How do we call a "burst of evolution"? I have in mind that evolution is not a constant / continuous process and that there are bursts of evolution.

Are there terms to refer to the concepts of fast vs slow evolution rates?

There are indeed periods of fast evolution and period of evolutionary stasis. The term "burst of evolution" is never used in the literature but below are three common terms when discussing these concepts.

First we have to realize that the term 'speed of evolution' does not mean much. We can be talking about change in phenotype through time (See Punctuated Equilibrium and Evolution and Ecology time scales) or speciation rate (See Adaptive Radiation and Mass Extinction). Also, we have to realize that we can talk about such speed of evolution on a given taxon or for the entire life on earth.

Punctuated Equilibrium

We often refer to the fact that there are periods of evolutionary stasis and periods of rapid evolution as punctuated equilibrium

  Punctuated equilibrium (also called punctuated equilibria) is a theory in evolutionary biology which proposes that once species appear in the fossil record they will become stable, showing little evolutionary change for most of their geological history. This state is called stasis.

Here is a representation (from the above wikipedia link) of phenotypic divergence following an extremely gradual view of evolution and an extremely "punctuated" view of evolution

Evolution and Ecology time scales

Since the 2000s, there has been increased recognition that evolutionary processes even matter on a ecological/demographics scale. That is ecological/demographics processes and evolutionary dynamics influence each other dynamically and the old view that evolutionary processes are much slower than ecological/demographics processes is sometimes wrong.

See the post History: Do evolutionary and ecological processes occur at the same timescales?

Adaptive Radiation / rapid diversification

The speciation rate also varies through time. There are "burst in speciation rate" if you like the term. A sudden burst in speciation rate is called an adaptive radiation

  In evolutionary biology, adaptive radiation is a process in which organisms diversify rapidly from an ancestral species into a multitude of new forms, particularly when a change in the environment makes new resources available, creates new challenges, or opens new environmental niches. Starting with a recent single ancestor, this process results in the speciation and phenotypic adaptation of an array of species exhibiting different morphological and physiological traits. An example of adaptive radiation would be the avian species of the Hawaiian honeycreepers. Via natural selection, these birds adapted rapidly and converged based on the different environments of the Hawaiian islands

You can find a list of classical examples of adaptive radiation on the above wikipedia link or at the post Is there a taxa that radiates faster?. If you don't want to be too extreme, you can as well just use the expression rapid diversification.

Mass Extinction

There are essentially two differences between an adaptive radiation and a mass extinction. 1) one is about an increase in speciation rate while the other is an increase in extinction rate. One is about a single taxon, the other one concern most of life on earth.

Because, a mass extinction sounds quite apocalyptic and because we seem to be at the start of a new mass extinction, most people are familiar with this term.

  An extinction event (also known as a mass extinction or biotic crisis) is a widespread and rapid decrease in the biodiversity on Earth. Such an event is identified by a sharp change in the diversity and abundance of multicellular organisms. It occurs when the rate of extinction increases with respect to the rate of speciation. Because most diversity and biomass on Earth is microbial, and thus difficult to measure, recorded extinction events affect the easily observed, biologically complex component of the biosphere rather than the total diversity and abundance of life.

I want to highlight that when thinking of a mass extinction, many people think of a single event clearing up the surface of the earth in a day but the reality is very different. In fact, a mass extinction can well last thousands of years.


What is this feather like bug with no legs? Seen on leaf in North Texas, USA in April 2017. Critter will attach itself to any object put next to it.

It is a specialized feather called "down" (like in down pillows, etc.)

  Down feathers have a rachis that is shorter than their longest barb. They are completely plumulaceous and have a fluffy appearance, which results from filamentous, noninterlocking barbules.

Anatomy, Clinical Presentation, and Diagnostic Approach to Feather-Picking Pet Birds


Is there an ecological scenario where terrestrial insect larvae can show food choices? I have been going through literature on insect food choices. I plan to study the effect of prior experience on food choices in both adults and larvae of the red flour beetle, Tribolium castaneum. There are plenty of studies that focus on larval and adult experience having an effect on adult preference. I would like to look at how larval experience changes larval choice, but only if it has some ecological relevance. However, I could not find a single study that provides an ecological relevance to larvae making food choices.

This appears to be due to the fact that larvae are usually sessile, and since adult females are the ones making the oviposition choices, therefore most studies seem to assume that the choices of the larvae don't matter. (Preference Performance Hypothesis)

Larval food choice might be ecologically relevant under conditions where females make "mistakes" during oviposition, say if the environment is spatially/temporally fluctuating. But if they show limited dispersal (or slower dispersal than adults), then does their choice really matter?

Does anyone know of any examples (published or unpublished) where insect larval food choice is ecologically relevant? It would help me out a lot to design my study.
Thanks in advance!

The diamondback moth (DBM), Plutella xylostella L. (Lepidoptera: Plutellidae) is one of the most important pests of cruciferous crops in the world.. A strain capable of complete development on sugar pea (Pisum sativum L. var. macrocarpon) has recently appeared. A recent study (Henniges-Janssen, Heckel & Groot (2014), "Preference of Diamondback Moth Larvae for Novel and Original Host Plant after Host Range Expansion"; link) compared the feeding preferences of L4 larvae reared during previous larval instars on cabbage and pea. Pea-reared larvae of this strain preferred peas, while cabbage-reared larvae preferred cabbage. L4 larvae of the original strain preferred cabbage irrespective of their previous diet. I don't think this example has been shown to occur in the field, but the two plants are both fed upon by these caterpillars in the wild.

There is also evidence that larvae of Cydia pomonella (codling moth), a marjo agricultural pest of orchards with a near-global distribution, learn to avoid apple flavoured with saccharine if they have previously encountered saccharine-flavoured noxious plants (Pszczolkowski & Brown, 2005); this probably meets your second criterion for ecological relevance more closely (evidence for learning to avoid odour/flavour cues encountered in a toxic plant, thereby increasing survival) but it's less relevant to a real-world field situation than the first example.

I also found an article on associative learning in insects here that may include some useful examples.


Immunotherapy for tumours which do not have TSA Is immunotherapy possible for tumours which do not have Tumour Specific Antigens (TSA)? If so, doesn't targeting those tumour cells also target other healthy cells, thus causing autoimmunity ?

Yes, in some circumstances.

In some cases the antigen being targeted, even if it leads to loss of normal cells, can be targeted. This is most evident in the targeting of CD19 to treat various forms of B-cell derived tumours. Example of such an application and response biomarkers are described here
https://www.ncbi.nlm.nih.gov/pubmed/28291388

Secondly, opportunities may be created by the generation of epigenetic states. Cancer-germline antigens are usually only expressed in gonad tissues (which enjoy immune privilege) but are often aberrantly reactivated in tumours, but not in other somatic tissues. This too can create specificity to immunotherapy even if the antigen is not truly tumour-specific, and is rather striking as a phenomenon in testicular cancer.

https://www.ncbi.nlm.nih.gov/pubmed/28555838


Should I dilute DNA with water or elution buffer? I've extracted DNA using a kit and final step is eluted with buffer. If I must dilute my DNA samples, do I use the same elution buffer or can I use milliq water?

I would generally recommend using the elution buffer (which is typically Tris-EDTA buffer) or TE-Buffer, as the pH and the conditions stabilize the DNA for a longer time, which is especially interesting when you want to store your DNA.

It also dependent on your downstream application - when they recommend diluting the sample in water (or another buffer) I would follow this advice. In my experience TE buffer is perfect for all molecularbiology applications (cloning, digestion, amplification, PCR, etc.). The EDTA will of course complex bivalent cations, but since the concentration in the buffer is only 1mM and the DNA solution is usually diluted further in PCR or digests, this plays no role in real life applications.


Coronavirus origin could be bat, why this happen while people have been eating bats for centuries? Sorry for my lack of understanding, Why now, when people been eating bats for centuries? If bats are simply a vector, where does that virus come from?

Bats are reservoirs of many important human pathogens, some are emerging infections (e.g., 2019-NCoV, the coronavirus in the news recently), and some are not (e.g., rabies).

Contact between humans and bats is certainly not a new phenomena, but there is more required for an emerging infection than a reservoir and a new host. There must be some bridge that allows a virus to cross a previously effective species barrier. For SARS, there was an intervening amplifying host, the palm civet.  We've now had long enough to study the molecular biology, so this is now quite well described:

  Once SARS-CoV had jumped from bats to civets, it underwent further mutations in civets. The first K479N mutation allowed SARS-CoV to jump from civets to humans and the second S487T mutation allowed SARS-CoV to transmit from human to human, leading to the severe SARS outbreak in 2002–2003.

It may be useful to understand that, as they are RNA viruses, coronaviridae have a high error rate, increasing the rate of mutation. Additionally, making a species jump may allow for novel recombination.


Can someone suggest me good opencourseware links for learning computational biology basics? My internet is slow and I have only 1GB data usage allowed for this month. And I want to make maximum out of it for learning some basics of computational biology.

Which are the best online course (freely available lectures) suggestions for me?

http://ocw.mit.edu/courses/health-sciences-and-technology/hst-508-genomics-and-computational-biology-fall-2002/audio-lectures/

Download all the slides if you want good resources.


Why is there a layer of moist lining the inner walls of alveoli? I'm taught that the walls of the alveoli are moist, so gaseous oxygen molecules can dissolve into this water. This then allows the dissolved oxygen (liquid state) to diffuse faster from the alveoli into the bloodstream through the basement membrane.

However, why is it faster for gaseous oxygen to first dissolve in water (transitioning into liquid state) then diffuse through the basement membrane and dissolve into the blood stream than for gaseous oxygen to directly diffuse through the basement membrane and then dissolving into the blood stream?

The second mechanism would eliminate the need for the moist layer lining the alveoli wall.

Is there some physical or chemical explanations to this phenomenon?

The fluid in the alveoli contains phospholipoproteins that act as pulmonary surfactant, which keeps the alveoli open during breathing.


Additive property of taste It might be a dumb question to ask, but I find it confusing.
Is the perception of taste additive?

Or to be more precise, can two tasty food items combine to give a more delicious product?

For me, this sounds logical. I believe that the sense of taste is due to some chemical reactions in our mouths, which in turn fire up our taste receptors to give some specific signals to the brain. So when two tasty foods combine, there would be more signals that are identified as 'Tasty' by the brain. That should give the food combination a stronger taste than its constituents.

But I found some contradicting examples.

I like to drink tea and coffee. But once, when I accidentally mixed a cup of tea with coffee, it wasn't tasty at all.
I have seen some specific 'COMBINATIONS' of foods that taste better than their constituents.

What does this mean? More likely, my understanding of taste perception is flawed.  If it is, then what is the real working mechanism of taste?

I would classify the neurological phenomenon of "taste" or "tastyness" as an emergent property (1), and therefore synergistic (i.e. not adequately explained simply by additive effects). For example, when something "tastes like chicken" that's a synergistic sensory pattern in your brain involving the specific ratios of the 5 basic tastes(2) on your tongue, along with your sense of smell, and the sensation of the food's texture in your mouth (is it moist, dry, viscus, etc). This helps explain why simply combining two tasty flavors (coffee+tea) does not necessarily yield something twice as tasty, and also why foods which might not be tasty on their own, can be tasty in the right combination (e.g. potatoes+onions+salt+oil+heat makes tasty hashbrowns, but none of those foods are especially tasty on their own).

Taste preference (tastyness) also involves a certain amount of neurological learning, which is partially why often people don't like the taste of something like coffee when they are young, but learn to enjoy it as they find it elicits a response from the reward centers of the brain.

In summary, "tastyness" is most likely an emergent and synergistic property of a system of complex sensory and neurological interactions, and not simply an additive.


Why does plasma protein saturation of a drug increase its volume of distribution and clearance rate? I need help understanding this statement from Goodman and Gilman's "The Pharmacological Basis of Therapeutics:"

  For a drug that is metabolized
  by the liver with a low intrinsic clearance-extraction ratio, saturation
  of plasma-protein binding will cause both V (distribution volume) and CL (clearance rate) to increase as drug concentrations increase.

This is how the textbook defines distribution volume and clearance.
$$\text {distribution}\ \text{volume} = \frac{\text{amount of drug in the body}}{\text{concentration in plasma or blood}}$$

$$\text{clearance rate} = \text{bioavailability} \ \cdot \frac{\text{dosing rate}}{\text{concentration at steady state}}$$

I think I get the grasp of it somewhat, but I would like to verify if my reasoning is correct.

The reason why volume of distribution increases is because the drug is distributed to tissues other than blood once the plasma proteins are saturated with the drug. As a result, the amount of drug in the body increases while the concentration in plasma or blood stays the same.  Hence, the increase in distribution volume.

As for clearance rate, it increases because the zeroth order reaction is always faster than the first order reaction in Michaelis-Menten kinetics.
However, I am not sure why the fact that plasma proteins are saturated matters.

For the distribution volume to increase, unbound drug concentration in plasma should stay constant while tissue drug concentration has to increase when more drug is administered. For clearance rate to increase, however, unbound drug in plasma needs to be able to increase when more drug is administered. What am I understanding wrong?

First a couple of clarifications:

You wrote:

For the distribution volume to increase, unbound drug concentration in plasma should stay constant while tissue drug concentration has to increase when more drug is administered.

Actually, it is the total drug concentration in plasma (bound plus unbound) which matters while calculating distribution volume.

Clearance is better defined as $ \frac{\text{Rate of elimination}}{\text{Plasma concentration}}$. The equation you mentioned above is a derived formula for calculation of dosing rates.

Now for the answer. The basic principle is: when plasma proteins get saturated, increasing drug concentration increases both tissue concentration and unbound drug concentration in plasma, because the drug has "nowhere else to go".

Thus your reasoning is correct when you say this:

The reason why volume of distribution increases is because the drug is distributed to tissues other than blood once the plasma proteins are saturated with the drug.

Of course, our understanding here is that the increase in total plasma concentration is marginal as compared to the increase in tissue concentration.

However, the following does not seem to be correct:

As for clearance rate, it increases because the zeroth order reaction is always faster than the first order reaction in Michaelis-Menten kinetics.

(Perhaps you are confusing plasma proteins with drug metabolising enzymes?)

The answer to the clearance part can be obtained when you recall that we are talking of a drug with low hepatic extraction ratio. Thus, clearance is proportional to unbound drug concentration. As already mentioned above, unbound drug concentration increases on increasing drug concentration.

Hope that answers your queries.

Reference:

Buxton ILO. Pharmacokinetics: the dynamics of drug absorption, distribution, metabolism, and elimination. In: Brunton LL, Hilal-Dandan R, Knollmann BC (editors). Goodman & Gilman's the pharmacological basis of therapeutics. 13th ed. New York: McGraw-Hill Professional; 2017. pp 13–29.


DNA damage theory of aging and sex If aging is due to accumulation of damages in DNA, then shouldn't the DNA in gametes also be damaged and so the next generation should be borne old! How does gametes avoid this DNA damage accumulation?

I've answered a related question, which was wondering why older people get more cancer from accumulated DNA damage and yet their children aren't immediately susceptible to it, here:
https://medicalsciences.stackexchange.com/questions/19915/why-do-age-related-dna-transcription-errors-not-manifest-in-children-as-readily/
Quoting from my answer there:

...a parent does not pass on all their mutations in all their cells, they pass on just one, which need not have any deleterious mutations at all, even if the parent has cancer themselves in some other part of the body.

If that one cell is defective in some way, it is less likely to be involved in creation of a successful pregnancy, and may lead to miscarriage. Therefore, the probabilistic process of reproduction tends to result in offspring from selection of healthier gametes.

There are in fact mutations that accumulate in gametes, but if any of those mutations are very serious, they are unlikely to support development of an entire new organism, and they are also relatively few. The burden of age on the genome is spread over all the cells in a body, and worst in types of cells that divide the most, when errors are most likely to occur.


Material on the analysis of (micro)array data I'm at the moment analyzing cytokine array data. The available material on the statistical analysis of these data is more than unsatisfactory. Since a lot of effort is being made in the analysis of gene microarray and MALDI-TOF proteome data, I seek to apply these methods on my cytokine arrays.

What is a good introductory text on microarray analysis, especially quality control and error estimation?

A good place to start would be Statistical Methods for Microarray Data Analysis. I'd also suggest papers from the labs of Terry Speed, Gary Churchill, John Quackenbush, and Gordon Smyth.

Also, I found some papers that specifically reflect on your exact issue: how to apply the methods developed for DNA microarrays to analyze protein arrays.

Eckel-Passow et al. Experimental design and analysis of antibody microarrays: applying methods from cDNA arrays. Cancer Res. 2005 Apr 15;65(8):2985-9.
Royce et al. Extrapolating traditional DNA microarray statistics to tiling and protein microarray technologies. Methods Enzymol. 2006;411:282-311.


term for species that produces males only to mate with mother or sisters In reading about unique reproductive strategies I've run into two closely related and comparatively unique mechanics.  Both involved a female who was born 'pregnant' with at least a male, but the male sole job was to impregnate the mother/sisters prior to immediate death, with the females never mating with a male other then their relative.  Thus, the outcome feels more similar to self fertilization of hermaphrodites then your traditional mutli-sex mating strategy.

I have heard of at least two species that did this.  One in which the son was born along with a batch of females that he immediately mated with, another where the son actually mated with his sisters while still in the womb, and the children would then eat their way out of the mothers corpse to be born (fun stuff!)

I also recall reading an article which said a mother would lay an egg to have a son who would mate with the mother to produce females and then immediately die.  However, this sounds so similar to the Haplodiploidy system that I wonder if the article I had been reading was simply misrepresenting a regular Haplodiploidy system by implying the males would never mate with other females (I read about it awhile ago so not sure, does anyone know if a species uses a haplodiplody system where the male never survive long enough to mate with other females?

I'm wondering if there is a name for this reproductive strategy.  Specifically for any strategy where a male is produced, but only as a means of providing DNA to mother or sisters; with no means to mate with non-familiar entities.

The non-random mating of individuals within a population is called Assortative Mating. Mating specifically with individuals that share similar traits is called Positive Assortative Mating. However, sharing similar traits doesn't imply being closely related.

The reproduction by two closely related individuals is called inbreeding. The opposite of inbreeding is outbreeding (a.k.a. outcrossing).

To my knowledge, a mating system where all individuals inbreed doesn't have a special term. Searching google.scholar for mating system inbreeding will show you a lot of articles that talk about mating systems where all individuals inbreed without needing to use a specific term for it.


Is hunting animals, crafting and attacking/defending from enemies intellectually equivalent to learning quantum physics? Our brains were shaped after natural selection. Which means that, as long as we were being affected by it, our brains were changing, evolving.

Once we stepped out of nature and stopped being targets of natural selection, our brains (structurally speaking) stopped changing.

Civilizations rose, humanities and science developed, and you know the rest of the story.

But the brains that we used to create all that is the same brain that was shaped by natural selection. A brain that was concerned with animal hunting, food gathering, fighting with enemies, relating socially and so forth. It is curious to notice that we used that same brain to develop algebra, geometry, physics, astronomy, arts, and so on.

So, would it be correct to say that all those activities from our ancestors living in nature (gathering, hunting, fighting) are INTELLECTUALLY equivalent to quantum physics, i.e.? Because our brain capacity is limited to what happened to it during natural selection (while we were living in nature), so would it be safe to assume that whatever complex thing we can think of (such as quantum physics) is actually as hard as those activities our ancestors performed in nature?

This may be a very stupid question, but I couldn't find fallacies or wrong assumptions in my thought, but my conclusion seems to be a bit... unexpected? Please, correct me if I'm wrong, I'd really like to know the answer to this.

Addressing some assumptions/presumptions apparently present in the question (this might be too long for a comment):

First, natural selection has not stopped. The sexual selection might be more active than ever, so there is ongoing "pro-fertility" selection and some segregation "pro-smarts". Not every member of contemporary potplation is capable, even with unlimited attempts at education, of doing something useful with quantum physics.

Second, surviving in the wild and fighting enemies are competitive enterprises. Which means that the task is of potentially unlimited difficulty: the better you are at survival, the more you procreate, the more pressure you put on limited resources of the environment, to harsher climates you spread. With enemies, especially those evolving along with yourself, this unlimited competitiveness is even more obvious.

So, the question could possibly be framed differently: how hard our ancestors, living in nature, made the intellectual part of the task of competing with each other? Apparently, about that hard.


What are the features on a microscope one needs in order to do lab work? By lab work I mean urinalysis, blood work(live as well), fecals, cytologies, histologies and all other.

I have read(partly) a book(from 2002) on lab diagnostics and the author did not mention anything about diagnostics. I've spent a lot of time searching on google as well and I did not get anything.

It sounds like you need a microscope for standard microbiology lab tests. At a minimum, any standard wide-field/brightfield microscope would work. If most of your histology work involves colorimetric stains (e.g., H&E, gram staining), you don't need any fluorescence capability. If you are working with a lower budget, look at the new lines of LED-based miroscopes, which dramatically drop the cost (I think around $10,000).

If you plan on doing a high volume, in particular of fixed histology/cytology slides, then you may want to invest in some of the automated slide scanner microscopes. They have a small benchtop footprint and can be programmed to image large areas automatically, for later analysis.


Is there a way to see what representations are currently displayed in PyMOL? I am using PyMol to visualize .pdb protein structures.

I show/hide representation a lot, and sometimes I get confused with what representations are currently displayed. So I end up with doing a lot of hides (basically trying to hide each representation).

Is there a command which shows me what representations are currently used.

For instance if I have used

show ribbon
show lines
show mesh
hide lines

and than use some sort of showRepresentation
it will return me ribbon, mesh

You can use "as" to switch to a particular style (http://pymolwiki.org/index.php/As
):

as cartooon, 11AS and chain a

You can also hide everything, to remove all representations (http://pymolwiki.org/index.php/Hide):

hide every, 11AS and not (n. ca+c+n and resi 5-10)

I'm a fairly expert user of PyMOL and I've never seen an API exposed which will show you what representations are being used. That's not to say that it doesn't exist, there are a variety of undocumented features and commands still.

The problem is it isn't as simple as ribbon,mesh.  Every single atom can be displaying any combination of representations, so as an API call or command, it would have to return the status of every atom in your selection. If the displayed representations are exposed somewhere they're probably in a very low level format like that, and not of use unless you're a programmer.


What is a good set of notes to study human's eye mathematically? I want to learn about the human eye. I could read a lot of online literature about it.

However, ideally I would like to study human's eye by solving some maths exercises. I suspect people have done this before. How would we have glasses otherwise?

Maybe you know good maths notes + PROBLEMS that would give me an insight into how an eye works?

The notes don't have to comprise a whole course. One chapter is enough, as long as there are some maths exercises attached.

Mathematical models of the human eye

Fluid mechanics

Mathematics of Eye

Physics of blinking
Thin layer approximation (lubrication theory)
Aqueous flow in eye chambers
Tonometry

Those two links provide quite a sufficient description of how to mathematically describe/analyze the human eye. It seems that you need to be fairly familiar with (at least) differential, integral and vector calculus in order to competently study the eye, mathematically. If you can get through (and understand) the fluid mechanics then you'll be well off.

And as for practice problems, aside from the examples in those links, I'm not sure you'll so easily be able to find sets of mathematical practice problems that specifically describe the eye. Or at least, I wasn't able to find any such  repository.


Primary function of the enzyme lipoprotein lipase I read here and here that the function of lipoprotein lipase is to facilitate fat uptake and storage in adipose tissue. Could anyone provide a slightly more expanded explanation, without going into too much detail, and without the use of too much jargon (I am not a biologist). I have read the wikipedia page, but sadly I didn't understand it....Thanks !

Edit: One of the things that is confusing me is what "fat uptake" means in this context.

Fat uptake means cells eating fat.

I'll try to keep it simple, so forget the many approximations. You need first to consider that most fat circulates in the blood under the form of triglycerides (TG). TG are not soluble in water, so how do they circulate? They are hidden inside cargo vehicles called lipoproteins. When a circulating lipoprotein touches a cell, if the cell expresses lipoprotein lipase (LPL), first LPL would trap the lipoprotein cargo, and then will start to catabolize the TG.

Importantly, there are no efficient TG cargoes inside the cell, so the function of lipoprotein lipase is to make fat easy to move inside the cell. TG are a chemical assembly of one glycerol and three fatty acids. Of note, there are good fatty acid cargoes inside the cell, so LPL will break TG into glycerol and fatty acids so that they can be further metabolized depending on the cell type.

Heart and muscle cells will bring fatty acids to mitochondria where they will be oxidized to produce energy. With reference to your question, adipocyte cells will bring fatty acids to other cellular compartments where they will be converted back to triglycerides and stored as fat. That's why you read that LPL facilitates fat uptake and storage in adipose tissue.


Why do high cholesterol levels result in a buildup of fat in blood vessels? As is well known, high levels of cholesterol can lead to a buildup of fat in blood vessels, which can lead to them being constricted which makes it more difficult for blood to pass through. In fact, this can end up with the formation of fatty deposits that, if they suddenly break, could result in a clot that causes a heart attack/stroke. Therefore, the resulting buildup of fat because of these high cholesterol levels is highly important.

My question is why do higher levels of cholesterol result in a buildup of fat at all? Why do fatty acids care that there's more cholesterol around? I know cholesterol and fats are both lipids, but beyond that, I don't see the connection.

The phrase "high cholesterol", and the measurement itself is a marker for high levels of a particular lipoprotein, Low density lipoprotein (LDL). Because cholesterol and triglycerides are not soluble in plasma, they are packaged by the liver into soluble particles called lipoproteins. Packaged in lipoproteins, these lipids are transported throughout the body, for use by different organs and tissues. As these lipids are dropped off, the lipoprotein is converted from one form to another, with characteristic biophysical and physiologic properties. The LDL is a late stage of a lipoprotein before reuptake at the liver (and other organs, but mainly the liver) via the LDL receptor. We happen to know that people who have high levels of circulating LDL are at risk for, e.g., cardiovascular disease because of The Framingham Study, and that if you can reduce circulating LDL levels you can decrease the risk for these diseases. The molecular basis of this risk was demonstrated to be, in large part, failure of clearance of LDL particles because of ineffective receptor mediated endocytosis, as described in this wonderful 1986 paper in Science.

From this presentation:

Some LDL cholesterol circulating through the bloodstream tends to deposit in the walls of arteries. This process starts as early as childhood or adolescence.
White blood cells swallow and try to digest the LDL, possibly in to digest the LDL, possibly in an attempt to protect the blood vessels.
In the process, the white blood cells convert the LDL to a toxic (oxidized) form.
More white blood cells and other cells migrate to the area, creating steady low steady low-grade inflammation in the artery wall.
Over time, more LDL cholesterol and cells collect in the area. The ongoing process creates a bump in the artery wall called a plaque. The plaque is made of cholesterol, cells, and debris.
The process tends to continue, growing the plaque and slowly blocking the artery.

There is a good overview of the general physiology here in Robbins The Pathologic Basis of Disease. Chapter 5, Genetic Disorders, reviews the physiology, and the relevance to disease, in the section on Familial Hypercholesterolemia. The review is relevant to hypercholesterolemia in general.


Why only 6 water molecules are formed in the aerobic degradation of glucose? I am studying the aerobic degradation of glucose and it seems that for every glucose molecule we should obtain $\ce{10H2O}$ molecules. However, it is known that we only obtain 6.

$\ce{C6H12O6 + 6O2 -> 6CO2 + 6H2O}$

(I am not going to focus in all products and reactants, but just in the important ones for the formation of water molecules)

First, in the glycolysis, for each molecule of glucose we obtain two water molecules, $\ce{2NADH+}$ and 2 pyruvate molecules. By the oxidation of two pyruvate molecules we obtain $\ce{2NADH+}$ and 2 acetyl Co-A molecules. So we are going to pass twice through the Krebs cycle, obtaining $\ce{6NADH+}$ and $\ce{2FADH2}$, and requiring 4 water molecules.

So, when we arrive to the electron transport chain, we have a negative balance of 2 water molecules, and we have $\ce{10NADH+}$ and $\ce{2FADH2}$. We have been told that for every of these molecules 2 electrons go to the electron transport chain, that means that a total of 24 electrons go to the system. The problem comes here:

$\ce{4e- + 4H+ + O2 = 2H2O}$

So, bearing in mind that we have $24e^-$, 12 water molecules should be formed, so at the end, we have gained 10 water molecules, but we know that the number of water molecules formed should be 6. So, clearly there is something wrong in my explanation. I would be very pleased if you could tell me what is wrong.

Thanks in advance.

Your confusion comes entirely from this equation:

$\ce{C6H12O6 + 6O2 -> 6CO2 + 6H2O}$

This reaction is the combustion of glucose. This is not how glucose is oxidized in cells! Why so many biology texts and courses present this equation when introducing metabolism is beyond me.

Indeed, your tracking of water molecules is correct: starting with one glucose molecule, 2 waters are produced in glycolysis, 4 are consumed in the tricarboxylic acid cycle and 12 are produced during oxidation of NADH/QH2 (ie FADH2). This gives a net total of 10 produced.

Why is this different from the combustion of glucose? The answer lies in the oxygens introduced by inorganic phosphate during substrate level phosphorylation. Consider the balanced net reaction for the biological oxidation of glucose (simplified by ignoring ATP produced by oxidative phosphorylation and substituting ADP/ATP for GDP/GTP):

$\ce{C6H12O6 + 6O2 + 4ADP + 4P_i + 4H+ -> 6CO2 + 4ATP + 10H2O}$

In particular, consider the formation of ATP from ADP and Pi (HPO42-). In both substrate level phosphorylation reactions (catalyzed by GADPH/PGK in glycolysis and succinate-CoA ligase in the tricarboxylic acid cycle), inorganic phosphate nucleophilically attacks the activated carbonyl (thioester) of the substrate and is then transferred to ADP (to form ATP):

The oxygens of the original inorganic phosphate are coloured red. The key point is that an oxygen atom from HPO42- is transferred to the substrate. This oxygen is later removed in the form of carbon dioxide, via oxidative decarboxylation, during the conversion of pyruvate to acetyl-CoA and in the tricarboxylic acid cycle. This occurs four times for each glucose molecule entering glycolysis and is accompanied by the reduction of NAD+ to NADH. Given that NADH is used to reduce molecular oxygen during the electron transport chain:

$\ce{NADH + H+ + 1/2O2 -> NAD+ + H2O}$

...this explains where the four, apparently extra, water molecules come from when comparing the combustion of glucose with its biological oxidation.


Why do we like to touch fluffy things? I read this article but it didn't explain much. Is the fact people like to cuddle pets with fur connected anyhow with our past when our ancestors had fur as well - and therefore could evolve an instict to enjoy hugging someone furry as an expression of friendship.

An answer I got from Jan Kolář of Charles University:

  I'm not sure that people prefer fluffy things just from the fact that
  they are fluffy. They like things that are soft to touch such like
  pillows. The popularity of fluffy things might have a simple
  explanation: There's no danger of getting cut.

So the fact we like to cuddle with dogs and cats has probably nothing to do with our furry past.


What are the differences between HPRD and BIOGRID databases? What are the differences between HPRD and BIOGRID protein-protein interactions databases?

What are their purposes? Why do we need two different databases?
How is data collected into each one?
How different are they in the interactions they contain?
Is one considered more reliable than the other?
Which one is more commonly used when benchmarking models?
Are there any other commonly used PPI databases?

Short Answer

In a nutshell, there are two major differences:

Species range: BioGRID integrates multiple species' protein-protein interaction (PPI) data, whereas HPRD focuses mainly on Human data.
Functionality: HPRD has some GUI tools that can interact directly with it's database (e.g. BLAST - for searching proteins and their binding partners via sequence alignment) whereas BioGRID is mostly just a database.

Long Answer

In bold are the unique features of each database.

About HPRD:

  The Human Protein Reference Database represents a
  centralized platform to visually depict and integrate information
  pertaining to domain architecture, post-translational modifications,
  interaction networks and disease association for each protein in the
  human proteome. All the information in HPRD has been manually
  extracted from the literature by expert biologists who read, interpret
  and analyze the published data. HPRD has been created using an object
  oriented database in Zope, an open source web application server, that
  provides versatility in query functions and allows data to be
  displayed dynamically.

  FAQ HPRD: Why did you decide to develop yet another database instead of integrating other existing databases?"
  We believe that biological databases are still in their early stages
  and no protein database can be considered as an established standard.
  We feel that a variety of databases trying to solve problems in
  diverse ways provide the biologists the possibility of choosing their
  favorite. Our approach is radically different from existing databases
  and we want to offer biologists the possibility of choosing instead of
  imposing one database by default. Besides, most of the databases are
  automated and ours is manually curated to avoid errors. We are also
  trying to provide information that few other databases provide.

About Biogrid:

  The Biological General Repository for Interaction Datasets (BioGRID)
  is a public database that archives and disseminates genetic and
  protein interaction data from model organisms and humans
  (thebiogrid.org). BioGRID currently holds over 720,000 interactions
  curated from both high-throughput datasets and individual focused
  studies, as derived from over 41,000 publications in the primary
  literature. Complete coverage of the entire literature is maintained
  for budding yeast (S. cerevisiae), fission yeast (S. pombe) and thale
  cress (A. thaliana), and efforts to expand curation across multiple
  metazoan species are underway. Current curation drives are focused on
  particular areas of biology to enable insights into conserved networks
  and pathways that are relevant to human health. The BioGRID 3.2 web
  interface contains new search and display features that enable rapid
  queries across multiple data types and sources. BioGRID provides
  interaction data to several model organism databases, resources such
  as Entrez-Gene, SGD, TAIR, FlyBase and other interaction
  meta-databases. The entire BioGRID 3.2 data collection may be
  downloaded in multiple file formats, including IMEx compatible PSI MI
  XML. For developers, BioGRID interactions are also available via a
  REST based Web Service and Cytoscape plugin. All BioGRID documentation
  is available online in the BioGRID Wiki.


Reducing the Proportion of Phenotype in Hardy Weinberg Population through Selection I was given the following question:

You travel to an unknown island and find a population of strangely colored
slugs! Upon close investigation, you notice that 16% of the slugs have a
shriveled tails, a most terrible condition you decide to name Yilunemia. The condition makes the affected slugs have a 50% chance of surviving to
reproduce. This is a autonomic recessive condition caused by a single gene,
and heterozygotes are not affected.

Assuming Yilunemia confers no discernible evolutionary advantage, how
many generations should it take for the proportion of slugs with the Yilunemia disease to fall below 5%?

Possible answers:

5
6
7
8
9

I've tried to apply usual formula for frequency after selection:

0.36 + 0.48 + 0.16 = 1

0.36 + 0.48 + 0.5 * 0.16 = 0.92

Divide by 0.92 gives:

0.39 + 0.52 + 0.087 = 1

If I keep doing this, after the 3rd generation, the frequency of Yilunemia condition is 0.045, which is less than 5%. However, this isn't an answer choice, therefore I must be doing something wrong.

Any suggestions?

The theory

You have to use the diploid selection equation (see here). Let $p$ be the the frequency of the recessive allele of interest, you get

$$p' = \frac{p^2 W_{aa} + p(1-p)W_{aA}}{\bar W}$$

, where

$$\bar W = p^2 W_{aa} + 2p(1-p)W_{aA} + (1-p)^2W_{AA}$$

You can simply iterate over with this equation. Do no forget to recompute $\bar W$ at each generation as the allele frequency changes, so does the mean fitness $\bar W$. Also, do not forget that we are looking for the generation where the frequency of sick individuals is lower than $0.05$, that is the generation where $p<\sqrt{0.05}$.

I don't think this recursion equation has any general solution unfortunately. This would mean that iteration is the only way to got.

The practice

I am a bit too lazy to compute everything by hand so here a short R code that will do the calculations for us.

frequencySickIndividuals = 0.16
p = sqrt(frequencyHomozygoteRecessiveMutants)
waa = 0.5
waA = 1
wAA = 1
for (generation in 0:10)
{
    frequencySickIndividuals = p^2
    cat(paste0("Generation ", generation, " frequency sick individuals = ", frequencySickIndividuals, "\n"))
    p = (p^2 * waa + p*(1-p)*waA) / (p^2*waa + 2*p*(1-p)*waA + (1-p)^2*wAA)
}

It outputs

Generation 0 frequency sick individuals = 0.16
Generation 1 frequency sick individuals = 0.120982986767486
Generation 2 frequency sick individuals = 0.0935350533786218
Generation 3 frequency sick individuals = 0.0738632061510922
Generation 4 frequency sick individuals = 0.0594638505565122
Generation 5 frequency sick individuals = 0.0487003101360286
Generation 6 frequency sick individuals = 0.0404940467744661
Generation 7 frequency sick individuals = 0.034123112395776
Generation 8 frequency sick individuals = 0.0290951856295452
Generation 9 frequency sick individuals = 0.0250680151553009
Generation 10 frequency sick individuals = 0.0217991643532054

So, it actually takes 5 generations to reach an allele frequency lower than $\sqrt{0.05}$.

Source of information on hardy-Weinberg problems

Note by the way, you might be interested in having a look at a tutorial on how to solve Hardy-Weinberg problems on the post Solving Hardy Weinberg problems.


What was the first piece of work in computational biology? What was the first piece of work in computational biology? I'm ideally looking for a paper.

I am not interested in works that involve data management or data analysis but work that model biological processes through numerical simulations or numerical approximations of analytical results.

I don't believe you'll ever find the first work in bioinformatics (or computational biology, as you put it), however the field really began in the times of accumulating data about protein biochemistry. Computational biologists (before they had access to the computer) would be writing and analyzing morphologies and types of proteins with pencil and paper.

But you can go even further back than this. "Alignment" is another old technique used in bioinformatics. This is establishing the amount of similarity between two DNA sequences, or rather the degree of similarity between any two objects or data sets in computational biology.

Your question, though, asks for a scientific paper (one of the oldest) on bioinformatics. This is arguably  M. O. Dayhoff's paper: "A Computer Program to Aid Primary Protein Structure Determination." (1962)

This is the first formal paper that limits the scope of computational biology to the definition provided by this BioPlanet article and generally agreed by many:

  Bioinformatics is the application of computer technology to the management of biological information.


What type of photosynthesis is performed by phytoplankton? I am not a biologist, but I know there exist three variants of photosynthesis, namely C3, C4 and CAM.

I would like to know what type is used by the ocean's phytoplankton? It might also be that different photosynthetic mechanisms are used by the bacteria vs. algae. I have searched the web, but the information I find is too broad.

I'm not sure that all phytoplankton perform the same type of photosynthesis.

Originally, people thought that they all performed C4, on the basis of genome sequencing, which revealed the presence of genes important for C4 photosynthesis.  However, experiments on individual species seemed to indicate that the phytoplankton were performing multiple types of photosynthesis (source).

EDIT: CAM is unlikely, as that is an adaptation for dry environments.

EDIT 2: and of course, some phytoplankton appear to have both C3 and C4 pathways. In short, you can't generalize.


How does zoo and laboratory animal feeding work? What steps are taken to ensure those animals are fed adequately? When dealing with larger populations of animals, how is it ensured that all of those animals received food during a certain time period, and not fed multiple times by different people working different shifts? Is there a procedure in place for identifying and treating animals with over and under nutrition?

I volunteered for 3 years at a large mammal laboratory where we diligently tracked the weight and caloric intake of each of our animals. Diets were weighed out each morning and total calories could be calculated based on the known caloric value of the particular food item.

We fed our animals during training sessions and would adjust the individual's food intake based on their appetite/motivation (i.e. if an animal was full, they'd drop the piece of food they earned or leave the session). This would indicate that we could decrease the individual's diet in small increments.

The animals were also weighed each week. Weight and caloric intake were recorded in daily logs using FileMaker Pro. This allowed us to view fluctuations of each throughout the year and compare to previous years. If an animal's weight was a bit lower at a certain time of year than it typically was in past years, we could increase their diet.

Diet items were selected based off of the animals' natural diet.


Evolutionary support for parenting book "The happiest baby on the block" The book by Dr Harvey Karp (MD) The Happiest Baby on the Block proposes that the duration of human gestation has evolved as a tradeoff between cranial size and development of the infant.  He hypothesizes that from an overall developmental perspective human babies are all premature and would benefit from additional time in their mother's womb; however, because humans have such big brains, and therefore our babies have big brains, the infant needs to be born earlier than would be developmentally ideal so that it doesn't get stuck in the birth canal.  The result is babies that have big brains but are highly vulnerable and dependent on their parents until their development progresses further.

I discussed this with some students in class as an example of the use of ideas from human evolutionary ecology and life history theory in the popular press, but with the disclaimer that I had no idea if any of Karp's ideas are backed up by any evolutionary or anthropological data.  Could anyone point me towards literature that support or contradicts Karp's claims?  For example, are human infants more dependent than those of other primates?

[The upshot of Karp's theories are that the best way to have a "happy" newborn is to mimic conditions that it would experience in the womb, such as swaddling.  Works for my child!]

How many more weeks in utero does Karp think would be ideal? I don't know Karp at all, but a quick search indicates he's known for soothing babies by swaddling. Great. My mother swaddled all her infants many decades ago.
If he is comparing human neonates to  primate neonates, he's correct. Baby primates are born pretty much knowing how to cling onto the mother with four extremities, necessary because primates are quadripedal, and need their arms to walk as well, meaning baby needs to hold on, aided by opposable toes. (Chimps and gorillas do support the baby with one hand longer, though.
But what evolutionary advantage would it serve for our infants to come out grasping? humans are bipedal, meaning we have arms that can be used to carry an infant. If we need our arms, we have the intelligence to fashion slings or carriers.
The same goes for any ability: sight, motor skills, etc. They don't need to be born with these skills, because they are cared for.
Antelopes drop a newborn which is up in minutes and able to see and run. Cats drop a newborn which can wiggle, crawl some, is blind and as helpless as a human.
Babies, through evolution, are able to live outside the womb (assuming no complications) without extraordinary maternal assistance from about 36 weeks on. A look at growth charts show steep rises in both cranial size and weight gain.

But you can see that a baby's head at the 10%ile takes at least six weeks to catch up to a baby the size of one born at 90%ile. Why doesn't that baby just gestate for 6 more weeks?
There is much more than head size going on here. There is the placental size, the amount of amniotic fluid, the possibility of meconium aspiration, etc.
Stillbirths are twice as common at 42 weeks and 4 times as common at 43 weeks.

Approximately 20% of postterm (41 weeks gestation) fetuses have fetal postmaturity syndrome, with chronic intrauterine growth restriction from uteroplacental insufficiency. These pregnancies are at increased risk of umbilical cord compression from oligohydramnios, [low Apgar scores], intrauterine passage of meconium, and short-term neonatal complications (such as hypoglycemia, seizures, and respiratory insufficiency). ...[T]he 4-fold decrease in the incidence of the meconium aspiration syndrome in the United States from 1990-1998 has been attributed primarily to a reduction in the postterm delivery rate [(induced delivery at 41.5 weeks)]. Postterm pregnancy is also an independent risk factor for neonatal encephalopathy and for death in the first year of life.[17, 18]

Maternal complications and death also increase with post-term deliveries.
Are term babies actually evolutionary preemies? I haven't read Dr. Karp's book or heard his reasoning, but it seems superficial to me. Medically, from an infant and maternal standpoint, a 38 week delivery is ideal. Over hundreds of thousands of years, the female uterus and pelvis, and the fetal placenta and amniotic fluid found the most favorable time for delivery into a human environment.
If we gestated for two years, like elephants, yes, our babies would be more capable at birth, but we aren't elephants, and mothers and babies would die.
Postterm Pregnancy (Medscape)
Elephant birthing and calves (Wikipedia)


Is it plausible that eukaryotic organelles like flagella and cilia are the result of endosymbiosis with spirochetes? This was a claim by Lynn Margulis explained over at this link.

  The sense organs of vertebrates have modified cilia: The rods and cone
  cells of the eye have cilia, and the balance organ in the inner ear is
  lined with sensory cilia. You tilt your head to one side and little
  calcium carbonate stones in your inner ear hit the cilia.  This has
  been known since shortly after electron microscopy came in. Sensory
  cilia did not come from random mutations. They came by acquiring a
  whole genome of a symbiotic bacterium that could already sense light
  or motion. Specifically, I think it was a spirochete [a
  corkscrew-shaped bacterium] that became the cilium.

And why would our bodies incorporate spirochetes as part of our basic functionality?

  There are many kinds of spirochetes, and if I’m right, some of them
  are ancestors to the cilia in our cells. Spirochete bacteria are
  already optimized for sensitivity to motion, light, and chemicals… If
  I’m right, the whole system—called the cytoskeletal system—came from
  the incorporation of ancestral spirochetes.

Well, since all cells in a multi-cellular organism originally come from the same precursor cells, it’s hard to argue that some of them have endosymbiotic compartments that are missing in others, and notably their precursor.

Notably, there are species which possess both ciliary and rhabdomeric photoreceptor cells, and their precursor is non-ciliary. This is incompatible with Margulis’ endosymbiosis hypothesis.

PZ Myers has a good summary of the relevant papers [1, 2].

[1] D. Arendt, K Tessmar-Raible & al., Ciliary photoreceptors with a vertebrate-type opsin in an invertebrate brain, Science 306, 2004.
[2] D. Arendt, Evolution of eyes and photoreceptor cell types, Int J Dev Biol. 47, 2003.


How much total RNA can be extracted from Drosophila brain I am wondering how much total RNA could be extracted from a single D. melanogaster brain.
I could not find this information from the literature.

The closest hit was this paper, that claims that 16-21.9µg of total RNA can be extracted from 100 brains, which translates to at least 160ng for a single brain.

I also found in the supplementary material of this paper that 1µg of total RNA was extracted from 5-10 fly brains, which would also make > 100ng for a single brain.

I am asking the question because I am envisioning to perform RNA-seq of single Drosophila brains. The standard Illumina TruSeq library preparation protocol works with 100ng of total RNA. Thus I am wondering if this is realistic, or if I should rather target low input library preparation protocols.

In my opinion you should try low input library prep protocols because in my experience even with a decent quantity of RNA, standardizing the sequencing is not an easy job. The manual says that this kit works with 10-20ng of RNA; always assume the higher limit to be true. There is a higher chance of loss (relative) during extraction also. Try doing precipitation with 5M LiCl and a little glycogen along with alcohol; but assuming your yield is 80ng you can still run replicates for statistical comparisons.


Less oxygen in winter? Since Oxygen is produced by photosynthesis, would there be less oxygen in the air in winter, where the trees shed their leaves and the sun generally shines a lot less? If yes, would that be a noticable difference?

Pretty interesting question: The short answer to it is: Yes, the seasonal O2 levels vary with the season and this can be measured.
The paper in reference 1 says that this is connected to two phenomena: Production of O2 by photosynthesis and also the uptake and release of O2 in the oceans due to higher temperatures (warmer water dissolves less gases).

The paper in reference 2 says that the northern and the southern hemisphere are basically decoupled from each other. The northern hemisphere reaches its peak of maximum O2 concentration in June/July while the southern reaches its peak around January due to the slow mixing in the athmosphere. They also say that due to more ocean area on the southern hemisphere the uptake/release processes in the ocean play a much more important role there.

The graph from paper 3 also shows that the CO2 concentration is inverse compared to O2, since during the photosynthetic period of the year CO2 is consumed.

The following figure is taken from the website of "2° Institute" and is interactive, so can actually check, when the concentration is at which level. The general O2 concentration is getting lower, it is assumed that this happens due to the human CO2 production, the source can be found here.

References (please let me know in the comments, if you can't access the articles):

Seasonal and interannual variations in atmospheric oxygen and
implications for the global carbon cycle
Seasonal variations in the atmospheric O2/N2 ratio in relation to the  kinetics of air-sea gas exchange
Seasonal and short-term variations in atmospheric potential oxygen
at Ny- Ålesund, Svalbard


Help me identifiy this moth? I found this moth in Bengaluru/India. Its body length was nearly 2cm. Brown colored with three yellow rings.

This looks to be a handmaiden moth (Syntomoides imaon) which has been observed in this part of India.

Source: India Biodiversity Portal


Why do we need two markers to measure a recombination rate? In calculating recombination,

Why is it necessary to take into account pairs of loci where one marker is heterozygous?

Why is it necessary to take into account pairs of loci where both markers are heterozygous?

If at least one locus is homozygous

If a recombination event happens between two loci where at least one is homozygous, then you would not see anything. Consider for example the following strand sequences in a diploid individual

-----A-----B----
-----a-----B----

Whether a recombination event occurs or not, the two possible chromosomes passed down to an offspring are

-----A-----B----
-----a-----B----

Therefore, you cannot tell whether recombination has occurred.

If both loci are heterozygous

Now consider the following individual

-----A-----B----
-----a-----b----

If no recombination event has occurred between the two loci of interest then the two possible chromosomes that will be passed down are

-----A-----B----
-----a-----b----

If on the other hand a recombination event has occurred between the two loci of interest then the two possible chromosomes that will be passed down are

-----A-----b----
-----a-----B----

Therefore, you can tell whether a recombination has occurred or not.


How do plants prevent infection from retroviruses? Why are plants not affected by animal viruses such as retroviruses? What prevents them from being infected?

Virus are extremely host-dependent because they need to enter the host, move inside of it, use its replication mechanisms and codon usage. There are virus that cross the family boundry (ToMV for example) but crossing the kingdom boundry is less probable.  For example, animal cells don't have a cell wall, which is a major change and requires a change in strategy for entrance to plant cells.
For retrovirus, they simply are virus that can integrate into the host genome.  Several articles [1, 2, 3] describe retroelements that have been classified as retrovirus, retrovirus-like particles, and retroelements encoding coat proteins. This can lead to the conclusion that there are retrovirus in plants.
It is worth noticing that virus are not the major pathogens of plants (fungi are) and resistance to virus can be acquired even without understanding the mechanism.   This leads to a lower level of interest, funds, and researchers in the area, which leads to a lower rate of discovery of new virus.
In conclusion, we have not found a virus that crosses the kingdom barrier but have families of virus that contain both plant and animal virus.


What is the metagenome like for other classes of animals? Lately there's been a lot of discussion around the many non-human cells essential to a healthy human body — called the microbiome, or metagenome.  Much of this is in the gut microbiome.  See this question, for example.

The Human Microbiome Project at NIH emphasizes we are just beginning to measure the specifics of this for the human case.

I assume this is similarly true for all mammal species, and I don't know how much farther.  Fish have a fairly different body plan than mammals, including a fairly different gut. And coelenterates have an even more different body plan in many ways, again including the gut.

Does a typical fish depend on as large a microbiome as a human?  Is there much known about that?  What about jellyfish?

There are multiple parts to an answer for this.

1) There is not only a microbiome in the gut. So microbiomes in general are very diverse. A fish microbiome on the scales will of course be very different to the one on a human skin.

2) Gut microbiomes are also quite different both in taxonomic and functional content, as they are in different ecological niches.

3) There are microbiome studies for nearly every type of organism I could imagine now. Fish, insects, snakes, you name it. They differ in diversity and composition of their microbiome, but also the used methods and databases do differ, so it is hard to compare them.

4) The further away from well studied microbiomes we get, the less specific will be our assignment of taxonomy and function, because we have not seen enough comparable microbes before. So more information will be hidden in the "dark matter" (in metagenomics: reads not assigned to a taxon and/or function).

Unfortunately I don't know of any jellyfish microbiomes so far. Their body (as far as I know ) seems to be much more "permeable" for sea water (-> their environment) and thus I would think that they generally would have aquatic bacteria in whatever corresponds to their gut. The sea microbiome is said to be very diverse and far too little studied, although there are cool projects like the Global Ocean Sampling Day to try and close this huge gap as best as possible.


Why is the strength of genetic drift inversely proportional to the population size? I saw a concept on the Internet that says "the strength of genetic drift is inversely proportional to the population size". I don't know why they are inversely proportional? Can somebody explain? Thank you all!

Plane Crash Analogy

4 people in a plane crash

In a small aeroplane, there are 2 people that wear a blue shirt and 2 people that wear a green shirt. The plane crashes, half of the people died. The 2 survivors are those wearing the green shirt… well, nothing so surprising!

400 people in a plane crash

In a very big aeroplane, there are 200 people that wear a blue shirt and 200 people that wear a green shirt. The plane crashes, half of the people died. The 200 survivors are those wearing green shirt… This is quite surprising!

Genetic Drift

The same logic applies to genetic drift. Genetic drift is caused by events that modify the reproductive success of individuals in a random way (independently of their genotype). We usually referred to this as random sampling. At each generation, individuals are randomly chosen to reproduce and some genotypes might just happen to be chosen more often than others at a given draw (=at a given generation). Genetic drift pushes the frequency of allele slightly away from what would be predicted. According to the Wright-Fisher model, the frequency of alleles (of a bi-allelic gene) in a haploid population (to make it easier) in the next time step is given by:

$$p' = \frac{p \cdot WA}{p \cdot WA + (1-p) \cdot Wa}$$

where $p$ is there frequency of an allele at time = $t$ and $p'$ is the frequency at time = $t+1$. $WA$ is the fitness of the genotype which frequency is $p$ and $Wa$ is the fitness of the genotype which frequency is $1-p$. If the population is infinite, the predictions of this equation are exactly correct.

Now if we say that meteorites fall and half of the individual get killed. The probability of getting killed by a meteorite obviously does not depend on genetic predisposition, it is a question of chance! If you look at a population of 1 million individuals, half of them having the genotype $A$, the other half having the genotype $a$. It is very unlikely that more than 60% of all individuals that get killed are of the same genotype. Therefore, the meteorites won't change much the frequency of the genotypes. If you look at a population of 4 individuals 2 are $a$ and 2 are $A$, 2 of them get killed by a meteorite. Well, you have a probability of one half that the two survivors are of the same genotype and that the genotypes frequency would have changed drastically.

Genetic drift refers to these changes in allele frequency which are due to random events (such as meteorites) and the strength of genetic drift indeed depends on the population size for probabilistic reasons. The greatest the population size, the lowest is the strength (or the relative importance) of genetic drift.

How to model genetic drift

There are three famous models of genetic drift that all lead to very similar expectations. I shall just name them here but I will not develop the underlying mathematics.

Wright-Fisher model of genetic drift

Not to confuse with the Wright-Fisher model of selection written above
It models genetic drift as a random sample of the previous generation and hence uses a binomial distribution.

Moran model

It is based on a birth-death model (a type of Markov model).

Kimura's diffusion equation model

It is an extension of the above two models for a case of continuous time.


skin colouration in thalassemia Now when i was studying about thalassemia, I read that anaemia is its major characterstic. I can understand that fact. But it was also written that the skin gets pale.

  Wikipedia says that the skin turns yellowish.

I want to ask firstly is it that the skin gets darker when the affected person is exposed to sun and is otherwise pale?

And also why does the skin turn yellow/pale in the first place? Does that have to do something with Iron?

Thalassemia is a genetic disease, in which either the alpha- or the beta-globins are missing or mutated. The hemoglobin of the blood is a protein complex which in adults consists of 2 alpha- and 2 beta-globin subunits. The ratio of these proteins needs to be exactly right, if one of them isn't produced enough or even missing, this leads to non-functional hemoglobin and subsequently abnormal erythrocytes.

These are then removed and broken down in the spleen (which is often abnormally enlarged), which also leads to the breakdown of the non-functional hemoglobin. The main product of the hemoglobin breakdown is Bilirubin, which is yellow. The yellow skin is a sign of jaundice, which is caused by high levels of Bilirubin in the blood.
The cause for the high Bilirubin levels in the blood of Thalassemia patients is the abnormal high rate of Hemoglobin breakdown.


What is the biology behind a skin "mole"? Are the dark marks aka "moles" on our skin a patch of dead cells? If so, why is it not cleared over time? In a (probably) similar vein, why do scar marks from injuries remain long after new cells replace the dead cells?

[Feel free to edit out the second question if the answers are unrelated]

A mole is simply a benign tumour, i.e. a proliferated cell growth that hasn’t become cancerous. So moles are not dead cells, they are very much alive. The colour is caused by a high concentration of the melanin, which is also responsible for normal darker skin.

Since moles are tumours, they can – but in most cases don’t – give rise to melanomas, malignant skin tumours, when they lose susceptibility to cell growth regulation and start invading surrounding tissue.

Scar tissue is entirely unrelated and due to regular regrowth of epithelial cells after injury forming a linear collagen structure (as opposed to the skin’s normal collagen structure, which resembles a “weaved“ structure).


What's the name of this green fruit with little pikes fallen from a city tree on the pavement? What's the name of this green fruit with little pikes fallen from a tree on Paris (France) pavement ?

It is horse chestnut it is very common to plant chestnut trees in public parks and a lot of people do have them around their property and by the side of many roads.
What you have in your picture is the fruit and the leaves on the ground confirms that this is horse chestnut.
Source https://en.wikipedia.org/wiki/Aesculus_hippocastanum
The nut is poisonus and the toxin can cause loss of coordination and tremors in horses if they eat the nuts.
Touching or handling the nuts do not cause any adverse effect to humans they are only dangerous to humans if they are eaten.
Horse chestnut contains alcaloid saponins and glucosides that have a toxic effect on mamals.


Is a sequential double transformation acceptable? Standard protocol states having two compatible vectors being transformed simultaneously during the same procedure. I've come across a situation in which transforming one vector, obtaining results, and then transforming the other is preferable. Is there any reason to think that this wouldn't work? Do I risk losing my first vector upon transformation of the second?

If the plasmids you wish to transform are very big (more than 20kb), the co-transformation might not be very efficient (you might not get any colonies). Electroporation should work though, as electrocompetent cells are more efficient than chemically competent cells. Alternatively, as you have read, you could transform your first plasmid and select for it, and then make these cell that harbor it competent and transform the second plasmid. As long as you select for the plasmids (with kan/carb/etc resistance marker), the cells that grow on the selective media will keep both of them. If I were you, I would try the co-transformation and then if it doesn't work I would do the sequential transformation.


Why do neurones use chemical signalling at synaptic junctions? When a neurone fires, it sends an electrical signal that jumps down the axon via the nodes of Ranvier very rapidly. At a synaptic junction, chemical Brownian diffusion signalling with receptor surface proteins is relatively slow and is often exploited by venoms and susceptible to toxins (on the plus side it's the reason a lot of medical drugs work). It seems flawed for evolution to have selected for this rather than some alternative quicker and more direct electrical interface.

Question. Why are chemical synaptic interfaces used in higher organisms at the synaptic junction?

This is the coolest part. Those synapses are the reason the brain is so complex! Basically you've got the first part right, the neurones are quicker and they transmit messages from one end to the other. The other thing you have to do is analyse and calculate. Signals from multiple neurones feed into a single neurone using a chemical synapse. Similarly the converse is true, a single neurone can feed multiple synapses. So when we for example walk, receptors monitoring our balance can feed this to our conscious and unconscious mind, but I'm grossly simplifying this. What our brain does is take hundreds and thousands of ports of information, with where the chemical synapse is and the type of synapse and the receptors and a million other things just slightly changing the information until it's perfect and then send that information a million ways however it likes.

The most important thing is this allows inhibition. Most of the brain uses inhibitory GABA rather than activating signals. Furthermore, the system uses the delay created. Different transmitters act for different durations and send a different volume of signal. An impulse is all or nothing, it's of a fixed amplitude, however a chemical signal can be fine tuned. Neurones can not only interact to inhibit themselves or other neurones to increase the resolution of a signal etc. Conversely a system of just physical connections allows little regulation, in fact it'd be practically a seizure.

Does that make sense?


What is a synonym of the word design that can be used in context of evolution? For example let's take two sentences; "engineer made a design for camera", "evolution made an X for eye". What is the best X that could be used?

I need it for an essay about evolution.

Although not ideal, "adaptation" is more appropriate than "design" as a noun describing something that has come about in an evolutionary context, even though not all evolution is adaptive.

In writing, though, I would not phrase it as you have, rather I would change the agency from something evolution does as some sort of "entity" which makes it sound like a goal-driven "designer" with whatever words you use, and instead say that "Eyes evolved from simpler photosensitive groups of cells." Eyes deserve the agency, because having eyes is what would improve the survival of an organism versus eyeless conspecifics and increase the proportion of eyed individuals in the next generation (I hope my simplification of the eye-evolving process as if eyes are a simple Mendelian trait isn't too distracting here, I mean it mostly as metaphor), rather than eyes being a "goal" of something called evolution.

Similarly, you would not say "Chemistry makes water from hydrogen and oxygen," rather you would say something like "Hydrogen gas reacts exothermically in the presence of oxygen gas to produce water." There is no agent "chemistry," that is just the word we use to describe the set of processes in the universe that govern how molecules/atoms/subatomic particles interact. Similarly, "evolution" is not an agent who does things.

One place I would differ in this guidance is in talking very big picture, such as saying that "evolution produced the wide variety of species present today"; in that example, there isn't anything more local to act as an agent, and it's appropriate to refer to the evolutionary process as a whole.


Total amount of CO₂ / Oxygen in Bloodstream in Humans How much carbon dioxide and oxygen from/for respiration are in the bloodstream at any one time? (mass per litre of blood or similar)

And would there be much more aside from the blood in tissue, e.g. muscle, brain, etc.

So far the figures I have are as follows (please double check for me, I dont have a clue)

O₂ molecules per red blood cell: 1 billion. Red blood cells per micro litre of blood in males: 4.7 to 6.1 million. Molecules per mole: 6 x 10^23. Therefore moles of O2 per litre of blood: approx 0.01 (correct?) This seems quite low, since an inhalation is typically 0.5L and about a quarter of the oxygen is absorbed (oxygen by volume, 5% of the air) (1 thousandth of a mole of oxygen absorbed per inhalation?)

Thanks

Your calculation for O2 is along the right direction, but missing a factor I think.

Each red blood cell holds millions of molecules of hemoglobin, each hemoglobin molecule, when saturated (at the lung), holds four O2 molecules.  So this is off by a factor of millions at least.  Wikipedia estimates that hemoglobin makes up about 35% of the total weight of blood.  We can use this figure and an average of 4.5 l of blood for a human being ( numbers vary, but it will be within 30%).

4.5l blood * 1.060 g/ml density of blood * 1000 ml/l water * 35% = 1667 g hemoglobin

4 molecules O2/molecule hemoglobin * 1667 g hemoglobin / (64000 g/mol molecular weight of hemoglobin)  = 0.104 moles O2

so I get:

0.104 moles O2 * 30 g/mol for O2 = 3.12 g O2 in the blood at a time.

In the muscle and tissues it gradually depletes so that all four molecules will usually end up somewhere in your tissue.  So this is all assuming that counting all the hemoglobin bound O2 will approximate the count of O2 in the body.

We know this is a crude estimate as myoglobin in mammal muscle will store O2 for use later, and the average hemoglobin is not in the lungs and will have given up some of its O2.  It also doesn't count the O2 which diffuses into the blood and is carried by the water.  This is about 0.035 g / l, which is why we need hemoglobin - total blood saturation would carry about 1.15 g of O2.  Hemoglobin multiplies the oxygen carrying capacity of blood by 100 fold.

CO2 is much more soluble in water (blood/tissue) than O2 is- about 1g/l.  There is I think only 2 CO2 binding sites for hemoglobin, which means it carries out only half the CO2 oxygen that it carries  in.  Hemoglobin is is only considered to account for 10% of the total CO2 carrying capacity of humans.  So calculating CO2 respiration by hemoglobin is not a good way to estimate blood CO2.


What regulates the timing of the motion of molecular machines during DNA Replication? This question is about this video I found on Youtube. I just want to know what is the mechanism which regulates the timing of motion of the parts of these molecular machines.

I know that those big molecules moves using mechanical energy from ATP molecules and take advantage of the electric forces specially the hydrogen bonds, they also take advantage of the Brownian motion of water molecules around them.

From what is see, the green floating molecule triggers the whole process by attaching the purple one, then some electric equilibrium is disturbed so the {purple+green} molecule is attracted by the horizontal cyan molecule...etc.

But the problem is: does the green molecule attaches to this group in a periodic timing ? or in other words does the Okazaki fragments have the same lenght evertytime ?

Thank you in advance !

That's a pretty neat video, I'll just give you some background information first. It's an illustration of the "trombone model" of DNA replication. The darker blue molecule is helicase, it unwinds the DNA and facilitates translocation (this is an ATP dependent process). The dark purple molecules are DNA polymerase, they catalyze DNA strand synthesis (an NTP dependent process) using an ssDNA template and 3'-OH primer (the primer:template junction). The green circular molecules are sliding clamps, they increase the processivity of DNA polymerase. The light purple molecule is the sliding clamp loader, unsurprisingly it loads the sliding clamp onto the DNA (ATP dependent). The light blue molecule is a flexible linker that connects everything together. The other green molecule (the one that contacts helicase) is primase, it synthesizes RNA primers (which contains the 3'-OH initially used by DNA polymerase).

Certainly intermolecular forces play a significant role in this (and every) biochemical process, but I'm not really sure what you're talking about when you're describing electric forces and Brownian motion.

Anyways, the answer to your question is no, Okazaki fragments do not have a fixed length. DNA synthesis, as mentioned above, occurs only by adding NTPs to a 3'-OH primer. Thus the length of Okazaki fragments is dependent on the spacing between primers on the lagging strand. This is dependent on when primase binds which in turn is dependent on primase concentration as well as its binding affinity with DNA and other replication fork proteins (especially helicase). High concentration and/or high affinity leads to a higher binding frequency and therefore shorter Okazaki fragments. The opposite is true for low concentration and/or low affinity. Note that most (or all?) primases have some degree of sequence specificity which means that specific DNA motifs will increase binding affinity. For example, Escherichia coli primase (DnaG) recognizes the trimer GTA.

This process also requires some degree of coordination between leading and lagging strand synthesis. Primer synthesis and DNA polymerase recycling on the lagging strand is much slower than the continuous synthesis on the leading strand. It has been suggested that primase acts as a "molecular brake" by halting the replication fork during primer synthesis to prevent the leading strand polymerase from rapidly outpacing those on the lagging strand (Lee JB, Hite RK, Hamdan SM, Xie XS, Richardson CC, van Oijen AM. 2006. DNA primase actas as a molecular brake in DNA replication. Nature. 439(7076):621-624.).


Is there a balance or feedback between O₂ and CO₂ in the atmosphere? Is there, globally, a balance of the concentrations of oxygen and carbon dioxide  in the atmosphere?

Plants convert CO₂ to O₂,
and with the concentration of O₂, the tendency of plants to oxidize to CO₂ increases. That is, plants burn better with more oxygen.

Based on this there may be a feedback of increasing CO₂ concentration to increasing O₂ concentration back to increasing CO₂.

This feedback requires that plant growth increases with increasing CO₂ concentration.

Otherwise there would be only a limit to the oxygen concentration as at some concentration of O₂, even a wet rainforest burns explosively.

Does a feedback loop like that exist?

Yes, increase in CO₂ concentration increases the rate of photosynthesis in plants. The rate of photosynthesis is linealy proportinal to CO₂ concentration in range up to 225ppm  and  slowly increases range 225-650ppm.[Limiting Factors in Photosynthesis, Plant Physiol. (1984) 75, 82-86] (Now CO2 concentration is about 400ppm).
You can read more in Educational article on Nature journal website or in
More scientific review on the topic.


Evolutionary history: did any organs start out as autonomous organisms? I've read that the cell nucleus was once an autonomous organism that was "enslaved" by the larger cell at the time of the Eukaryotic Revolution. Are there any organs in the human body that we know of that started out as autonomous organisms (of course they would be unrecognizable in their current form)?

Very short answer

No!

Long answer

It is not the nucleus who was an independent organism but the mitochdonrion (organelle) (One might discuss this point and say that both are correct, it is just a philosophical issue of the identiy of the eukaryotic cell). The plastids (the chloroplasts for example) were also independent organism. In consequence, in every cell, we have DNA in the nucleus and DNA in the mitochondria. The mitochondria is contained in every cell of our body and is transmitted via the ovule (and not the spermatozoid) to the offsprings.

Now let's think about your hypothesis that one of our organ (let's say, our liver) might have been an independent organism in the past. Therefore, this organ would contain different DNA than the rest of the cells of our body. How would you transfer the DNA of your liver to your offspring? Well, it is hardly imaginable.

Moreover, it has been argued that because we now have a complex and efficient immune system, a endosymbiose would be very unlikely.

But no, none of the cell in our body come from a previously different organism. But every cell of our body is some kind of chimera of two previous cells. Note: the vast majority of our DNA are present in the nucleus and not in the mitochondrion.

For more information about endosymbiose, have to look to this and this (wiki articles)

It seems much more easy to have two organisms that stay together during reproduction when reproduction is mediated by striking.

You may find some funny examples (border cases) of two organisms that don't separate during reproduction in corals (zooxanthella), leafcutter ants (and their fungus), parasitoid bees (and the virus that females create in their ovary) and lichens


What are the consequences of drinking water with food? Does drinking water with a meal release lesser energy/glucose into the blood stream due to a diluted digestive mixture ?

For simplification : If a person eats 100 grams of cooked jasmine rice with no water in take, when digested in 90 minutes  releases, say, a 100 calories. Then, if  the person eats 100 grams of cooked jasmine rice and drinks 50 ml of water along with it (during/after) (basically, halving the power of the digestive juices) then will the energy released be 50 calories ?

A moderate amount of water while eating will not dilute digestion
...according to Michael F. Picco, M.D. and the Mayo Clinic:

There's no concern that water will dilute the digestive juices or interfere with digestion. In fact, drinking water during or after a
meal actually aids digestion.
Water and other liquids help break down food so that your body can
absorb the nutrients. Water also softens stool, which helps prevent
constipation.

Water, after all, is the "universal solvent" which should help break food and organic materials down further.
Effect of Stomach Acid Dilution
This is a total myth, especially if you consider it from totally a chemical perspective.  Stomachs secrete about 400 to 700 mL of gastric acids per meal. Just to be conservative, let's say 500 mL.  Also, the average stomach has a pH of about 2.  Now let's look at the formula for pH and what the effects of adding water might be:
pH = log(1/(mols/volume))
2 = log(1/(mols/0.5L))

Now solve for mols, and we get mols = 0.005
Now let's assume our meal contains about a quarter of a liter of water in it.  We'll also assume that our food is completely pH neutral.  This is probably a little high on water concentration, but let's see its effect on our stomach's pH.
Since it has a neutral pH, the mols does not change, but our volume does (0.5L [previous contents] + 0.25L [from the food] = 0.75L).
pH = log(1/(0.005 mols/(0.5L + 0.25L)))

Now solve for pH and we get pH = 2.18.  No problem here, since normal digestion occurs between a pH of 1.5 to 3.5.
Finally, let's say we drink a lot of neutral pH water with our meal now.
pH = log(1/(0.005 mols/(0.75L + 4.25L)))
pH = 3

So we are still within a normal pH of digestion, even though we just drank over 4.25 liters (~1.12 gallons) of water with our fairly liquid meal of 0.25L!  We would need to drink about another 45 L of water to knock our gastic pH above 4.  But don't worry, we would die of water intoxication well before that ever happens.
Furthermore, our stomachs (and digestive tract) are incredibly good at adapting their secretions to the consistency of a meal.
Water and Speed of Digestion
Perhaps another way that water may change caloric intake is to increase the speed at which solid foods exit the stomach.
This is thought to reduce the meal’s contact time with stomach acid and digestive enzymes, resulting in poorer digestion.
As logical as this statement may sound, no scientific research supports it.
A study that analyzed the stomach’s emptying speed observed that, although liquids do pass through the digestive system more quickly than solids, they have no effect on the overall solids’ digestion speed.
Bottom Line
Water during meals should not decrease the amount of calories absorbed.  With all that being said, digestion is a very complex system, and there are still many unknowns as well as individual responses.  Before making drastic changes concerning your health and digestion, you should consult a medical professional.  This answer should in no means necessary replace any medical advice or treatments, but rather aid in your understanding of how digestion works.
A Final Word of Caution
I feel obligated to include that however you found this question/answer, staying hydrated to aid in digestion is a very healthy function, especially in considering weight loss and 'feeling full for longer.'  However, obsessive water consumption aimed at decreasing food consumption/appetite ("fluid loading" or "water loading") is a common symptom of eating disorders.  If this is a concern for you or someone you know, please, seek professional support and help.

Sources:

NCBI - Adaptive Secretions

NCBI - Digestion Speeds

www.mayoclinic.org

water.usgs.gov


What does “energy transfer in cells” mean? "ADP and ATP are involved in energy transfer in cells."
I know what is ATP and I know how ADP is formed, but I don’t understand what “energy transfer in cells” means.

Cells require a constant supply of energy to generate and maintain the biological order that keeps them alive. This energy is derived from the chemical bond energy in food molecules, which thereby serve as fuel for cells.

Cellular nutrients (components in foods that an organism uses to survive and grow) come in many forms, including sugars and fats, so food molecules are rich sources of energy for cells because much of the energy used to form these molecules is literally stored within the chemical bonds that hold them together.

Cells release the energy stored in their food molecules through a series of oxidation reactions. Oxidation describes a type of chemical reaction in which electrons are transferred from one molecule to another, changing the composition and energy content of both the donor and acceptor molecules. Food molecules act as electron donors. During each oxidation reaction involved in food breakdown, the product of the reaction has a lower energy content than the donor molecule that preceded it in the pathway. At the same time, electron acceptor molecules capture some of the energy lost from the food molecule during each oxidation reaction and store it for later use. Eventually, when the carbon atoms from a complex organic food molecule are fully oxidized at the end of the reaction chain, they are released as waste in the form of carbon dioxide.

They (Cells) do not use the energy from oxidation reactions as soon as it is released. Instead, they convert it into small, energy-rich molecules such as ATP and nicotinamide adenine dinucleotide (NADH), which can be used throughout the cell to power metabolism and construct new cellular components.

Sources :

How Cells Obtain Energy from Food ?
Cell Energy and Cell Functions

For more informations :

What Are Nutrients ? - Definition & Examples
Cellular energy production


Do scars generally continue to undergo beneficial changes after maturation? I understand that succumbing wound healing, a modulated scar would go through a process of scar healing which I understand to be remodulation and maturation.

Do scars generally continue to evolve in beneficial ways throughout the life of a human?
That is to ask; might it be that a scar's evolution could be comprised of two major stages "primary" and "secondary" and that the primary stage is consisted of remodulation and maturation and the secondary is comprised of "post maturation" evolution which could last during all life of a human?

In general, scars do get changed after being "healed", at least by general bodily changes from aging effecting all tissues in general (including the scar tissue), but there might also be a "post maturation evolution" as well.

The collagen that holds together scar tissue is continuously degraded and replaced. (Plastic and Reconstructive Surgery, 1976) If collagen synthesis slows down, due to scurvy for example, old wounds can in theory reopen. Historic records of sea voyages contain descriptions of long-healed wounds opening back up in scurvy victims, and these cases are cited authoritatively in some papers (e.g. Annals NYAS 1961), but it is difficult to test experimentally.
I would describe this more as 'maintenance' of the scar, rather than as 'continuous healing', but it may be of interest to you.


Why do floaters in the human eye appear to have a squiggly-line, tubular shape? If you intentionally try not to tune out visual floaters in the eye, you can see them very clearly and they seem to have a squiggly line shape but with a volumous tubular look. Why is this?

They almost look like some kind of microbe as seen through a microscope, but that seems like a naive guess, and I'm curious to know the scientific explanation of why these entities look the way they do.

Eye floaters are usually small flecks of collagen floating inside of your eye (the same substance that is present in the extra-cellular matrix) and as you age they can clump together and cast shadows on your retina.
They may look like microbes to you because the clumping gives the appearance of a thread-like or rod shape, commonly associated with microbes. The light falling on the eye will enhance this by making them look transparent and somewhat like microbes. But rest assured they aren't, because if they are, then you certainly have superhuman eyes!


Do lysosomes play any role in cell division? My biology textbook includes a point that lysosomes stimulates cell division without further elaborating. But studying it, I felt eerie about this function of lysosome. Then, I checked on the internet; found nothing relating cell division to lysosomes.

Maybe, autophagy of lysosomes can play a role in this regard. Killing cells and thus 'stimulating' cell division. But this reasoning doesn't seem plausible as autophagy doesn't occur without extreme conditions.

Nothing else is coming into my mind.

So, is this point included in my book wrong or right?

It is actually not completely correct to include it as a fact in textbooks. The main cause of it is that there is not much research on this topic. See this article for reference. According to Allison and Mallucci (1964), during cell division, lysosomes either released an unspecified activator or some hydrolase that inactivated a repressor. Apart from this, Allison and Paton (1965) showed that treatment of human embryonic lung cells in tissue culture with photosensitizing agents allowed high frequency of chromosome breaks on irradiating the cells with light from a high intensity tungsten source. They claimed that these effects were observed only at lysosomal sites, from which they concluded that a cytoplasmic event was giving rise to structural alteration in chromosomes. This event was suggested to be release of deoxyribonuclease from the lysosomes. However, Chevremont et al, 1959 showed different results through their experiments. They grew mammalian cells in tissue culture in the presence of acid deoxyribonuclease. This treatment inhibited cell division, but allowed DNA synthesis to proceed and did not appear to alter the nuclear DNA. Hence, the contribution of lysosomes in cell division is not yet completely established and still comes under debate.

So, it should not be considered a total false, but is also not reliable enough to be printed in textbooks. Overall, we don't yet know whether lysosomes do play a role or not.

References:

TUATARA: VOLUME 18, ISSUE 1, JULY 1970
THE LYSOSOME
ALLISON AC, MALLUCCI L. LYSOSOMES IN DIVIDING CELLS, WITH SPECIAL REFERENCE TO LYMPHOCYTES. Lancet. 1964 Dec 26;2(7374):1371–1373.
Nature 227, 707 - 708 (15 August 1970); doi:10.1038/227707a0;
Chromosome Breakage by Deoxyribonuclease;
GILLIAN R. PATON & A. C. ALLISON
CHEVREMONT M, CHEVREMONT-COMHAIRE S, BAECKELAND E. [Action of neutral and acid desoxyribonucleases on living somatic cells cultivated in vitro. III. Histoautoradiographic study after incorporation of tritium-labelled thymidine]. Arch Biol (Liege) 1959 Oct-Dec;70:833–849.


Folding of bulliform cells How do bulliform cells cause a leaf to fold in half when the leaf looses water? Also, how would these bulliform cells be arranged to cause the cell to instead curl up?

Curling up is due to turgor pressure. Quoting from wikipedia

  Loss of turgor pressure in these cells causes leaves to "roll up" during water stress

More scientific reference , on morphology,  on mechanism, on development, some genetics and on physics.


mRNA synthesis for in vivo injection I found a commercial reagent called in vivo-jetPEI® from Polyplus-Transfection that is able to delivery mRNA in vivo. I'm planning to do an experiment with it, but I'm worry about how to synthesise mRNA and purify them clean enough to inject to living body.
I also found a recommended Kit called HiScribe T7 High Yield RNA Synthesis Kit that can help me to synthesise mRNA but I'm not sure if I can use the final product for an in vivo injection. Anyone have any experience with it?

You should purify your RNA after transcription from any buffer/enzyme contaminants. There are several kits available in the market for that. One is GeneJET DNA & RNA Cleanup and Concentration that uses standard silica-beds packed columns to absorb nucleic acids. You can then elute them in pure water and you should be ready to go. Once the RNA is purified you will use the vivo-jetPEI for the delivery.