division allows the growth of the organism. Cell division does not necessarily contribute into making a new multicellular organism.
Fragmentation
Fragmentation is a type of non-sexual reproduction. An organism gets split ("intentionally" or "unintentionally") and the different fragments develop into independent mature organisms. Sometimes, on fragment is small than the other one, so that one fragment can be seen as the "parent" and the other one as the "offspring".
Budding
Budding is a type of reproduction by fragmentation, where the splitting occurs due to a specific developmental pathway and not through some external environmental cause (such as getting cut in two by a researcher's knife, a falling tree or the bite of a predator). In other words, in budding, the splitting is "intentional".
More information

wikipedia > Cell Division
wikipedia > Fragmentation (reproduction)

P.S. You won't need to know this biology stuff to get a good score at your TOEFL. On an unrelated personal note, I found this exam particularly unpleasant when I had to take it. Especially when we have to converse with a microphone while somehow ignoring the accents and english mistakes your neighbours are making while talking into their respective microphones. Good luck for your exam by the way :)

I really appreciate your answer. Although you told me these knowledge are useless, nonetheless, these distinction from the textbook, you native speakers made. Thank you very much and much appreciation.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Is this an imprint of a fossil?
I found this stone in the arizona desert. Sort of far from humans on the side of a Butte

Could you please add the size if that stone/imprint?

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How does shortage of oxygen halt the NADH dehydrogenase complex?
I understand that in the absence of oxygen the functioning of cytochrome c oxidase stops because it is its substrate. However I don’t understand how stopping cytochrome c oxidase also stops the previous complex (the NADH dehydrogenase complex).

At a basic level this is quite straightforward if you look at an old-fashioned simplified diagram of the electron transport chain, such as the one below that I filched from the web.

If oxygen is absent then there will be a build up of the reduced forms of each cytochrome. Starting from the bottom, in the absence of oxygen cytochrome a is not reoxidized; if there is no oxidized cytochrome a then reduced cytochrome c cannot be reoxidized, and if there is no oxidized cytochrome c then cytochrome b cannot be reoxidized. The latter is the substrate of the NADH dehydrogenase complex — NADH-Coenzyme Q reductase in the figure — so this reaction stops for want of oxidised cytochrome b.
(Years ago I demonstrated on a standard undergraduate laboratory class using rat liver (or perhaps beef liver) mitochondria, where you inhibited different stages and detected the reduced forms by their colours in the visible spectrum.)


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What triggers the switch between aerobic and anaerobic respiration?
I understand that when there is a shortage of oxygen cells convert the pyruvic acid from glycolysis to lactic acid to regenerate NAD+. What I don’t understand is how they switch to anaerobic metabolism occurs. Is there a certain chemical message that triggers this?

Are you referring to human cells?

Yes, the respiration in human being cells.

The simplest method of control of metabolism is by substrate concentration. So if the concentration of NADH and pyruvate is low, lactate dehydrogenase cannot function. When they build up it can and will.

The situation is more complicated than this, because pyruvate will only build up if it is not converted to acetyl CoA by the pyruvate dehydrogenase complex (see Berg et al. section 17.1.1):

Although the overall reaction is oxidative, and ultimately requires NAD+, the latter is not directly involved in the initial irreversible reaction. It is presumably for this reason that the reaction is also controlled, either allosterically (in bacteria) or by phosphorylation (in mammals). In either case the regulators are the small molecules the concentration of which is altered by the lack of oxygen: NAD+/NADH and ATP/ADP. The figure below and its legend is also from Berg et al. (section 17.2.1) — available through NCBI Bookshelf.

[The complex is inhibited by its immediate products, NADH and acetyl CoA. The pyruvate dehydrogenase component is also regulated by covalent modification. A specific kinase phosphorylates and inactivates pyruvate dehydrogenase, and a phosphatase actives the dehydrogenase by removing the phosphoryl (group). The kinase and the phosphatase also are highly regulated enzymes.]
The actual situation is quite complex and this is something of a simplification.

Thanks, can you give me the link so i could read more about the over all change that will make lactate dehydrogenase function?

@kgemp Done. You can only search (not browse) books on the NCBI bookshelf, but the two links I have given should provide a reasonable starting point.


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Why are red blood cells not attacked by NK cells?
All cells containing a nucleus present MHC-I, while some specialized cells present MHC-II in addition to that. Since erythrocytes lack any MHC why do natural killer cells not attack them?
It is my understanding that any cell which starts presenting foreign peptides on MHC-I will undergo apoptosis after Th finds them, or if they stop presenting anything at all, they will be eliminated by the NKs.
So what mechanism prevents erythrocytes from being destroyed by the immune system?

Too bad the duplicate has an answer, such as it is, only in a comment under one of the three "Answers".

I'm voting to reopen. The linked question is not a duplicate and doesn't have a suitable answer for this specific question.

The question states, not quite correctly, that "if they stop presenting anything at all, they will be eliminated by the NKs".  In fact, simply not having MHC is not enough to trigger destruction by NK cells.
NKs have a two-part trigger. Part 1 is an activator; part 2 is a suppressor. When the activator is present, and the suppressor is not present, then NK cells will destroy the target.
The suppressor is typically MHC class I, which is present on almost all normal cells. That means that NK cells will not destroy normal cells. There are many different activators, but most normal cells have at least one of the activators also present. That means that NKs are normally primed to destroy, but refrain from destruction because they also sense the suppressor.
With that explanation, it should be clear why RBC are not destroyed by NK cells. Even though they lack the suppressor, they also lack any activators. Since there are no activating signals, the NKs don't need to be also suppressed, so the lack of MHC doesn't lead to an attack.
Sample references:

Two-signal requirement for activation and effector function of natural killer cell response to allogeneic tumor cells
Controlling NK Cell Responses: Integration of Signals for Activation and Inhibition

It's also possible that RBC further protect themselves by showing a "marker of self" on their surface (Role of CD47 as a Marker of
Self on Red Blood Cells) but that doesn't change the important point about NKs mode of activation.


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Hydrophobic interactions in the helix-turn-helix
This slide states that the second helix works to stablize the configuration of the two helixes via hydrophobic interactions. What exactly is this hydrophobic interaction? In other words, what molecular interaction does the second helix have with the recognition helix?

Welcome to SE Biology. The slide does not say anything about "reaction" which involves a change in covalent chemical bonding, but "hydrophobic interactions" which are described here. I have edited your question to fix this.

To quote Sir Max Perutz, in general, the insides of proteins tend to be "waxy", while the outsides of soluble proteins tend to be "soapy."  Those two alpha helices are interacting in a space that is energetically unfavourable for a polar solvent, like water.  Since the outside of the DNA double helix tends to be highly charged, and the edges of the stacked base pairs also have H-bond acceptors and donors, the portion of the alpha helix that interacts with the DNA sequence, will also contain charged amino acid side chains.
In contrast, the portion of the alpha helix that faces inwards, towards the interior of the protein, will have largely non-polar side chains.


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How to determine if the amount of manganese chloride will change neural resting potential
If I am treating an organism in MnCl2 dissolved in water, how do I determine if the amount of Cl (in MnCl2) will change the neural resting potential Oor if it will influence motoneurons?

For theoretical calculations with other ions, you need to know the concentration and permeability of each of the major ions inside and outside the cell, both with and without the added substance (in your case MnCl2), and then use the Goldman equation/GHK equation to calculate resting potential before and after. Approximations would probably be sufficient.
However, chloride can be a bit complicated because the intracellular chloride concentration can fluctuate with extracellular chloride moreso than the other major ions. Therefore, depending on the sensitivity of your experiment, you may need to perform whole-cell patch clamp recordings to measure the resting potential directly.
If the change in chloride is a small percentage of the total, you can probably consider the influence to be negligible.

As the previous answer states you will need to know, or estimate, the concentration of ions and their relative permeability.
Knowing these values you can estimate the change using the following link:
http://www.physiologyweb.com/calculators/ghk_equation_calculator.html
Do you only have MnCl2 in your solution? Are there any other ions?

My solution consists of MnCl2 in water

Then you will greatly affect the resting potential. Probably since you don't have potassium or sodium outside you'll  generate an hyperpolarization.


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Have there been any "chopstick gene" mistakes in genetics?
I've heard of the "chopstick gene" fallacy - wrongly assuming an association between genetics and some characteristic, confounded by non-genetic factors.
Has this fallacy happened in real life?
I'm not really interested in cases deliberately focusing on race, where people have argued that there's an innate difference between people of different races based on certain genetic differences, such as the putative "warrior gene" ("warrior allele"?) being described as more common in Maori people. As far as I can tell, the "chopstick gene" isn't about arguing that Asian people are better with chopsticks because of genetic differences between Asians and non-Asians.
I'm more interested in research that was done in good faith, which ignored the possibility of genetic variations having different frequencies in different groups, that produced erroneous conclusions.

If something is a fallacy, then how, by definition, could it actually have occurred? If you are asking if there are examples of genetic differences that separates ethnicities based on physically performable traits, then there are some examples. Sherpa's are able to live normally a very high altitudes and is related to genetic traits that were selected for because they were an isolated population in a selective environment. http://news.sciencemag.org/archaeology/2014/07/tibetans-inherited-high-altitude-gene-ancient-human

@AMR I was thinking of a scenario where a scientist publishes something, then either they or someone else notices this problem.

Have a look at this time article from a couple years ago.
A concept that you should think about is nature vs nurture. You can think of nature (your genetics) as controlling part of the potential of what you could become (for example, many long distance athletes have genetics that are beneficial for their sport) where as nurture encapsulates the environment that you grow up in (a nutritionally deficient child will not reach maximum potential height that you might predict based on genetics alone).
When scientists are studying a gene in relation to a phenotype, they statistical methods to determine how much a genotype contributes to a phenotype. This process would minimize these types of fallacies since different alleles in different populations would be considered. However, sampling biases can occur and most human variation studies are done on people of european, asian, and african descent.


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Why sudden stresses cause stuttering and/or other impairs in children?
The question is simple: Why sudden stresses cause stuttering and/or other temporary or permanent impairs in children (and even adults)?

The stuttering issue has an answer on http://cogsci.stackexchange.com/questions/8895/why-do-some-people-stutter-only-when-they-are-nervous/8911#8911.


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Determining a patients biological age?
I am looking for an algorithm that shows the exact coefficients some variables that have on a hospital patient's chronological age versus their biological age.
I understand a lot of the variables that go into determining ones biological age (i.e. Blood pressure, diet, family history of disease, obesity etc.) but not the amount of impact that it has on the actual scoring of their age.
I have found many sites that will calculate it, however I need the actual variable coefficients and influence in order to produce a proper score for thousands of patient records.
Thanks in advance for your input!

How is a "biological age" defined? It doesn't sound like it would have a precise definition, but maybe I am ignorant.

Biological age is considered one's "real" age based on how their body is behaving versus someones actual age.

So for example. A 65 year old who still works out, and eats healthy and is of normal weight has a biological age of 55.

There is no rigorous standard for "biological age".  It makes no sense.  A fit 65 year old might have a heart that, in some tests, performs as well as the "average" 55 year old, but that's just one organ, and one set of tests.

As the definition of biological age is very ambiguous, I propose that to generate an algorithm, you first need to create a quantifiable definition. I submit:

Biological age is a measure indicating what portion of one's calculated life expectancy is already expended, adjusted proportionately for the average life expectancy of their major demographic.

Wow, that's a mouthful! So, let's break it down.
Life expectancy is calculated :

Ascertain a person's major demographic (Geographic residence, Race, Gender and Generation).
Find the average life span of that demographic.

This is negligibly speculative as a living person's Generation has not yet fully perished
Statistical outliers, such as infant mortality, are generally excluded from this calculation

Adjust for known major factors that have accepted statistical impact.eg:

Lifestyle
Current medical conditions
medical history

Average Life expectancy of subject's demographic was calculated in #2 above.

So, now let's throw in some sample numbers.
Statistical Facts: (totally made up)

Caucasian males living in the France, born in the 1970s have an average life span of 72 years.
Exercising 30 minutes or more daily increases life expectancy 6 years
Smoking decreases life expectancy 7 years
Not smoking increases life expectancy 2 yearsHold on a second?! Wouldn't not smoking already be accounted for in the "Smoking..." section? Well, no, because our demographic sample are all "unknown" so having specific knowledge would statistically change the results in either direction
Heart Disease decreases life expectancy 8 years
Devout religious affiliation increases life expectancy 6 years.
Family history of diabetes decreases life expectancy 2 years.

Two subjects both Caucasian, french males born in 1974 (40 years old chronologically):Their mom's actually shared a labor and delivery room!

Beavis - known: Smoker with heart disease.
Butthead - known: Devout Buddhist, very athletic, non smoker with a family history of diabetes
Beavis' life expectancy is 57 (72-7-8)Butthead's life expectancy is 84 (72+6+2+6-2)
Beavis has expended 70.2% (40/57) of his life expectancyButthead has expended 47.6% (40/84) of his life expectancy
Despite sharing a birthday:Bevis' biological age is 50.5 years (.702*72)Butthead's biological age is 34.3 years (.476*72)

Note: It's almost 6 hours past my bedtime, so please excuse any stupid mistakes or miscalculations.  The general concepts are what is important

From the way you phrased your question, it sounds like you are doing this programmatically.  As that was not explicitly stated I reserved this suggestion for the comments:  I would recommend storing the statistical factors with both true and false adjustment values (like we did smoking above) as, inherently, any factor's inverse will also have an impact. Then when a factor is unknown you just don't apply any adjustment. Also, in the unlikely event where a factor's inverse is negligible or unknown you can just store an adjustment value of zero.

The problem with calculations like this is that the time-spans (smoking lets you die 7 years earlier) are based on population wide statistics. They include healthy, 95 year old smokers, which smoke 2 packs a day as well as 35 year old smoking lung cancer patients. What you can derive from this are general recommendations, but hardly specific calculations, as they have to include a lot of personal factors which are unknown.

@Chris Agreed wholeheartedly. This flaw is inherent in statistics universally and is why we use non-precise titles like "life expectation". Additionally, using the following statement highlights the accepted variability:
"Adjust for known, major factors that have accepted statistical impact."  There are literally infinite variables in play, some may have nanoseconds in actual lifespan impact some could eliminate a teenage athlete mid stride. An infinitesimal fraction of these variables are known, a smaller fraction are studied and the minority of those have an accepted statistical impact.

Thank you for your input @trex005, I have taken your factors and took a adapted approach with my data variables and took some additional factors from the cdc life tables as well as Moran E. Levine from his article: Modeling the Rate of Senescence: "Can Estimated Biological Age Predict Mortality More Accurately Than Chronological Age?" and from L. Galzigna and M. Cecchettin their article "a simple procedure for calculating biological age."


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How does the number of chromosomes evolve through generations?
Mitosis is a complex mechanism that, through mutations and crossover, determines how a chromosome is composed. But at that point, the number of chromosomes is already determined: how can this number evolve through generations? What mechanism is involved?

A mutation is a general term referring to any alteration of a nucleotidic sequence. It includes small mutations like indels (insertion or deletion of a single nucleotide) and substitutions, or bigger mutations such as e.g. chromosome fusions, whole chromosome duplications, Robertsonian translocation, whole genome duplications and gene deletions. Some of these bigger mutations can affect the number of chromosomes (and ploidy number).
Such of these mutations can typically be caused by the non-disjunction of homologous chromosomes during meiosis.
Most of these mutations are deleterious but some aren't and might eventually fix (fixation = reach a frequency of 1.0) in the population.
A very common example of such mutations in humans is the mutation that is causing the Down syndrome.

Note that I mainly recycled this answer of mine but as the question is phrased in a much more pleasant way, I did not want to mark it as a duplicate.

your answer is interesting, thanks. Do you have some source you can suggest to read?

It appears to me that very introductory source of information tend to neglect those types of "big mutations" (e.g. evo101) and after that you're only left with slightly more advanced source such as a good textbook or directly in the scientific literature....

... I am not sure what to point to like that. I would advice you to just have a look at the wikipedia entries of gene duplication, Robertsionian translocation and others and go into the scientific literature (you can use GoogleScholar to search in the scientific literature) if you have a more accurate, clearly defined question about it.

Sure, but when a mutation reduces - in one individual only - the number of chromosomes like it happened some time ago for humans (chr. 2 fusion), how can it pass into the germ line with a population having one mutant only and all other indiviuals with a different karyotype. Pathenogenesis being ruled out.


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Are mutations random?
The following claim

Mutations are random

or just the use of the expression

Random mutations

are very common among lay people.
The claim is very common among lay people. The claim is often made by OPs (such as here, here for example) but also in answers (such as here for example).

What does it mean exactly?
Are mutations really random?

A bit of a straw horse? However I have taken it by the horns (biology was never my strong suit) and provided an answer that explores a rather different aspect from you.

genetic recombinations are fairly random, but mammals have more efficient mutations than birds, owing to their 2x times bigger genomes. when the chromosomes devide and combine, segments shuffle around a bit like when you mix up colored socks in a draw. the mutations are carefully balanced, not random at at all, as in randomly growing a nose on your elbow.

@comprehensible No offense but outside the fact that birds have smaller genome than mammals, I don't think anything from your comment makes any sense.

@David You're right! Thanks for that. I've removed my link to wikipedia from my question (and my previous comment). I would not think anyone would argue that the claim is not a common one but I did quickly link to three SE posts who talk about "random mutations".

OK. I've deleted my comments on Wiki as they are now redundant.

Short answer
The claim is unclear but is essentially misleading and wrong. However, IMO, for lay people, it is a good approximation to just think that mutations are random!
Here, on Understanding evolution is a great source of information on what it means to say that mutations are random
Long answer
What is a mutation?
A mutation is an alteration of the DNA sequence. There are different types of mutations, consider for example the following Single Nucleotide Polymorphism (SNP)
Original Sequence

ATTATCTG

Sequence after mutation of the 3rd nucleotide

ATGATCTG

Note that mutations can have much more drastic effects such as the duplication of a very long sequence of DNA for example.
You might want to have a look at What is the definition of a mutation? and eventually Effect of mutation on phenotype.
What can be random?
A variable can be random. So is the term mutation a variable?
IS "MUTATION" A VARIABLE
Consider first this discussion about the term house. You can measure the height of the house or the number of windows and both the height of the house and the number of windows so that both the number of windows and the house of houses are variables but house itself is not a variable.
A mutation is an event but, just like with the house, there is no obvious number associated with the term mutations. The number of mutations occurring in a reproductive event is a variable. The effect size on fitness of a mutation is a variable. So claiming that mutations are random is unclear as we don't know what property of the mutation the claim is referring to.
WHAT IS RANDOM
Fully discussing the concept of randomness will require doing quite a bit of math and philosophy. I will not attempt to do so and will intentionally make some oversimplifications here.
The concept of randomness only makes sense if we formalize a model. The outcome of flipping a coing may seem random to you but this is true only if you assume you don't know the forces at play on the coin (the movement of the thumb, the speed of the wind, etc...). A physicist would be happy to consider a coin flip being a perfectly deterministic (deterministic = not random) process.
If a process is deterministic, it means that for a given input there is a single possible output. If a process is stochastic, then there are several (potentially an infinite number) of possible outputs. Now, stochastic does not mean fair or uniformly distributed and therefore a process can be stochastic and yet we can have some predictive power on what range of values the outcome will likely take. For example a weighted die/dice may turn up certain numbers more often, but it's still random, it's just that the distribution of expected outcomes is not uniform.
So, to talk about the claim mutations are random, ideally one would need to fully specify a model of consideration.
RANDOM AS DIRECTIONLESS
Often by random, people mean "directionless" (or "fair"). This is clearly not what the term random means but I will still discuss the case of "direction" (or "fairness") as it is often what people mean. If a mutation is directionless, it means that this mutation is not more likely to increase the value of the variable than to decrease it. For example, if the variable of interest is the height of the individual, assuming that mutations are truly directionless, a mutation is not more likely to increase the height of an individual than to reduce it.
Is the number of mutations random?
VARIATION IN MUTATION RATE
The mutation rate varies dramatically among species and along genomes roughly speaking from a rate of $10^{−2}$ to a rate of $10^{-10}$ mutation per nucleotide. For example microsatellites (repeated sequences) are highly mutable.
EFFECTS OF NEARBY SITES
Note also that the probability of a given nucleotide to mutate depends also on the exact nucleotides that are around it (Rob Ness; Personal communication).
PLASTICITY FOR MUTATION RATE
The mutation rate is also a plastic trait (and is therefore under selection) in some species (of plants and bacteria typically) (Chary et al. 1993; Bjedov et al. 2003). The environment affects the mutation rate and the environment can be chosen by some species (avoidance) or even constructed by others (niche construction).
AGE OF THE PARENTS
In multicellular organisms, the age of the father correlates with the number of new transmitted mutations as well. See the post Gender and age-specific mutation rate in plants (and its references) for more information.
EPIGENETICS
Epigenetic changes (do not concern all species) can also affect the mutation rate and even influence what new nucleotide the old nucleotide will be mutated into (with a given probability).
CONCLUSION
Many things affect the mutation rate. However, the exact number of new mutations an offspring will carry is not perfectly deterministic.
Type of mutations
Mutations are more likely to be transitions than transversions. But again, it is not a perfectly deterministic process.
Effect of mutations on fitness
DISTRIBUTION OF FITNESS EFFECTS
Different mutations have different effects on fitness. We talk about the Distribution of Fitness Effects (DFE).
The DFE varies from one sequence to another. In conserved sequences, mutations tend to have a higher impact on fitness.
ARE MUTATION EFFECTS ON THE FITNESS DIRECTIONLESS?
No, most mutations are deleterious or neutral. Only few mutations are beneficial.
Effect of mutations on the phenotype
Again, some phenotypes are more sensitive to new mutations than others. The increase in phenotypic variance due to mutation at every generation is called the mutational variance.
ARE MUTATION EFFECTS ON THE PHENOTYPE DIRECTIONLESS?
It can be the case, but it is not necessarily true. When mutations are not directionless, we talk about mutation bias (see for example Eyre-Walker 1998, Harr and Schloterrer 2000 or Shah et al. 2010).
Conclusion
Yes, there is some randomness in many of the variables associated with mutation events. However, it would be wrong to think that we have no predictive abilities in the number of mutations or effect of mutations, it would be wrong to think that a mutation is as likely to increase fitness than decrease it and it could be wrong to think that a mutation is as likely to increase a phenotypic trait than decreasing it.
Related posts

Are evolutionary mutations spontaneous?
What are the major causes of mutations in DNA?

Source of information in evolutionary biology
Understanding Evolution by Uc Berkeley is a good, short and very introductory course to evolutionary biology.

I think you could add to your discussion of "what is random" some recognition that "random" does not necessarily mean "uniformly random": a weighted die/dice may turn up certain numbers more often, but it's still random, it's just that the distribution of expected outcomes is not uniform. You touch on this later but I think it's a really key part of what "random" means to a biologist/statistician versus what it means to a 'random' individual.

@BryanKrause I added a paragraph (3rd paragraph) including a sentence form your comment. Please feel free to edit if you can improve that. I agree with you it is important to clarify this point to the readers. Thanks

It would be more considerate to other answers if you could set out your answer using a smaller size of type for your headings (and perhaps fewer of them). Try using caps or italics at the default size in your hierarchy instead. As it is I and others have to scroll more than three screens-full on my laptop to get to the next answer (admittedly two screens-full and my own).

@David I'm sorry your laptop has a small screen! Reproaching someone of not being considerate because his/her answer is too visible feels rather strange. Also, changing the title sizes won't change much to the overall length of the answer unfortunately. But anyway, I did change all titles. It rather decrease the quality of the format I think.

Thank you. The quality of the format is limited by the extent to which one can manipulate the underlying HTML. Even on my 27in iMac your answer still takes up over two screens. But very large type is ugly and not what you would see in a professionally printed document.

The claim is unclear but is essentially misleading and wrong. - No, if something is unclear to you, it is not misleading and wrong.  Only clear things can be misleading and wrong.

Mutation is an event causing an alteration in the DNA sequence where the mutation occurred.  - It's nonsense. It means: Mutation is an event causing an alteration in the DNA sequence where the event causing an alteration in the DNA sequence occurred. //// An event causing an alteration in the DNA sequence is not the same as mutation.

@user1425 Thanks! Indeed the phrasing was wrong. I am not sure I fully understand what your issue with it was but I changed the phrasing to something that, to me at least, seems correct.

What has been meant historically by random mutation?
I am not an evolutionary biologist, so I was surprised that the poster — whom I believe is — does not discuss the origin of the term. As original conceived ‘mutation’ could have had nothing to do with DNA, as DNA was not established as the genetic material until the Avery experiment in 1943. It is more reasonable to thinkg that a mutation was thought of as some unspecified heritable change in the genetic make-up of an organism.
I did a Google Books ngram search for “random mutation” with the result shown below:

Perusing the books that came up, I found two snippets from the 1907 Proceedings of the American Catholic Philosophical Association:

The pure chance that causes mutation, we are told…

and

[…de]termined in advance. From which random mutation can be distin[guished]

Unfortunately, more of the context is not available there (the completions in the second snippet are my own deduction) but is evident that ‘random’ is being used — not in a strict mathematical or statistical sense — but in opposition to ‘determined’. It was, of course, all to do with evolution and religion. Indeed that type of concept of ‘random’ has a hard scientific pedigree: Einstein, albeit in another context, maintained that “He [God] is not playing at dice”. (Original German: Jedenfalls bin ich überzeugt, daß der nicht würfelt.)
Another example is a biology text book from 1937:

To some biologists these evolutionary trends cannot readily be fitted
  into a random mutation-natural selection explanation of evolution.
  Consequently, to account for them some of these biologists have
  suggested orthogenesis hypotheses, ..

And although I had never met the term orthogenesis, the Wikipedia entry suggests it is a religious or quasi-religious antithesis to mutation and random selection in which evolution is directed by some (supernatural?) force.
How would the term be viewed by a modern molecular geneticist ignorant of history?
Perhaps a modern scientist, unaware of the historical usage and uninterested in the historical and long-settled antagonism to evolutionary theory would regard random mutation as meaning something like the following

That there is an equal chance of any base-pair in the genome of an animal undergoing a mutation, hence there is an equal chance for genes of the same length to undergo mutation.

Are Mutations really random?
Yes: in the historical meaning of the term — there is no evidence for a directing force.
No: in the modern sense of the term, there are factors that can make particular regions of DNA more susceptible to mutation than others.
The poster, in answering his own question, mentions this point but does not elaborate on it. Being, perhaps, more concerned with biology at the molecular level, I shall give a few examples from my own knowledge, and encourage others to contribute more.
1. CpG dinucleotides mutations
The paucity of these in the human genome is thought to be because of their methylation to 5-methylcytosine, which slowly deaminate spontaneously to thymine.
2. Trinucleotide repeat mutations
For example, CAG repeats can expand in length due to mismatches in crossing-over.
3. Somatic hypermutation in immunoglobulins
Perhaps this is not strictly relevant as it occurs in somatic cells, but it is thought to operate on the DNA, and it is of interest in that it targets a particular region of particular genes.
4. Mutational hotspots

Mutation frequencies vary significantly along nucleotide sequences
  such that mutations often concentrate at certain positions called
  hotspots

I take this quotation from the summary of a review by Rogozin and Palov in Mutation Research. The interested reader is directed to his university library etc. for the full text, which is not freely available.


text:
Why do the calicheamicins bind to DNA at the minor, rather than the major, groove?
I am trying to understand why some drugs bind only to the minor groove and not to the major groove. More specifically, I am interested in calicheamicins.

They target DNA and cause strand scission. Calicheamicins bind with
  DNA in the minor groove, wherein they then undergo a reaction
  analogous to the Bergman cyclization to generate a diradical species.
  This diradical, 1,4-didehydrobenzene, then abstracts hydrogen atoms
  from the deoxyribose (sugar) backbone of DNA, which ultimately leads
  to strand scission.[7] The specificity of binding of calicheamicin to
  the minor groove of DNA has been demonstrated.

It would be helpful if you could provide a source for the extract you quote, preferably with a link.

this particular quote is from wikipedia, https://en.wikipedia.org/wiki/Calicheamicin

Accommodation in the major or minor groove
I am not in a position to generalize about all drugs that bind to the major groove of DNA, but at least one well-known example, actinomycin D, does so because it intercalates between the base-pairs in the double helix. Although other weak chemical interactions stabilize this binding, much of it is through base stacking with base-pairs. Hence binding requires it be inserted into the major groove in which the base pairs lie (see e.g. PDB 101 Molecule of the Month article).
Binding of calicheamicins, in contrast, involves interaction with two parts of the molecule. The ‘head’ of the molecule makes specific interactions with a TCCT sequence in the DNA (in the case of calicheamicin γ1), which is achieved from the minor groove (intercalation is not necessary) allowing the saccharide ‘tail’ to fit into the minor groove. (Ikemoto et al. 1995).

(Constructed from 3D Structure images on the Protein Data Bank website)
Sequence specificity
A concern of the poster is the fact that the interaction of calicheamicin is sequence specific (there is apparently a preference for d(T-C-C-T).d(A-G-G-A)) whereas access to the bases is restricted in the minor groove. This is addressed in the paper by Ikemoto et al., but without illustration, assuming you are able to visualize the chemical interactions in your mind. I have used Jmol to view the structure 2PIK, have prepared a couple of screen shots to help illustrate the details I shall quote from the text of the paper.

Cleavage of the DNA is performed by the enediyne aglycone (R), which does not make contact with the bases. Two of the regions that do interact with bases are the thio-sugar ring (B) and the aromatic ring (C). These are shown below in the complex of  calicheamicin (coloured yellow) with a deoxy-oligonucleotide duplex, together with a close-up of the interactions of these rings.

In the left-hand frame the DNA has standard cpk colouring, and the phosphates (orange–red) lining the minor groove are evident. The base-pairs are perpendicular to the plane of the image. In the second frame I have tilted the image slightly to allow the rings of the bases to be seen, and coloured the bases (actually the whole nucleoside) red/white/green/blue for A/T/G/C. Quoting from the Ikemoto paper:

The thio sugar B is positioned edgewise in the minor groove and contacts the A20 residue through van der Waals and hydrogen bonding (B ring hydroxyl to N3 of the base) interactions. The aromatic ring C is positioned between the walls of the minor groove with its iodine and CH3 groups directed toward the floor of the minor groove.… The S-carbonyl linker, which adopts an orthogonal alignment relative to the plane of ring C (favored by the steric demands of the ortho aromatic ring substituents), bridges the minor groove and makes van der Waals contacts with the opposing walls of the groove.

This may not have the clarity of, say, Watson and Crick base-pairing, but neither does the interaction of proteins with particular DNA sequences — one needs to examine the multiple interactions that occur. What I think it does show is that this drug can make specific contact to bases, even though it binds in the minor groove.

thank you a lot for your reply. however still I cannot fully understand..I thought that binding with minor groove is non-specific, in contrast with binding with major groove that is specific. So that's why I wondered since the binding is not specific and major groove is wider than minor, why calicheamicins act only in minor groove. thank you in advance!

@marilu — Generalizations have their uses, but biology is full of exceptions, and if you are talking about interactions you are talking about individual chemistry. One needs a representation with drug and DNA in stick representation to see the interaction, although then the grooves are not obvious. Unfortunately the original paper does not have a suitable picture. I'll see what I can find and then flesh out my answer. May take a few days.

thank you a lot!

@marilu — That's the best I can do. If you need more detail you'll have to grapple with the paper yourself and get to grips with a molecular graphics program like Jmol. (It can be fun, but there is a learning curve.)

I am so grateful!THANK you so much for your time and help!!!I get it now!:)

@marilu — You are welcome. I learned something from your question.


text:
Protein-coding introns in mitochondrial genomes
I am studying the mitochondrial genome and have read that some contain introns. However, these introns code for proteins. I cannot really understand this. Could someone tell me what intron in which mitochondria genome this refers to?

Can you please share the exact sentence and the reference to the paper/textbook mentioning this? I tend to think that introns are by definition the portion of genes that does not cod for proteins (although some exception may apply, such as intron retention). I would therefore be curios to investigate the issue.

unfortunately my references are in Greek, so not helpful I guess. if i translate it says sth like that: ORFs inside introns of group I and II. ORFs usually encode for GIY-YIG or LAGLI-DADG  endonucleases

Pehaps the mitochondrial proteins are encoded (with introns) in the nuclear genome, and then transported to the mitochondria?

Mitochondrial genomes differ greatly in size, coding potential and even whether they are circular or linear. Mammalian mitochondrial DNA is small (11–28 kbp) and intronless. However the mitochondria of certain other organisms range up to 1000 kbp in size.
Certain sponges (demosponges) with large mitochondrial genomes contain type I introns and type II introns.  Although introns were initially thought to have no other function than to separate exons, the introns of certain nuclear genes have been found themselves to contain genes. This turns out also to be true of some of the mitochondrial introns. To quote from then introduction to a paper I found through an internet search:

Most Group I introns encode homing endonuclease genes (HEG) and/or
  maturase of the LAGIDADG † family, while most Group II introns encode a
  reverse transcriptase (RT).

These introns are found in genes such as that encoding cytochrome oxidase subunit 1 (COI).

† This appears to be a misprint for the LAGLIDAD mutases, which are also endonucleases, and are involved in splicing the introns in which they reside.


text:
Why is facial symmetry of the opposite sex attractive?
Why do we give so much importance to the symmetry of face in the opposite sex? Why do we yearn to reproduce with a person with a beautiful face? How is it important for survival, if at all? Is there a biological explanation for this?

Who exactly is "we" here?  From my own experience & observation, I hardly think it is universal to regard the face as all that important in attractiveness.

Well it does seem like symmetric faces are more attractive (to both genders; Grammar and Thornil, 1994)

@Remi.b: I think you misunderstood what I was trying to say.  I'll accept that symmetric faces are more attractive than non-symmetric ones; what I'm questioning is the idea that the face, whether beautiful or not, is more than a minor factor in overall attractiveness.

@jamesqf What does it matter if its minor or major factor? My question was about the fact that it clearly has some importance in survival why else would people care about facial symmetry?

@user10093863: The problem is your assumption that "we yearn to reproduce with a person with a beautiful face", which at least from my observation isn't generally true.  I could cite any number of examples, from the feminist complaints about men not looking at their faces, to the cruel description of a fat woman as "but she has such a pretty face".

@jamesqf You clearly are living in a dreamworld or have never been to a normal school or college, let alone an outdoor setting like restaurant or a bar. If you genuinely believe that people don't give any importance to facial symmetry in the opposite sex, then I think you are living in the world of non-smelly farts and invisible poops.

@user10093863: At the risk of descending into crudity, are you living in a dreamworld where you've never heard the expression "just put a bag over her head"?  Do a thought experiment (or a real one if you can get funding :-)).  Take your bar or whatever, dress half the people in revealing clothing but have them wear masks, have the other half show their faces but wear something that completely conceals the body.  Now which half do you suppose is going to get the most interest from the opposite sex?

@jamesqf Wow that makes no sense. My question is regarding facial symmetry, it has nothing to do with the body.

@user10093863: No, you asked explicitly why "...we yearn to reproduce with a person with a beautiful face?"  The answer to that is that WE don't.  Now maybe some people do, because different people find different things attractive.  But if beautiful faces were a major factor in sexual attraction, Playboy could have been a success with nothing but head shots :-)

@jamesqf The reason you won't admit to the fact that you and I and everyone else is highly attracted to facial symmetry is because you want to live in a world where we are attracted based on important things like someone's intelligence rather than their looks, however, I hate to break this bubble for you but humans are still pretty primitive when it comes to attraction. Our brains have not evolved much for thousands of years and we used to be attracted to others based on their facial symmetry and physicality. So, what makes you think that it is any different nowadays?

@user10093863: You've entirely misunderstood what I've been trying to point out, which has nothing to do with whether I'd like intelligence to be sexually attractive.  (I don't think I've even mentioned intelligence AT ALL.)  It's that when it comes to sexual attraction, the face plays little part, at least for men.  (I think also for women, but I have limited data, not being one.)  To be crude (since nothing else seems to get through), most men look at tits, ass, legs, waist &c long before the face, and will pretty much ignore the face if the rest is attractive enough.

@jamesqf As I have mentioned before, you live in a dreamland. Producers hire pretty faces for lead roles because they know that more people are going to watch. Why do you think people want to watch pretty faces? Because it is soothing to the eye? No, because people are more attracted to pretty faces and find it hard not to look at them. What do you think this phenomenon is if not sexual attraction? Ever heard of the phrase 'sex sells'? If it was merely about 'tits, ass, legs, waist, etc' then wouldn't they hire based on physique rather than facial symmetry? Its so hard to get through you.

@user10093863: The first problem with your reasoning is that anyone movie/TV producers hire (for other than character rolls) is already several standard deviations out on the T&A bell curve.  You don't see them hiring the fat girls (or men) with pretty faces, do you?  The second problem is assuming that movies (other than porn, of course) are all about sexual attraction.  While I'm not a movie fan, people do seem to watch them for reasons other than sex. And if it seems hard to get through to me, it's because you insist on holding to an obviously false thesis :-)

Are you claiming that face symmetry is unimportant for gay people?

@swbarnes2 Are you virtue signalling here?

Why is it 'virtue' signaling' to acknowledge the existence of gay people?

Because biology.

Facial symmetry is currently believed the be a sign of developmental stability and good health and thus good genes.  More precisely a sign of genetic diversity in a potential partner.

Parasites, disease, or injury can cause asymmetries. The complexity of the face, and our visual sensitivity to facial features, makes us most sensitive to subtle symmetries and asymmetries in facial features.
Therefore facial symmetry is a sensitive and reliable indicator of health. Healthy mates are more likely to possess good genes to pass on for strong healthy offspring. Healthy mates are also likely to be more physically capable of producing and raising offspring.
Any individual who possesses a gene that causes attraction to symmetric partners is more likely to select such a mate. That individual is therefore likely to produce more offspring, and more likely to produce strong healthy offspring.
Therefore the gene for attraction to facial symmetry is more likely to survive and spread.

Welcome to Biology.SE! Your answer sounds reasonable, however, it is likely to receive a more favorable response if you include supporting references (primary literature is best). ——— Please also take the [tour] and then consult the help pages for additional advice [Answer] effectively on this site and then edit your answer accordingly. Thanks!


text:
What is the highest concentration of sodium chloride for the oceans to be able to sustain life?
What is the maximum concentration of NaCl for life in the oceans to be possible?
Was it fortuitous that the concentration was originally no higher, in which case the evolution of life on Earth would not have occurred?

This is more of a biology question than a physics one. Try the Biology stack exchange.

Apart from answers given, here are some reference for you: https://royalsocietypublishing.org/doi/10.1098/rstb.2018.0011, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2329653/, https://link.springer.com/referenceworkentry/10.1007%2F978-3-642-30123-0_57


text:
Glucose 6-phosphate dehydrogenase: reaction mechanism
I have searched the internet for the reaction mechanism of G6PD but couldn't find it, so I am asking whether anyone here knows its mechanism and whether they could recommend some sources that give detailed info about enzyme mechanisms generally.
I would be grateful for this because it seems difficult to find enzyme mechanisms on the internet.

How did you search the Internet? As the Internet contains sites for all the journals in which enzyme mechanisms are published, it seems more likely that your search strategy needs improvement or that you don’t have access to the journals. Did you search PDB and work with the source papers? Have you bibliographic software (eg Endnote) that allows you to search PubMed? Did you try Google scholar?   Did you follow the links in the section of the Wikipedia article on the enzyme’s structure? “But I couldn’t find it” is insufficient to demonstrate that you tried to research the topic yourself.

@David actually I searched in Wikipedia and other journals (like springer ,pub med and even PDB), but I just find info about the enzyme structure and the complications of its deficiency but I never found its mechanism .

But one of the main points of determing structure is to throw light on the function, especially the mechanism, by identifying residues at the catalytic centre where the substrates bind. I can help you but to conform to the ethos of this site I need to know if this is some sort of "homework" question, and if not why are you asking as you don't appear to appreciate the relevance of structure? Oh, and as a new user to the site, please finish reading the Tour — we can see you lack the "badge" for doing so.

@David I am not a student in biochemistry as my major subject, I study medicine and in my college we don't have to know mechanism, it is some sort of individual effort from me (not homework) to better understand biochemistry and because I am hobbyist of biochemistry, I understand acid base catalysis and other simple mechanism but I don't have enough information to be able to confirm that I can predict mechanism from active site structure and that's why I asked here to see how experts can predict and know the mechanism of catalysis and that's why I also asked for good sources on this topic

@David I am really thankful to you and I would be more thankful if you recommended some good source :books or websites (if you could also mention the source from which you get the info in your answer, I would appreciate it a lot) and thanks in advance

Disclaimer
I am not an enzymologist and this answer is based on work published in 1998, and the latest paper I consulted was 2000. Hence I cannot exclude the possibility that more recent work has modified the model shown here.
General Approaches
The general approach to elucidating the mechanism of action of enzymes has been as follows.
Historically, and before a structure is (or was) available:

Hypotheses of possible types of mechanisms would be made on the basis of the known mechanisms of non-enzymic chemical reactions.
Experiments with inhibitors might suggest what class of residues of the enzyme might participate in the reaction.
Experiments would be performed to get indirect evidence for the residues involved, e.g. by examining the effect of pH in relation to the pKa.

More recently, with structure determination less difficult and more common:

The structure would be determined and an attempt to identify the active site made on the basis of the position of a bound pseudo-substrate or inhibitor.
Residues near the substrate that might participate in the reaction would, thus, be identified.
A hypothesis of the role of these residues would be made in relation to the known chemistry (as in historical 2, above).
Experiments would be performed to test the participation of the residues — often by modifying them — and their proposed role.

Proposed Mechanism for Glucose 6-phosphate dehydrogenase
The structure of glucose 6-phosphate dehydrogenase (G6PD) was published in 1994 by Rowland et al. in Structure 2:1073-1087. To test their hypothesis of the mechanism, Cosgrove and coworkers constructed performed site-directed mutagenesis on G6PD and determined the structure of the mutated protein. On the basis of this they published a paper in Biochemistry 1998 37:2759–67 in which they proposed the reaction mechanism shown below.

The Nδ1 atom of His-240 is hydrogen bonded to the Oδ1 atom of Asp-177, forming a catalytic dyad. The Nε2 of His-240 is poised to act as a general base by abstracting a proton from the C1-OH of G6P, allowing transfer of the C1-hydride to the C4 position of the nicotinamide ring of NAD(P)+.
They summarize this as follows:

“The results support a mechanism in which His-240 acts as the general
  base that abstracts the proton from the C1-hydroxyl group of glucose
  6-phosphate, and the carboxylate group of Asp-177 stabilizes the
  positive charge that forms on His-240 in the transition state. The
  results also confirm the postulated role of His-178 in binding the
  phosphate moiety of glucose 6-phosphate.”

Suggested reading and search approach
The classic text on enzyme mechanism is Alan Fersht’s Enzyme Structure and Mechanism published in 1984. This is clearly based on a limited range of enzymes, so its importance is not in finding the mechanism for a particular enzyme, but for understanding the principles involved. (You can pick up a second-hand copy very cheaply). Fersht has a more recent (2017) book in the same area — Structure and Mechanism in Protein Science but this is much more expensive. You can view the contents on Amazon.
Other suggestions are welcomed as comments.
My approach to searching for an answer here is worth mentioning as the question indicates the poster failed in his attempt. First I just did a Google search “reaction mechanism, glucose 6-phosphate dehydrogenase”. This wasn’t very useful, but alerted me to the fact that Google was prioritizing pages related to G6PD deficiency, a clinical condition on which much had been written. To avoid this I decided to focus specifically on structure, assuming that some of the papers would be proposing mechanisms. I tried three of the following four approaches (while idly waiting for a computer program to run).

Google search on “glucose 6-phosphate dehydrogenase, structure”. This did not appear to give me a direct hit, but brought up the three other sources I went on to try.
The Wikipedia entry on glucose 6-phosphate dehydrogenase. Half way down the page is a section on structure with a diagram of the substrate binding site, so I knew I was on track. The references on this page were not very useful, but the diagram indicated the structure was PDB 2BHL.
The Google search also brought up a Protopedia page, which I actually looked for directly. At first I was disappointed by the lack of information other than the structure, but the third of three references was a Cosgrove paper from 2000 which contained the words “catalytic diad” in its title. I went for that, and it led me back to their 1998 paper.
I could have tried the Protein Data Bank and searched for 2BHL (or just for the enzyme). 2BHL would have led me to a later paper in Acta Crystallographica, which does mention the 2000 Cosgrove paper in its introduction.


text:
What is the substance that tumors release that stimulates growth of blood vessels but suppresses its release from other tumors?
I'm currently in high school and I am working on a cancer research project. My project consists of a cancer, and different ways to treat it. I have a set of benign tumor and I was thinking of immediate way of treating it without using a drug like Taxol to destroy parts of the cell is to simply remove the tumor.
However, I remembered learning about a 1 1/2 years ago about a substance that tumors release to stimulate the growth of blood vessels towards them, but this same substance suppresses the release of itself by another tumor (hopefully this makes some sense). I made some drawings that are attached here:
Scenario 1: The 1st tumor in the blood flow releases an unknown substance, which promotes blood vessel growth, but suppresses the release of the same substance from another tumor behind it.

Scenario 2: The 1st tumor is removed, and now the 2nd tumor starts to release the substance, because the 1st tumor's release is not suppressing the 2nd tumor's release anymore.

Does anyone know the name of this substance, and can someone help me learn more about it? Thanks.

One very important signal for angiogenesis are the Vascular endothelial growth factors (VEGF)  (a small group of ~5 similar proteins). They generally promote generation of new blood vessels & migration of these towards the source of VEGF expression.
Blocking VEGF signalling (mostly be blocking the receptors with antibodies) has been a pretty good strategy in cancer treatment, since tumors can't grow over a certain size without blood supply by new grown vessels.
However, I am not aware of any blood-vessel specific signalling mechanism that stops it's own expression at a secondary site. (This may be possible though, especially for specific signals)

Galectins are family of beta-galactoside-binding proteins implicated in modulating cell-cell and cell-matrix interactions. These proteins are produced by tumor cells and promote angiogenesis.
These secreted Galectins are used by endothelial cells to enhance migration and proliferation. And play various roles during development of tumor such as cellular adhesion, cell mobility,  tumor-induced angiogenesis, and apoptosis.
Via:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5855652/
https://www.ncbi.nlm.nih.gov/pubmed/27649167


text:
What does "regulatory genomics" mean?
I have read about basics of molecular genetics ,although its not a thorough in-depth knowledge. I would like to know about "regulatory genomics". What is it actually?

As I understand it, it is the study of regulatory mechanisms in gene or protein expression in populations and especially how these mechanisms vary between closely related lineages.

Can you tell us, in which context you read about it?

@Chris : I was going through an institute website ( http://www.imsc.res.in/biology_imsc ). There a professor is specializing in regualatory genomics, and research programme for computational biology is going on.

The genome may be divided into two classes of sequences - those that code for proteins and those that do not. Those that do not code for proteins may be again divided into classes consisting of actively transcribed sequences that have biological activity (such as long noncoding RNA, microRNA, competing endogenous RNA and so on) and those that aren't.
These untranscribed noncoding regions may be involved in regulating the activity of protein coding and actively transcribed regions by binding to transcription factors or transcriptional coactivators/corepressors that control whether certain genes are expressed or not - this can happen close to the start of the gene (i.e, promoters) or far away (at enhancers). Distant enhancers can still affect gene expression because they and the genes they affect can be close together in three-dimensional space (The genome is folded in cells!).
Regulatory genomics is, simply put, the study of these regions, which are called genomic "features" and how they regulate genes. A great example of studies in this area are offered by papers published as part of the ENCODE project http://www.nature.com/encode/#/threads

Thanks for the effort in answering. Good answer too, I got the essence. But I didn't completely understood. Since my subject is not biology I don't understand things like binding. Can you suggest me some reference for beginners other than papers.

Not to discourage you, but you're getting into some fairly advanced topics in molecular biology so you may want to read some basic biology/biochemistry textbooks first to get the prerequisite knowledge.

@canadianer : I completely agree with you. I will have to see the basics.

Alberts' Molecular Biology of the Cell or Lewin's Genes would be a good starting point if you are looking for textbooks; alternatively, check out Scitable http://www.nature.com/scitable/topic/gene-expression-and-regulation-15


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What does chromosome CHR_Un, CHR_MT in the ftp site of NCBI mean?
I am not a biologist. But need some genetic data. So I searched internet and reached NCBI's website. I came to know from the FAQ page that I can the complete genome data of organisms from ftp://ftp.ncbi.nih.gov/genomes/. So I went to the FTP site and opened the homosapien section ftp://ftp.ncbi.nih.gov/genomes/H_sapiens/. I found folders CHR_1 to CHR_22, CHR_MT,CHR_Un, CHR_X and CHR_Y.
My doubt is this : Normally there are only 23 pair chromosomes right? 1 to 22 pairs OK. XY make another pair. Then what are MT and Un ?
And the folder which I am looking is a genome of male right?

chr_MT: List of variations that map to the mitochondria
chr_Multi.txt.gz: List of variations that map to multiple chromosomes
chr_UN: List of mapped variations that are on unplaced chromosomes
see here for more information.
This is the reference genome for human, as far as I know there is no discrimination for it into male/female.

If it was female genome , do we have to consider X twice.

@terdon : Do you mean the AGTC sequences as 'List of variations'?

@dexterdev I did not answer this, Chris did. I just edited which is why you see my name there. I don't know what Chris meant by that since I can't find that file on the FTP site nor see it mentioned in the FTP's README (which, by the way, you should read).

OK @terdon I will read it.

@dexterdev "List of variations" simply means variations from the reference sequence.

@Chris I will have read more to understand these. For example what is the "reference sequence" here then?

The reference sequence is the sequence of a genome which is considered to be the "normal" sequence of this species. This varies from individual to individual due to a individual set of insertions, deletions, polymorphism and so on.


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Do there exist publicly available Genome sequences of a family?
I would like to explore the genome sequence of a publicly available genome sequences of a family (like mother, father, son, daughter...). If such human genome sequences are not publicly available at least any animal's family data is also OK. :)  I am not a biologist, but aims to just understand things more clearly.

For animals and other organisms, NCBI has a database for publicly-available sequences:
https://www.ncbi.nlm.nih.gov/guide/howto/retrieve-seq-org/

I know that 1000 Genomes has sequenced Mother-Father-Child genomes from populations around the world (I think at least some of these samples were obtained from HapMap) and their data is publicly available by following the links in their website.


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What information do microarray image convey?
OK I have read that a cell generates 4 kinds of digital (to be precise discrete) data namely DNA, RNA, Protein (sequences that can be encoded as string sequences of nucleotides/ amino acids) and micro array image. I am not a biologist, but my interest is in the statistics and information theory of these data. I would like to know what information do DNA micro array image convey? For example after processing it with the aid of a suitable software, what sort of information we do obtain?
Sample micro array image:

In the general case the color simply indicates how much of a specific RNA or DNA is in your sample. What you get out of this depends heavily on the exact experiment you're performing.

Where can I get more information? What is the relation of micro array image with gene expression?

http://en.m.wikipedia.org/wiki/DNA_microarray In the context of an expression level experiment, each spot represents a unique oligonucleotide probe. The relative colour intensity of each spot tells you the relative abundance of RNA in the cell that hybridizes to that probe.

The color is because of a fluorescent tag (Cy3/Cy5) attached to the DNA that you hybridize to the array.

Each spot overlaps with an oligonucleotide probe, that is designed to identify a specific nucleic acid sequence. Gene expression arrays have probes which are complementary to sequences derived from the exons; therefore they will hybridize with these sequences.
Before hybridization the cDNA (in this case) is labeled with a fluorescent molecule such as Cy3 or Cy5 (two dyes can be used to differentiate treated and control). Note that each spot will have many probe molecules.
Fluorescent intensity is proportional to number of hybridized DNA strands, which in turn is proportional to its expression in the sample.
Extensive amount of texts are available on microarray data analysis which you can find quite easily.


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What are the application areas of Pattern formation studies specific to biology?
I was reading about reaction-diffusion processes, morphogenesis concept by Alan Turing and works of Murray in describing pattern formation on animals etc. But one question which came to my mind was even if we describe these processes in mathematical and physical contexts, are there any application areas awaiting for the results?

What do you mean "awaiting for the results?" Do you mean, are there unsolved problems in pattern formation that would have implications for biology, if the answer was known?

Yes. Specifically can such advancements help in any area like repairing an organ or so?

Ok, I'm not quite sure if we are at the repairing an organ phase, but here are a few interesting examples:
1. Philip Maini at Oxford has used pattern formation to give insight into jaguar patterning: Paper. He also has a book chapter Pattern formation and wound healing that could of of interest, although I'm not sure if this is a direct application as much as a heuristic understanding of how wound healing happens.

From the biomedical side, Michael Levin at Tufts is doing amazing work in regenerative medicine, and a lot of what he does is inspired by pattern formation as well, although I am not sure if it explicitly uses the theory - his papers.
This paper is one of my favorite from Ron Weiss - engineered pattern formation. Will most likely have important biomedical applications some day, although not currently.

It is quite interesting to know this. Tissue engineering, biomaterial fabrication and
biosensing.


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Parasite - host equations
The Lotka–Volterra equations describe how predator–prey interactions affect population growth. Do these equations describe parasite-host interactions? If not, how would they change by adding these interactions as well?

Parasite vs predators
In terms of ecological interaction, a parasite is essentially a predator. As such, of course the Lotka-Volterra equations apply to host-parasites interactions.
Lotka-Volterra equations
However, Lotka-Volterra equations are very simple and very general. So much so, that in order to make good prediction about the real world, one most often have to build more advanced models.
Host-parasite interaction models
There exist a whole set of models specific to host-parasite interactions. You should have a look at the wikipedia entry for epidemic model which is a pretty good overview and introduction.
Most models of host-parasite interactions fall into the category of the SIR (or SIRS and other derivatives) model. The term SIR comes from Susceptible-Infected-Recovered. The whole point of the SIR models is to categorize host individuals on whether they are Susceptible, Infected of Recovered (hence the abbreviation SIR).
The SIR models are very much used by national and international centers for epidemiology and underly many of the decisions of vaccination and other methods of disease control.
Host-parasite co-evolution
Of course, the Lotka-Volterra model and the SIR models assume absence of evolution and only track changes in population size (within each category for the SIR models). There are models that also take into account that populations also evolve in response to the interaction and demographic events that the interactions are causing. Such models are much more complicated to keep track of and we often (I think) make use of technics such as separation of time scales. These models are essential though typically for to control viral epidemic but not only. But these models are outside the scope of your question.


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Are there birds that don't vocalize?
I am wondering whether there are birds that do not vocalize at all.
I know about the distinctions between songs and calls in passeriformes.
I know that there are species that vocalize very little, like the Ruff (Philomachus pugnax).
I was curious to know whether there is a species in which vocalizations, acoustic communication, do not play any role at all.

There are birds with non-vocal sound only. However, there might not be any bird without producing any sound. Thus, all birds appear to have some way of acoustic communication.
A better known example of a voiceless or near voiceless bird is stork per multiple credible sources.

Storks are voiceless or nearly so, for lack of a fully developed syrinx (vocal organ), but some of them clatter their bills loudly when excited.
https://www.britannica.com/animal/stork

Wikipedia claims that storks have a syrinx and rarely produce some sound with it and adds credible citations.

Although it is sometimes reported that storks lack syrinxes and are mute,[7] they do have syrinxes,[8] and are capable of making some sounds, although they do not do so often.[4][9] The syrinxes of storks are "variably degenerate" however,[8] and the syringeal membranes of some species are found between tracheal rings or cartilage, an unusual arrangement shared with the ovenbirds.[10]
https://en.wikipedia.org/wiki/Stork#Morphology

Even, just clattering is an acoustic communication between storks:

Identification of the sex of birds is important for captive breeding of endangered species. In the oriental white stork (Ciconia boyciana), an endangered species, both sexes produce an acoustic signal called "clatter" by rattling their mandibles together to generate sounds. https://pubmed.ncbi.nlm.nih.gov/15333993/

The only birds without syrinx might be New World vultures but they do produce sound also.

No New World vulture possesses a syrinx,[35] the vocal organ of birds. Therefore, the voice is limited to infrequent grunts and hisses.[36]
https://en.wikipedia.org/wiki/New_World_vulture#Description

Here is a relevant quote from ornitology.com about Non-vocal Sounds:

Kiwis stamp their feed when annoyed. Boat-billed Herons, Storks, and Albatrosses rattle or clap their bills. Woodpeckers drum. The Ruffed Grouse drums with its wings. The nighthawk and hummingbirds often make sounds with their wings or tails. A number of birds make whistling sounds as they fly through the air- may or may not serve a purpose.


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Can an attenuated virus cause infection in some rare cases?
I just read in some comments, that some children got measles one week after getting the MMR shot. Afaik. MMR contains attenuated live virus, and the incubation period of measles is 10 days (+/- ? days). Can we be certain, that they didn't get infected by the vaccine?

There are two possibilities for getting the measles directly after a vaccination:

The kids where infected shortly before the immunization. Since it takes about two weeks to develop humoral immunity, it is possible that these two events overlap. The measles have an incubation period of 7 - 21 days (see reference 1), with a rash occuring around day 14. So if the kid was around day 7 of his infection, this would fit.
Since the measles vaccination is a live attenuated virus, it is possible to get a rash from it. However, these are relatively rare cases (depending on the source between 2 and 5%) and the infection is mild and not contagious. See also reference 2.

References:

Measles (from the CDC)
Measles: Questions and Answers

"About 5% of people develop a mild rash." - This is in your second reference. Is it 5% or 1/10000%?

@inf3rno I put in a wrong number, don't ask me why. Thanks for the notification.


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Why there are no plants that offer salt fruits as opposed to sweet fruits?
Why there are no plants that produce salt fruits?
Is it because other animals do not like salt to the same degree of humans?

If you could mark the question as answered that would be awesome! :)

Soil salinity and sodicity cause severe problems in agriculture worldwide, and salt tolerance in crops is an extremely important trait and a major focus of research. Detrimental effects of high salinity on crops are multifaceted and affect plants in several ways: drought stress, ion toxicity, nutritional disorders, oxidative stress, alteration of metabolic processes, membrane disorganization and reduction of cell division and expansion (Hasegawa et al. 2000; Munns 2002; Muscolo et al. 2007, 2013; Zhu 2007; Sidari et al. 2008). As a result, plant growth, development and survival are reduced (Muscolo et al. 2011; Schleiff and Muscolo 2011). Two major stresses affecting plants under salinity are osmotic and ionic stresses. Osmotic stress, occurring immediately in the root medium on exposure to salts, can result in inhibition of water uptake, cell expansion and lateral bud development (Munns and Tester 2008). Ionic stress develops when toxic ions (e.g. Na+) accumulate in cells causing increase in leaf mortality, chlorosis, necrosis and decrease in the activity of cellular metabolism including photosynthesis (Yeo and Flowers 1986; Glenn and Brown 1999). In fact, excess Na+ and Cl− have the potential to affect plant enzymes, resulting in reduced energy production and other physiological processes (Larcher 1980; Morais et al. 2012a,b). Ionic stress results in premature senescence of older leaves and in toxicity symptoms (chlorosis, necrosis) in mature leaves due to high Na+ and Cl− which affect plants by disrupting protein synthesis and by interfering with enzyme activity (Munns and Termaat 1986; Hasegawa et al. 2000; Munns 2002).

Source: Effect of saline water on seed germination and early seedling growth of the halophyte quinoa
Salt is really good at inhibiting enzymes and biochemistry, which translates into not being great for seeds. So to have a fruit that has a high concentration of salt is really risky and not likely to be successful. Sugars on the other hand attract a multitude of other organism that would help move seeds around or create an ideal growth environment. To have crops that are resilient to salt would be useful but would require a lot of wasted energy to maintain osmoregulation. So it's not so much that animals wouldn't eat a salty fruit but more that it would be harmful to the seeds.

Also the only places where salt is common enough for plants to stuff their fruits with it are the very places animals do not need more salt as they can get plenty from the environment.


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Do male humans have a mons pubis?
Wikipedia writes:

In human anatomy, and in mammals in general, the mons pubis (also known simply as the mons, and known specifically in females as the mons Venus or mons veneris), is a rounded mass of fatty tissue found over the pubic symphysis of the pubic bones. In human females, the mons pubis forms the anterior portion of the vulva. It divides into the labia majora (literally "larger lips"), on either side of the furrow known as the pudendal cleft, that surrounds the labia minora, clitoris, urethra, vaginal opening, and other structures of the vulval vestibule.

The Foundational Model of Anatomy suggests that the feature also exist in the non-gender specific pelvis concept. Does it?

Technically men do have a mons pubis but it is less pronounced. With increased estrogen in females it becomes more pronounced.
Wikipedia

Please add some references to your answer.

pronounced = expressed?


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Identify this bird
I have attached below the image of a bird that I see everyday from my balcony. Since I do not have a good camera, I searched the image of the bird on Google. It feeds on insects. I live in Satna (Madhya Pradesh), India.

You are probably seeing an Indian Roller (Coracias benghalensis).

Which is similar but not the same to the picture you posted; which is a  racket-tailed roller (Coracias spatulatus) a similar species of Roller  found in Africa.
However in India do occur other 2 species of Roller, the European Roller and the Dollarbird. You can check pictures of this other 2 species online and compare them with the bird you see every day.

Your guess is that the bird in question is an Indian Roller. However, you also said that there are two species of rollers found in India. Therefore, what I want to ask you is whether the Indian Roller is different from the European Roller or the Dollarbird?

Yes they are different as you can quickly see from a rapid google research. I guessed based on the most common species given in your area and asked you to check.


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Seizures and blood pressure
A seizure is basically a synchronized firing of neurons as opposed to the more common unsynchronized firing taking place during normal neural activities. However, I am uncertain if the exact technical definition of a seizure restricts this synchronized nerve activity to the brain only .
I wonder whether a wave of synchronized firing can propagate up to or occur in the area of brain controlling the blood pressure level and hence affect the blood pressure of the individual going through a seizure? Or can the impact of a seizure propagate to other areas and hence affect other functions like cardio-vascular system and hence the blood pressure? Or can neurons connected to heart, but not necessarily present in brain, exhibit synchronization as in a seizure and thereby affect the blood pressure of an individual undergoing seizure?
Summarizing my question is: can seizures affect blood pressure?

Yes, seizures can affect autonomic function including blood pressure. Such symptoms can even result in death. Note though that not all seizures are the same: there are many different types with many different causes, and they can affect different parts of the brain. There can also be different effects before, during, and post-seizure.
The effects described seem to be more related to overall discharge rates rather than synchronous firing in the periphery per se. The autonomic nervous system does not directly control heart rate, for example, but rather modulates the rate. The heart beat or vasculature would not entrain to any sort of seizure activity, for example, because the neurotransmitters involved in autonomic regulation of heart rate and blood pressure are comparatively slow-acting relative to the rate of seizure activity (essentially those functions are taking a moving average of neural input, rather than responding specifically to each impulse).
The relationship between autonomic function and seizures need not be unidirectional, either; circulatory changes can also be triggers for seizures.
References

Devinsky, O. (2004). Effects of seizures on autonomic and cardiovascular function. Epilepsy currents, 4(2), 43-46.
Nei, M. (2009). Cardiac effects of seizures. Epilepsy currents, 9(4), 91-95.
Penfield, W., von Sántha, K., & Cipriani, A. (1939). Cerebral blood flow during induced epileptiform seizures in animals and man. Journal of Neurophysiology, 2(4), 257-267.

Thanks a lot . Does this kind of synchronous firing occur in neurons in any other part of the body ,other than the brain ?

The brain has some network architecture that isn't really found elsewhere. You could possible make some analogies with fibrillation in the heart, but the actual structure and causes are completely different. In other nervous tissue like that of the gut, a particular synchronous rhythmic pattern is important for gut motility and digestion, and you can certainly have cramping that occurs with overly synchronous activation along a stretch of gut tissue, but again, the networks aren't constructed the same as in the brain so I think it would be a distant analogy at best.

So no known cases where a synchronous oscillation of brain propagates to other neural networks ?

I'd hesitate to say "no known cases" - that's a pretty big leap that I can't make (hard to prove a negative), certainly you can have rhythmic clonic muscle activity in seizures, so does that count? It just isn't how the CNS is coupled with autonomic functions that makes me think it's unlikely you would have that sort of propagation. Like if you were driving a car and rhythmically pump the gas quickly, the car is going to speed up fairly continuously, because the engine doesn't respond immediately to the accelerator press and the velocity doesn't respond immediately to the engine.