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How much variation is there between DNA molecules from the same organism
If different but in tact molecules of DNA were extracted from my body, for example hair sample, blood sample, and mouth swab, how much variation would there be between DNA molecules?

That would depend on age since we accumulate mutations our entire life.

From my understanding, individual DNA molecules would have those mutations, passing them on, but I see no way in which all DNA molecules uniformly change, like they're quantumly entangled. I may be wrong, but how do individual DNA molecules communicate their code to all other DNA molecules in the body?

There are several answers to this question, depending on exactly what you mean.
Cells in the body will accumulate random mutations as they divide and multiply
The cells in the body that are not part of the reproductive line are referred to as "somatic cells". These cells are typically derived from a single fertilised egg. Every time the cell divides, DNA must be duplicated, and each time it is duplicated there is a chance that there will be a random mutation. These random mutations will be passed on to any cells which are later derived from this cell. Most work in this area is on single-nucleotide variations (see the answer from Martin Klvana) but there can also be insertions, deletions, and duplications as with other mutations.
Damage from radiation and other mutagens can cause DNA mutations
Cells are subject to damage all throughout their lives, and some forms of damage cause breaks or alterations to the DNA of the cell. There are complex repair mechanisms in place to deal with this damage but they are imperfect so over time this damage can result in differences in the DNA sequence of the cells in your body. This will increase with age.
Some cells have mechanisms for deliberate, random mutation
Certain cells in the body have evolved to be randomly different from each other. The most obvious example of this is in the immune system where random re-arrangments of specific sections of DNA are used to create a vast array of different antibodies.
Mobile genetic elements can activate and re-arrange through the body
The human genome, like that of other organisms, is full of transposons and other genetic elements that contain genetic machinery for relocating themselves within the genome. The activity of these elements in the somatic cells of the body can lead to differences in DNA sequence.
Not everyone has all their cells from a single fertilised egg
It can happen that rather than deriving from a single fertilised egg, a person is derived from two or more fertilised eggs, so that their body is made up of cells of distinct genetic origin that are effectively siblings to each other. This can result in large genetic differences between cells.
Furthermore, in women who have had children, it is common (found in around 50-75% of women) for some cells from the fetus to enter the mothers' body and permanently take up residence in a phenomenon called fetomaternal microchimerism. Again this can lead to large genetic differences between cells.
Differences in DNA go far beyond mere differences in sequence
All the mechanisms I have discussed so far will lead to differences in DNA sequence, however the DNA in a cell is more than a mere repository of sequence information, and its function is mediated both through chemical modifications, most notably DNA methylation, and interaction with proteins, most notably through the histones which mediate DNA folding in the cell, or through the selective inactivation of one X chromosome in the Barr's body if you are female. These modifications have profound effects on the activity of the DNA within the cell and shouldn't be ignored.
All of this means there is no single answer to your question since it changes with time, varies between individuals, and depends on exactly what you mean.

II love this answer but I got confused when you said DNA was a cell. I had always thought of DNA as a molecule within a cell.

@JimmyG Yes, DNA is a molecule within a cell. Where do you think I was unclear about that?

I must have misread. Follow up question: what are the "non-somatic" cells? You mentioned somatic but not their counterpart, which I assume exists.

@JimmyG. Non-somatic cells are germline cells, that is sperm or eggs - and their precursor cells - in humans.

So are they called germline cells or non-somatic cells? Or both?

@JimmyG. Both. And some other names besides :)


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Does drying meat in the sun make digesting it easier?
I was looking into the relationships between man, fire, brain size, evolution, etc. and I learned about other methods of food preparation that eased digestion, but did not use fire. Then, this question popped into my head. Specifically, I am wondering how much easier is sun-dried meat to digest; how much of a benefit is gained in the amount of energy needed for the digestive process?

I doubt it's easier to digest, the point of drying to make it harder for bacteria to digest which should make it harder for humans but our sheer mass means we can power through. You might find a better answer on the culinary stack. We also expect you research it yourself before asking it here.

Various food processing methods, such as cooking, can make meat easier, that is faster, to digest. The purpose of drying meat is to extend its shelf life, not to make it more digestible. Drying removes water from the meat and somewhat physically (but not really chemically) change it.
The amount of calories used for digestion is not that high; probably less than 100 Calories per day, so meat prepared in different ways does not likely significantly affect the amount of calories burnt.

Depends on how you define digestion.
If you consider chewing to be part of digestion, then this actually makes it more difficult as dried meat ("jerky") is harder to chew (into small pieces that are easier to digest) and harder for liquid (including saliva) to permeate.
Otherwise, ease of digestion is best defined at the molecular level. Tough fibers tend to be difficult to digest; pure protein can generally be hydrolyzed except in specific cases of structures specifically designed to withstand digestion. No idea if sunlight causes significant enough structural changes to change how digestable the meat is - that would depend on if the sunlight causes chemical reactions that "tenderize" the meat.

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Why are bed bugs attracted to Carbon Dioxide?
All over the Internet it says bed bugs are attracted to Carbon Dioxide. This is why they congregate around beds. Your bed is the only place you are stationary for long enough periods of the day to exhale enough Carbon Dioxide. So, I grant that there seems to be a consensus that they are in fact attracted to Carbon Dioxide. But, why? Certainly they're not breathing it. (Are they?) I was under the assumption that all animals are aerobic.

Can you please some link for the space on "all over the internet"?

For the second part of the question: No, the bed bugs do not breathe carbondioxide and especially do not use it for respiration. Instead, carbon dioxide environment is used to kill the begbugs - "Elevated CO2 levels cause insect spiracles to remain open, resulting in death from water loss" - Nicolas G. Sillans D.. 1989. Immediate and latent effects of carbon dioxide on insects. Annu. Rev. Entomol.  34: 97–116.

@dmishra https://www.bedbugsupply.com/blog/treatments/truth-diy-bed-bug-traps/, https://www.terminix.com/blog/education/what-attracts-bed-bugs/, https://www.ncbi.nlm.nih.gov/pubmed/24020296, https://www.epa.gov/bedbugs/bed-bug-myths

It's nothing to do with what they breath, they're attracted to carbon dioxide because it's generally a good indication of the presence of a larger organism (such as a person) so they're simply following the "scent" (for want of a better euphemism) to their food (in this case you, or whoever happens to be in the bed), the traps in your links just take advantage of this to trap and kill them.

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Has there ever been a recorded incident of mule deer bucks raising fawns?
I live in Colorado Springs, Colorado. According to Colorado Parks and Wildlife, there are two species of deer in CO, mule deer, and white-tailed deer. According to CPW:

There are two species of deer in Colorado. Mule deer "mulies" have rope-like tails, evenly forked antlers and extravagant ears. White-tails have smaller ears, antlers with a single main beam bearing smaller tines, and, of course, broad white tails. Mule deer bound with stiff-legged gait, the tail held down; white-tails move with a graceful lope, the flag-like tail held erect.

Given this, I am pretty sure that I saw three adult male mule deer, and one baby mule deer. The four were in a parking lot. There were two bucks that were close to, MAYBE appeared to be guarding, the baby, then a third buck came from out behind a wall, sadly limping, to follow the others away. I found a website that gives example antlers based on age. Judging by these antlers, one of the bucks protecting the baby was probably about 1.5 years old; the other buck protecting the fawn was probably about 2.5 years old; and the third, injured buck was probably 4.5 years old.
As for the fawn, I found this WikiHow page on determining a fawn's age. Judging from this, I would guess that the fawn was around 4 months old. Reason being that the fawn still had most of white spots, and I would guess that it weighed probably between 40 and 60 pounds.
As for mule deer behavior, according to the National Parks Service, mule deer:

live in a multi-generational family of related females and their offspring. Bucks older than yearlings often group together or remain solitary. In late summer and fall, mixed family groups form larger groups that stay together for protection throughout the winter. They break into smaller groups again by the next summer.

So, to be clear, it is not surprising that these three bucks were together. What is surprising is that there appeared to be no female in the area, yet there was a baby with the three bucks. Elsewhere, I have found it specifically stated that for white-tailed deer that bucks play no part in raising. I have nothing so direct relating to mule deer. Likewise, I find no direction mention of bucks playing any role in the rearing of offspring.
So, the question is, has this been viewed before? Is it a known phenomenon that male deer, take care of the offspring in the absence of a mother? Obviously this would not be possible if the fawn was still nursing, but according to the National Deer Association, fawns are usually done nursing by 3-4 months.
The other scenario I thought was possible was that one of the bucks was keeping the fawn around as a mate, but since the fawn has not yet reached sexual maturity, which according to the National Wildlife Federation doesn't happen until 18 months of age, I was not sure how likely this was. Any insight anyone could provide would be greatly appreciated.


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What did cyanobacteria gain from photosynthesis?
As far as I understand, cyanobacteria began performing photosynthesis long before plant cells as we know them arrived on the scene. But cyanobacteria do not seem to use polysaccharides in the same way as plant cells do (building materials, for example). So what evolutionary benefit did cyanobacteria gain from photosynthesis, that could have made them continue to produce oxygen generation after generation?

But cyanobacteria do not seem to use polysaccharides in the same way as plant cells do (building materials, for example)

The Calvin-Benson cycle produces glucose which is the starting
material for a lot of biosynthetic pathways including that of the
nucleotides (ribose from the pentose-phosphate pathway). Glycolytic intermediates are also involved in the synthesis of amino
acid, isoprenoids etc. Essentially all the carbon that cyanobacteria
contains comes from fixation of carbon (from CO2) via
photosynthesis.
Cyanobacteria also store starch as an energy reserve (Suzuki et
al., 2013). They also produce other polysaccharides (Phillipis
and Vincenzini, 1998). Moreover, the peptidoglycan cell wall has a "glycan" part which is a glucose derivative (a polysaccharide).
Moreover, cyanobacteria cannot produce ATP via the photosynthetic
electron transport chain in the dark and ATP in dark conditions
is generated (though significantly less) via substrate level phosphorylation in glycolysis.

Why do you think that the only benefit from photosynthesis is polysaccharide synthesis? Photosynthesis allows an organism to convert photons into chemical energy. That chemical energy can be stored as polysaccharides and used as a building material, but it can also just be converted into some other compound, or just used to run the organisms metabolism, which is the real significance of photosynthesis and the reason it supports most of the world's ecosystems.

I just know polysaccharides are a big deal. I am asking what other things cyanobacteria would use photosynthesis for that made it powerful enough to keep doing it at that scale.

Literally everything an organism does requires energy. Photosynthesis provides an electrochemical gradient that can be used to make ATP - which is then used in many, many chemical reactions throughout the cell as an energy source. DNA synthesis requires ATP. RNA synthesis requires ATP. Protein synthesis requires ATP.

So the ATP proces did exist in early cyanobacteria? Was it mitochindrial?

ATP is found in  all known organisms, so there's every reason to think it would have been. Bacteria don't have mitochondria, so no, it wouldn't have been mitochondrial.

Sorry, I meant that there was a photosynthetiv ATP, i.e. a more powerful one than in non-photosynthetic anaerobic organisms.

Mitochondrial oxidative phosphorylation and cyanobacterial photosynthesis are really two special cases of electron transport chains, which come in endless forms. They all follow the same principle, namely the transfer of high energy electrons redox acceptors, favourable reactions which release energy that can be harnessed. The donor of high energy electrons can be anything (NADH in oxphos or P700 for photosynthesis) and the electron acceptor just has to have a more negative redox potential than the donor. As long as the transfer of the electron from the donor to the acceptor releases..

energy, it can be harvested. In the case of photosynthesis, donor electron is only so high in energy because the reaction centers transfer energy to it from the sun's radiation. By contrast the donor electron in oxphos is high in energy initially, with the energy input coming from the initial synthesis of food molecules. There is really an amazing variety of these electron transport chains, which often use similar enzymes and electron transfer machinery, but have extremely varied high energy donors and oxidizing acceptors. It could be both are inorganic compounds like sulfur and nitrates.

Often the energy is used to pump ions across a membrane to synthesize ATP using the stored energy of the electrochemical gradient, as occurs in the mitochondrial membrane. In most bacteria this occurs in the cell membrane, which nicely illustrates the endosymbiotic (bacterial) origin of mitochondria. Some phototrophs transfer energy to electrons using the sun's radiation, but then simply use that energized electron to form a chemical bond (instead of pumping ions), which can be broken to release energy and the low energy electron. So, there even are ways to store food aside from sugar and ATP.

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At which voltage will the conductance decrease due to the narrow pore in a voltage-gated potassium channel?
If you have a voltage-gated potassium channel that do not inactivate, at which voltage would you see decrease in ion conductance related to the narrow path in the pore?
With that said I know that in a solutions with other ions there is a possibility that the high driving force eventually will lead to blockage of the pore by other ions. This is more of a theoretical question.

There is a point where diffusion into the pore can be a limiting factor in the channel's conductance. If the trans-membrane voltage and the recording solution viscosity are high enough, unitary ionic current departs the Ohms law; approaching a plateau. This asymptotic saturation amplitude represents the diffusion limited rate with which ions approach the channel entrance. The bigger the pore entrance, or the higher the ion concentration, or the larger the diffusion coefficient, the higher is the limiting asymptotic current. The pore entrance is measured as the capture radius.
The diffusion limited maximum unitary current (iDL) is directly proportional to the capture radius of the channel ($r_c$):
$$
iDL=2π z e_o r_c D C
$$
z is the valence of the ion, $e_o$ is the elementary charge, C is the bulk concentration of the ion, and D is its diffusion coefficient.
Here you can find a case in which single channel current is not linear with voltage and an example calculation of the capture radius of shaker $K^+$ channel.

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Genes related to senses and their variation across animals
Animals often have very different numbers of active genes related to any sense. For instance, most fish or even aquatic mammals have very few olfactory receptor genes, whereas this is higher in terrestrial animals. Even among them, there is huge variation; compare dogs and humans, for instance. But this comes at a cost; for instance, dogs are dichromatic, the blind mole is, well, blind. So there is a compensation across the senses which is not merely a plastic change. I was wondering if there is any way to reconcile this with some notion of conservation of the total proportion of active genes involved with sensation.

There are two notions I could think of

There might have a trade-offs about where to spend ressources (energy and nutrients). If an organism spend a lot of ressources in, say, vision (incl. the part of the brain that deal with interpreting the input), then there won't be much left for other things.
When a sensory system is well enough developed that the other sensory systems would bring up only marginal benefits, it is better to just not spend unecceesary ressources on building these other sensory systems.

Please note that

The above two hypotheses are just guess work from me and I did not support any of what I said with an actual evidence.
I assumed that there is a negative correlation between the "quality of the different sensory systems" (whichever way that would be defined) but I don't know whether this is true or not.


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Why do people cut back on kilo-calories?
I am learning about specific heat in science and I learned about how the specific heat for water is called a calorie, but that is different to what is on the food label.
On the food label, that calorie is actually a kilo-calorie. My teacher went on to explain that if somebody handed you a bowl of ice-cream that contained 500 Calories (i.e. Kilo-Calories) then, that was enough to raise 500kg of water 1°C.
If a kilo-calorie is just raising your body temperature, why do we cut back on calories?? What effect does a kilo-calorie have on your body other than raising your temperature?

P.S. How can we burn calories?? This seems, at least to me, like an abstract thing... burning heat....

Yeah. Burning calories is a misleading term. Actually pretty unscientific. What it basically means is that you are converting X calories of your reserve chemical energy (in the form of fat) to some other form such as mechanical energy, thereby getting rid of it. We don't really burn the fat and heat that is produced is much less than what you would get by combustion (even though both are oxidation). The combustion engines in automobiles actually convert chemical energy to heat (by burning the fuel) and subsequently heat to mechanical energy. Our body works differently.

The calorie is a unit of energy. Our body uses the energy found in food to create ATP (a molecule that is handy to deal with energy) with the help of oxygen (that we breath in). ATP can then be used for plenty of tasks such as importing ions through a cellular membrane or more ultimately walking, talking, warming up your body, etc...
Saying that some food contain 100 calories (not kilo-calories) does not mean that it will heat up 100 grammes of our body water by one degree (Celsius). It only means that we are ingested the same amount of energy than the one that is needed for warming up 100 grammes of water by 1 degree (Celsius).
You might to have a look at CrashCourse video on ATP and respiration.


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How did parasitoid wasps evolve their life cycle?
I know there are a variety of wasps with various strategies for acquiring and controlling hosts. Do these form a rough picture of how these life cycles could have developed in the first place? What is the most recent speculation?

This is similar to the seahorse problem, in that it requires a distinctly non-mammalian perspective. Parasitoid Wasps, Natural Enemies of Insects provides a more in-depth explanation.
Existing wasp strategies may illustrate the possible transitional forms. It is not a linear transition: all of these have branched off and there are multiple parasitic strategies.

Solitary wasp, captures prey to feed to its larvae
Ectoparasitoid wasp, which lays its egg directly on prey that is paralyzed or otherwise unable to resist as the larvae eats it alive
Endoparasitoid wasp, which has formed a symbiotic relationship with a virus that disables the prey's immune system thus allowing eggs to be laid inside the prey
Hyperparasitoid wasp, which preys on other parasitoid wasps

This has the beginnings of a great answer, but needs a bit more detail before it answers the question fully.

@arboviral: Thank you for your comment. I was becoming peeved that my question would never be answered and all my google searches revealed expensive textbooks and papers behind paywalls.

No problem! If you need to get paywalled articles and are on Twitter you could try #icanhazpdf (https://en.wikipedia.org/wiki/ICanHazPDF).


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Are there transposons which create homozygous genotypes in offspring?
Transposons copy or cut and paste gene sequences. Alleles are passed down from parents and offspring may be heterozygous or homozygous for an allele (assuming diploidy).
Are there any transposons which ensure the frequency of a given genotype in a population by converting heterozygous zygotes into homozygous zygotes?

I study transposons for my PhD; I am not aware of any that preferentially insert through an active mechanism to an un-inserted allele.
There are tranposons such as R1/R2 which have a 'favorite' insertion site and will insert/compete for that sequence. That's kind of similar to your question but not generalizable.
The predominant factor I can think of which would cause such a thing to arise would be gene conversion in which the insert allele is used as a repair template for an un-inserted allele. Gene conversion is rare but can explain how the TE insertion is found on multiple haplotypes.
It's very unlikely that the alternative hypothesis occurs in which the same type of TE inserts at the exact same position in two different haplotypes and that TE doesn't have a preferred insertion site.


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How would circular dominance of alleles be determined on the genetic level?
The distinction between dominant and recessive alleles seems to be due to loss or gain of function in the proteins they code for. Alleles have been observed exhibiting incomplete and hierarchical dominance.
Another type is "circular dominance," which is modeled in some computer programs but it isn't clear whether this occurs in nature. In this case, the dominance of alleles works similarly to rock-paper-scissors.
Would circular dominance exist in nature? How would alleles determine circular dominance?

Thomas Lenormand did some work on the subject if I am not mistaken. If I am not mistaken empirical evidence of such type of dominance suggest specific sequence of the expressed protein that will directly bind to the other allele causing reduction of its expression. It is therefore easy to imagine such circular dominance.

@Remi.b: So the proteins interact like a literal game of rock-paper-scissors? Do I understand that right?

Yes, exactly. I did not post my comment as an answer because I don't know much and failed to provide a reference for my claim. So you should wait for a good referenced answer and not just take my word for granted.


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Storage of energy in muscles vs fat depos
How does the body control, where consumed energy (fat, glucose) is stored? And what is its strategy?
More specific:
1) How does the body control storing glucose in muscles and not as (subcutan) fat? (E.g. exercise lets more GLUT4 translocate in muscle cells; because of this, do muscles in total simply have more transporters to suck in glucose than all fat cells, or is there another mechanism? How does the liver refills its storage)
2) Same question as 1) but regarding FFA and not glucose.
3) What is the overall strategy for energy storing? (Can it be stated as simple as "Fill the liver and muscles until they reach full capacity and then store extra energy as fat?")

Funny, that you think that is "homework" :D
I am a sports enthusiast and would like to have a deeper understanding in the "technical" details...

The  regulation of metabolites and signals in general (glucose (Glc) or FFA in this case) and their selective uptake by cells, depends on the number (from few hundreds to many thousands) of receptors expressed and displayed to the surrounding environment, the type of receptors (what they can bind, and do as a result) and their properties.
The regulation of glucose storage and use in muscle cells is determined largely by the dynamic energy state of the cell, which is can be described (to first approx at least) as the cellular equilibrium between ATP<-->ADP<-->AMP. The key here is to be aware that nothing is happening in isolation and the whole metabolism of the cell is one giant equilibrium. You make a change at one place that will result in proportional changes elsewhere to compensate.
If you start exercising, that is using ATP rapidsly, suddenly AMP spikes, the increase in [AMP] results in the upregulation of key enzymes in Glycolytic and TCA pathways, which causes and increase in ATP producting. How much is made? Whenever possible always just enough enough to meet the demand (assuming cell has resources to supply it and manufacture it).
Absolutely, in the same way, the energy state of the cell, and the availability of Glc in and outside the cell (which it knows, because increase in blood Glc causes insulin to be release, muscle cell can bind to insulin, which results in activation of more GLUT4 to be expressed and expressed) directs how Glc is used, stored as glycogen, converted to FFA etc. When cell energy state is low, or exercising, signaling from muscle cells to liver (via lactate in blood/ Cori cycle) tell liver to release stored Glc into the blood.  l
If Glc in high in blood, insulin released from the pancreas, which tells the liver, to start sucking up Glc from the blood, and the way it does that is a lot better than muscle. Why? because of the binding properties of the different isozyme receptors expressed (same function but slightly different physical properties).
FFA metabolism is a same general concept, but different key enzyme players. The increase in metabolite availability causes or is a signal, which results in the appropriate response to balance level out the steady state dynamic equilibrium.
The strategy is basically, if available in excess and can be stored it's stored until the limit of cell is reached, which is determined by the thermodynamic equilibrium of metabolite inside and outside the cell.
Nelson, D.L.,Cox, M.M.(2013) Lehninger Principles of Biochemistry, 6th Ed.
In response to your comment questions,
In general, like I mentioned, the strategy for coordinated fat uptake holds.
Majority of insulin-stimulated glucose uptake occurs in skeletal muscle, with about 10% of insulin-stimulated glucose uptake occurring in adipose tissue. However When it comes to FFA, these are largely delivered, absorbed and stored (as triglycerides) from bloodstream into adipose tissues. This process is definitely actively controlled and regulated, as you do not want fat globules floating around in your bloodstream. When energy state of the organism as whole is low, adipose tissue can sense and release FFA that can be take up by other cells (muscle, liver) and energy in molecules extracted during FFA catabolism pathways. How exactly adipocytes translate changes in glucose uptake or storage into signals that affect global energy balance is not completely understood it seems.
For a good place for much more detail, check out
Leto D., Saltiel A.R (2012) Muscle and adipose tissue in energy homeostasis, Nature reviews of Molecules Cell Biology, 13, 383-396
http://www.nature.com/nrm/journal/v13/n6/box/nrm3351_BX1.html

Thanks for the answer! What is still unclear to me is: are muscle cells preferred over fat cells for storage and how? Again, is this because of different properties of the isozyme receptors?
Does the mentioned storage strategy also hold for fat cells? I.e. is the fat cell "actively trying" to fill its storage (when the mentioned conditions (equilibrium in/out side) are met)?

I updated my response to hopefully address you questions more specifically


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Physical activity in fasted state: Glucose for brain vs muscles
Let's consider this scenario:
You do sports in the morning in a fasted state (i.e. without consuming any calories after waking). Your brain of course needs glucose and your liver probably still has some of it in stock. So it keeps releasing it. Is there a mechanism to prevent the working muscles from consuming the glucose (so that the brain can be supplied longer)? If yes, how does it work?
(Please answer not too technically, so that people outside this area can also understand it.)

In general it is the reciprical action of the hormones of the fed and fasted state — insulin and glucagon — that are responsible for this, together with the differences in hormone-sensitivity of the glucose transporters in muscle and brain. See the accepted answer to this question: During starvation, does the human body do anything to prioritize which organs receive nutrients?.


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Why do I feel my schoolbag to be heavier after meals?
I am not sure this is related to psychology or not.
My friend casually commented to me that he feels his bag to be heavier after his meal. So I started observing my perception of weight of school bag after every meal. I did this for 3 weeks ( 1 log per day i.e. lunch, 5 days a week, 15 observations).
For 15 observations, 13 times I felt my bag to be heavier. These 13 times I had regular class after lunch. The other 2 times, I had an exam an hour later my lunch.
Is it psychological and / or body function related ?

Could certainly be physiological. After eating more blood is diverted towards the smooth muscles around organs for digestion. This will mean your skeletel muscles have decreased blood flow so less nutrients such as Glucose available to make contractions. As you have less energy available to contract the skeletal mucles you're more than likely to feel slightly weaker.
On the contrary it may he purely psychological! :) Good question though!


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Unidentified insect seen in southern UK, near North Downs
This creature was seen in southern UK, near North Downs, just this weekend.
https://youtu.be/5VJYOrMJXaQ

Though it might resemble a woolly aphid (https://dengarden.com/gardening/Woolly-Aphids-Whats-that-Fluffy-White-Stuff-on-my-Tree). I'm more certain that it is a mealy bug instead (https://puffycarrot.com/little-fuzzy-white-bugs/). the fact that it is not on a plant is what confuses me since both these species are usually living on plants which is where they grow.
here is some images i found that look almost identical to the photo you have and give other angles to the species, you can compare it with the images in the other links:
https://www.flickr.com/photos/unique127/2539022716/
https://www.ecosia.org/images?q=white+furry+insect#id=DDEE9FF71839419EF585778C7DA8F1E1545E98D1


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Is it possible to identify this microscopic particle?
So I was playing amateur scientist with my 11 year old.
This photograph is from rainwater in a bird-feeding bowl in south England, at 300x.
It looks biological, but I have no idea what this is. Is it possible to know, beyond speculation, what this item is?

@theforestecologist  It was not moving, that I could tell.

This is an plain old ice crystal. Welcome to the microscopic world! When water evaporates, high-energy molecules escape, leaving low-energy molecules of water. The droplets cool this way, and they freeze - the dirt or debris in the crystallizing droplets make curious patterns. Here are some in my samples I made last week, for comparison:

How about a close-up?

Here's one I made by accident, this time featuring a fluorescent dye.

Notice how cooling droplets never freeze the same way twice. You'll never find two identical crystallized droplets!
If you want to avoid these, prevent evaporation by putting nail polish or glycerol around and between your coverslip and slide, so that water cannot escape.
OFFTOPIC: You should also encourage your kid to try make some of his/her own crystals. You can use food dyes to make beautifully patterned art. Good moment to teach your kid about nucleation; why water doesn't freeze at 0° C, but rather at temperatures that tend to decrease as the volume of the water decreases and as the water impurity increases. And maybe sneak in a funfact about how the freezing of small water droplets into ice is an important process in cloud formation.


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Memory storage in the brain
So I asked Google,

how many neurons in the brain
how many neural connections in the brain

The answers were, respectively:

86 billion
100 trillion

There are, I think, 8,589,934,592 bits in one gigabyte. (Am I correct?)
100 trillion divided by this number gives us approx 11,642 GB of storage, assuming that:

One neural connection stores one bit (I'm not sure what that would even mean)
The entire brain is used for memory storage

11,000 GB sounds like a lot. Laptops these days can have around 100 GB of disk storage.
A 4K film can need about 15 GB per hour of film. So the number above gives approx 776 hours of "recorded film" memory. That's 32 days. This calculation tells us the brain can store about a month's worth of memories.
But a human memory (well, my memories at least - I can't vouch for others ;) isn't just a high quality vivid visual + audio "film" recording - it contains other bodily sensations (smell, movement, space, muscular sensation, temperature) and also emotions, speech, thoughts, conclusions, intentions and other less definite content.
Additionally, I have on occasion surprised myself with just how early I could remember. For example, with parents saying to me, aghast, "You remember that house?" So I reckon one month of storage is orders of magnitude insufficient.

Is my thinking on this even vaguely in the correct direction?
How do theories of physical memory storage account for this?
What's the best theory of human memory storage we currently have?
Do memory theories focus exclusively on the brain, or are there any "whole body" theories, or theories involving cellular memory?

(As you may be able to tell, I am a layman on this. I have high school biology, and undergrad level physics knowledge.)

Hi Stewart. You should stick to one question per post. Also, some of your questions are far to broad to answer in a medium like Stackexchange "What's the best theory of human memory storage we currently have" is not something that can be conveyed in a few paragraphs. Be sure to take the guided tour of the site  (listed under the help button) to see what questions are appropriate.

It doesn't make much sense to measure biological/neuronal memory the way you measure bits in computer memory. Connections aren't binary, we store things conceptually not like pixelwise video.

11000 GB can be easily less than a single hard disk. There were SSD in laptops as small as 128 GB, but they get cheaper and bigger. HDD at the time were much bigger.

https://biology.stackexchange.com/questions/19614/is-there-any-size-limit-to-the-amount-of-information-a-human-or-other-brain-ca

The brain is much, much more sophisticated than a computer. Memory depends so much on so many things, from "working memory" available in any situation, to emotions associate with them, timing of synaptic pruning and even to olfactory-associated memories. This question is too broad. VTC.

Cellular memory? Here's stuff to look into: There's obviously DNA (and shortening telomeres with each cell division), but also search for "methylation" in relation to cell function.

Thank you all for these useful comments - particularly the leads of what to look up next.

@Mithoron Both questions which you linked, and their answers, are indeed helpful. Thank you.

There was this 2003 paper titled "Uncovering the Capacity of Human Memory" by Yingxu Wang et al. that estimated it at a whopping 10^8432 bits, based on synaptic connections
Current estimates are more like a few petabytes apparently.

Welcome syndrop. The paper is available on Researchgate and is titled "Discovering the capacity [....]". You can use the [edit] button to add the URL. It might be helpful if you were to summarize the contents to help explain how the number was derived also.

10^8432 bits is a huge number!

@Stewart And rather nonsensical. I doubt whole observable universe would be enough to store this much information.


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doubt with a multiple choice question
Permanent decrease in population would occur due to-
A) Migration B) Natality C) Emigration D) Mortality E) Territoriality .
It's obvious that C) & D) options are possible . But I'm confused about which one is more correct and what is the cause ?
The answer is given : C

please see this post and this post

Emigration is a permanent phenomenon. Mortality, on the other hand, is dependant on various factors such as epidemics, health, life expectancy, etc. A change in these factors leads to a consequent change in the mortality rate. For instance, if an epidemic plaguing a country is eradicated, then the rate of decrease in population would slow down. Hence, it can lead to an increase in population as compared to the population during the epidemic.

Aside the fac that the post is off-topic, It is definitely a poorly phrased question. Is it really the way the exact way the question was phrased? There was not even the term "size" after "population"? Both C and D sounds equally correct.

@ Remi.b : The question was on my MCQ book & i didn't commit any changes as i had doubt with the answer . If you have problem , Do an edit or don't give advices

I don't know if this is just me, but I'd consider this a pretty badly worded question. For models of population dynamics, the rate at which the size of a population changes over time is normally accepted to be the net balance of four fundamental processes: Birth, Immigration, Death, and Emigration ('BIDE'; see for example here). Birth and immigration increase a population, death and emigration decrease it. Unless you exterminate a species then it's going to be pretty difficult to assert that a population decrease from either source is 'permanent' - new individuals are likely to be born into the local population and/or immigrate eventually.
An example that specifically refutes the assertion that 'emigration results in a permanent decline in population size' would be a source-sink metapopulation, in which emigration repeatedly/constantly occurs from the 'source' population but it doesn't permanently decrease in size.
As a lesser quibble, although 'migration' can be taken to refer to temporary movement/resettling, it is pretty common to consider immigration and emigration to each be components of migration.
So I would certainly argue that for the question as asked, 'D' is at least as valid an answer as 'C', but in both cases it is impossible to say a permanent decrease would occur. At the same time, if it was changed to 'could occur', you could make a case that 'A' could be a valid answer (since 'migration' includes emigration).

A and C is more obvious answers.
Mortality and natality are two sides of the same coin there is a balance between them and are dependent on several factors.
Migration is temporary (Wiki: An instance of moving to live in another place for a while), whereas emigration is to permanently move and populate that area.

Through Migration , i tried to mean Immigration

anyways, I feel the question is incomplete.


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Relationship between lifespan and reproductive age?
I remember reading a while ago that there is a "general rule" in biology between an animals lifespan and when they reach reproductive age.
In other words, an organism that reaches sexual maturity after a short amount of time (for example, less than a year) will have a short lifespan (for example, 2-3 years) and an animal that reaches sexual maturity after a long time (elephant, 10-12 years) will have a much longer lifespan (40-60 years in case of elephant).
Is there a special name for this "law" or "rule"? Are there any major papers/theories supporting it that also attempt to propose why (perhaps from an evolutionary perspective) this trend exists?
Some quick supplemental questions:
1.) Is there also a trend between lifespan and animal size?
2.) Is there also a trend between lifespan and base metabolic rate?
3.) Do the two aforementioned "trends" or "rules" have technical names that I could look up as well?

Don't forget that some species (most notably humans) used to live for a lot less time, therefore we reach sexually maturity early in our lives which is not related to our current lifespan.

Actually, I'm not sure that is completely true. The average lifespan was certainly lower, but there are records of people living to ripe old ages of 80+ in ancient civilizations if they managed to avoid getting sick/being killed. Anyways, I think its fair to leave humans out of this question since we have developed ways of artificially extending our lifespans.

I think the only "general rule" in biology is that there are no "general rules". Take for example the central dogma of molecular biology where it was for a long time believed that RNA could not be reverse transcribed into DNA - until they found retroviruses.

The sort of thing you're talking about would be called a Life History Invariant: a dimensionless ratio between two life history traits $A$ and $B$, such that although the traits themselves vary widely between species, the ratio $\frac{A}{B}$ is relatively constant.
Eric Charnov has written a lot about this, including a book.

One of the invariants which has been suggested is the ratio of age of maturity $\alpha$ to adult lifespan $E$. Charnov claims that it is relatively invariant within taxa, but has a different value for eg. fish vs. mammals vs. birds vs. reptiles.

From Charnov and Berrigan, "Dimensionless Numbers and Life History Evolution: Age of Maturity Versus the Adult Lifespan", Evolutionary Ecology (1990).
(If the ratio $\frac{A}{B}$ is invariant, then plotting $A$ vs. $B$ for different species on a regular graph will give you a straight line passing through the origin. The slope of the line gives you the value of the invariant.
Sometimes, in looking for an invariant researchers will instead graph the quantities on a log-log plot: they then look for whether the curve is a straight line with slope 1 (whose height gives the value of the invariant), with a good fit. This method has been criticized: the fact that some quantities are just about necessarily a fraction of other quantities (eg. you can't really lay an egg bigger than yourself), together with the fact that log-log plots "squish down" variance about the regression, opens the possibility of observing artifactual yesses. I tried to give an intuitive explanation of this criticism in a quora answer. Charnov and company have dismissed it as not applying to the invariants they found, however.)
This invariant is slightly different than the one you describe, in that they deliberately ignore pre-maturity deaths. (If infant mortality were high enough then it would be possible for average lifespan to be less than the age of maturity.) Also, they measure the ratio of pre-maturity lifespan to post-maturity lifespan $(\frac{\alpha}{E})$ instead of the the ratio of pre-maturity lifespan to total lifespan $(\frac{\alpha}{\alpha+E})$. These are just two different ways of talking about the same thing, but the former has an upper bound of 1, while the latter has no upper bound.
Finally, it's important to note that even if a quantity is relatively invariant, it can't be expected to be perfect; you have to decide how much noise you want to allow while still finding an approximate invariant interesting.

There certainly is a general trend of later reproductive age and longer lifespan. This is simply because the organisms need to live at least until their reproductive age to be able to reproduce. However, other than that I think there is no definitive correlation that animals normally live approximately eight times as long as their reproductive age (as your Elephant example seems to suggest). For example, many Insects such as the Mayfly only live until they reproduce and then die quickly (speaking of a "magical first time").
To your supplementary questions:
1) Similar to the above there is a general trend of larger body mass and longer lifespan. This is because a larger body requires longer to grow. Again, beyond this very basic correlation, I would be careful of trying to find rules there as you will find very different lifespans in animals of similar size. Take for example the mole (lifespan 6 years) and the naked mole-rat (31 years).
2) No there is no general correlation between body size and metabolic rate. Metabolic rates vary greatly with habitat, warm blooded/cold blooded animals etc. If you restrict yourself to a certain family of species, such as mammals, you may find a weak correlation. For example, many smaller mammals have a higher metabolic rate, because their larger surface to volume rate requires a fast metabolism to keep their body temperature up. However also here you will find many exceptions (think of hibernation).
To summarize: It is tempting to try to find "general rules" in biology. However, while you will find many trends and correlations, particularly within certain families of species, calling them a rule is dangerous as it may lead people to believe they are generally true which is usually not the case because you will find exceptions everywhere. This is also the reason why you will not find names for such "rules" in reputable scientific literature.

When I say "general rules" I am obviously referring to named observations of trends like Cope's Rule, Von Baer's Law, Allen's Rule, Mendels 'Rules' of Inheritance, Dollo's Law, etc etc.

Most of the laws and rules you are quoting have since been found incomplete, inaccurate or plain wrong.

I can't find a very fine writings/documents to support this or satisfy your question.
I think, it's related somehow. Let's take a sample: (It's not super accurate but you can make a search)
 ------------------------------------------------------------
|  Creature        Lifespan              Reproductive Age    |
 ------------------------------------------------------------
  Butterfly        7 week           Until become a butterfly
     Dog        around 14 yrs            around 9 months
    Human       around 80 yrs            around 10 yrs
   Whale        around 80 yrs             around 8 yrs
  Jellyfish    can be immortal        depends on a situation

The data above is some-kind the "usual" but still it's not the 100% of proof. There are other factors that affects the lifespan and reproductive age relationships like:

Usual/Common ability to produce no. of offspring/s --- Like whales or elephants, they can't produce a ton of offspring in one shot so their lifespan can be longer. Or those cockroaches, they have short lifespan but they can produce a ton of baby roaches in one egg.
Environment Capability --- If one can survive longer in one place, then there's a possibility of late reproduction maturity but when a creature has less of percent of survival in one place then there's a possibility of early production of offsprings. It all depends on the environment.
Lifestyle --- Bad habits and unhealthy foods can shorten ourlives but good habits and healthy foods can help use for longer lives.


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Do alleles, by definition, code for the same trait?
A trait is defined as an inherited characteristic, like eye color and height.
A phenotype is defined as the specific physical manifestation of a trait, like blue eyes and 6 feet, respectively.
Now, genes code for traits. And because alleles are different versions of the SAME gene, they must code for the same trait. Let's say gene A codes for hair color (trait). Gene A(1) (allele) codes for brown hair (phenotype) while gene A(2) codes for blonde hair. Therefore, alleles code for the same TRAIT, but differing PHENOTYPES.
Here is the problem. When I google: "heterozygous", I get a bunch of websites defining it as "referring to a gene pair in which the two alleles do not code for the same trait"
This is not correct because a gene-pair refers to genes located at the same locus on a chromosome. In other words, they are alleles of the SAME gene and code for the SAME trait. They only code for different phenotypes associated with that trait.
So. Either my definition of traits is wrong. My definition of alleles is wrong. My understanding of alleles being different versions of the same gene is wrong. OR. The internet loves to be imprecise with their language and interchangeably use terms that mean different things.
Which is it?

Depends on what you call a trait. One gene (allele) can contribute to multiple traits and vice versa. IMHO, terms like "trait" and "phenotype" have little relevance in modern genetics.

I disagree that (1) the issue behind the question is related to the definition of trait and (2) that the concept of phenotype has no room in modern genetics. I don't think many geneticist, evolutionary biologist, medical geneticist or anyone would really agree that anything in modern genetics remove relevance of the concept of phenotypic traits.

I fear you won't get a definitive answer on this. A survey indicates both usages of trait all over the Internet. As a teacher, I generally used trait to apply to the gene. This made teaching the "central dogma" clear: DNA -> RNA -> protein -> trait. Of course this simplification gets added to later as the course progresses.
One interesting question this poses is in the case of skin color. Is that a trait? Last I read, at least four different genes interact to produce skin color.
I'd side with you on this but acknowledge the fact trait doesn't seem to have the consistent, well-defined meaning that allele does.
On the other hand, a visit to UC Berkeley's evolution site shows them applying trait to the variations due to allele combinations.
Hope that helps! :)

I appreciate your answer! I think you're probably right. NOTE: I would argue that skin color is indeed a trait. And you can have multiple genes code for one trait. In fact, that is the definition of a polygenic trait!

What is a trait?
Many people have talked about the issue of defining a trait. Of course a trait can be anything and there is no objective way of delimitating or counting the number of traits of an organism. However, the issue in this question is completely unrelated to the definition of traits, it is an issue of semantic of causality.
Semantic of causality
The whole issue boils don to what you mean by code for the same trait. In reality, this expression makes little sense. To explain the semantic behind this concept I'll use the existing semantic from probability theory (which applies not only as a vague analogy).
Semantic issue explained in probability theory
If you have some basis in probability theory, you know that you can consider a covariance between two random variables but it doe snot make any sense to consider covariance between the outcome of a random variable and another variable. For example, it makes sense to ask whether footedness is related to handedness, but it makes no sense to ask whether right handed is related to footedness.
Above semantic applied to genetics
Following the above logic, consider a locus (=position on the genome, may correspond to a gene) as being a random variable and the alleles at this locus being the possible outcomes of a random variable. Trait is another random variable which outcomes are the different trait value. It makes no sense to ask whether a given outcome (a given allele) affects a trait (random variable), but only if a locus (random variable) affect a trait (another random variable).
In other word, one can only consider whether variation at a given locus affect variation for a given trait, and not whether a given allele codes for a trait. A locus can indeed affect several traits. Typically, an allele will cause investing into building trait A, while the other allele at the same locus will cause investing into building trait B. As such this locus explains variation for both trait A and trait B but one could not say that an allele code for A, while the other codes for B.
The above case where one locus affect several traits is called pleiotropy. When several loci affect a single trait, it is called epistasis.

The way I see it, the semantics in this area of genetics are somewhat loose and you are correct about all your definitions.
I think the word 'trait' is not currently used as much as it used to e.g. in early 20th-century genetics, or earlier. The meaning of 'trait' can be compared to that of 'feature' (i.e. does it refer to 'having eyes' or 'having blue eyes'?).
In short, I would use 'phenotype' rather than trait when you refer to the  different alleles, and if necessary use 'trait' as height, eye colour, etc.

Really? Every modern introductory genetics book I've encountered definitely use the term "trait" to describe a characteristic...

in other words, it is mostly used in Mendelian genetics... so it will not be a problem you will encounter in more advanced genetics, in my opinion


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Why is the formation of an enzyme-substrate complex endergonic (induced fit model)?
In the section about the induced fit model for enzyme substrate binding, my MCAT textbook claims that "The substrate has induced a change in the shape of the enzyme. This interaction requires energy, and therefore, this part of the reaction is endergonic."
As a chemist, I am a bit confused here because induced fit suggests that some kind of bonding must be happening between the enzyme and substrate (hydrogen, ionic, covalent, etc) that would induce a change in structure of both enzyme and substrate. Any kind of bond formation is STRICTLY enthalpically exothermic, so why is the formation of an enzyme-substrate complex endergonic?
Am I missing an entropic component here? Or is my assumption wrong, regarding how the induced fit chemistry operates?
I would assume that it would TAKE energy to then cleave/break all the bonds that induced structural change and release the catalyzed substrate...

Most reactions require an activation energy to cross an energy barrier (this you may already know) after which the reaction is downhill. Even though enzyme catalysed reactions have a relatively lower activation energy compared to that of an uncatalysed reaction, there is still a transition state that has a higher free energy compared to the products. This transition state corresponds to the enzyme-substrate complex.

            Image Source: https://en.wikibooks.org/wiki/Structural_Biochemistry/Enzyme/Activation_energy

Free energy has enthalpic and entropic components (ΔG=ΔH-TΔS). Even though formation of bonds may reduce the enthalpy, the locking of the substrate and enzyme in a conformation also decreases the entropy. This could lead to overall increase in free energy (See here. For more details you can refer to this book- The Enzymes: Mechanisms of Catalysis by Paul Sigman. ISBN: 0121227200).


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Is it possible to use PCR to test for Machado-Joseph disease?
Machado–Joseph disease (MJD) is a rare inherited neuromuscular disease that is caused by a mutation in the gene ATXN3. The protein encoded by this gene contains "CAG" repeats in the coding region, and the expansion of these repeats from the normal 12-44 to 52-86 is the most common cause of the disease.
It is well known that amplification of repetitive DNA by PCR is prone to errors, mainly caused by misalignment/slippage of the polymerase during the elongation phase.
Does anyone know if there exists a specialized PCR protocol or polymerase that could accurately amplify the repetitive region of ATXN3 such that one could then use gel electrophoresis or Sanger sequencing to approximate the number of CAG repeats?

This paper describes an allele-specific PCR protocol to detect CAG repeat expansion in MJD patients:
Maciel P, Costa MDC, Ferro A, et al. Improvement in the Molecular Diagnosis of Machado-Joseph Disease. Arch Neurol. 2001;58(11):1821–1827.


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Is there more diversity in marine species?
I was reading about how life emerged from oceans, and the following question occured to me. Do land species suffer from the founder effect and is there more (genetic) diversity in marine species? A quick google search pointed to the fact that a majority of species live on land. Is that a paradox?

I know that marine habitats have a higher phylogenetic diversity (see also Faith 2006) than terrestial habitats, even though they host far fewer species, which is a result of their deeper evolutionary history. Unfortunately, I cannot find a good reference to this claim right now (see http://biodiversity.europa.eu/topics/ecosystems-and-habitats/marine for some support though).
I wouldn't really call the difference in species numbers a paradox though, since speciation rates depend on habitat complexity and dispersal rates (which are generally higher in marine habitats). In either case, the knowledge of marine habitats and species living there are much poorer than for terrestial habitats, so differences in species numbers are highly tentative.

The estimated diversity, in this case species richness, is higher on land than in the ocean. To resume the state of knowledge of biodiversity, here's an excerpt from an open-access paper by Mora et al. (2011) How Many Species Are There on Earth and in the Ocean?
"...(our analysis) predicts ∼8.7 million (±1.3 million SE) eukaryotic species globally, of which ∼2.2 million (±0.18 million SE) are marine. In spite of 250 years of taxonomic classification and over 1.2 million species already catalogued in a central database, our results suggest that some 86% of existing species on Earth and 91% of species in the ocean still await description."


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How are unnatural amino acids modelled using insilico tools?
When the structure of an unknown protein containing amino acids other than the 20 known natural amino acids is modelled which method is primarily used in bioinformatics to solve the structure? what is the significance of such model obtained??

when you say "unnatural amino acids" do you mean those not found in humans or just non-protein coding, or something else? can you clarify?

You use the words "modelling" and "solve the structure" and refer to "bioinformatics tools" and an "unknown protein" but it's not clear to me what you mean, and I suspect you are not clear either. Presumably you have the sequence of the protein and it contains something like selenocysteine. Are you talking about prediction of the structure de novo from the sequence or trying to impose the sequence on a similar protein of known structure? Why do you think a modified amino acid would cause a problem? You'll have to explain if you want an answer.

An amino acid is an organic molecule containing a carboxylic acid ($-COOH$) group on one end and an amine ($-NH_2$) on the other end. There exist in nature many more amino acids than the 20 proteinogenic α-amino acids. Examples include selenocysteine, pyrrolysine, and carnitine. The structure and character of these are all known, so there would be no difference in the computer model from a "standard" amino acid like threonine. They are not "mysterious" or "unnatural" at all.

In nature we have only 20 amino acids, but there is one more amino acid which is synthesised in laboratory

@Nik did you even read my answer? I defined what an amino acid is in chemistry terms, and provided evidence that there are 20 proteinogenic amino acids, and many more that occur naturally. There is an essentially infinite number of amino acids that can be chemically synthesized, varying the length of the carbon backbone, its structure, and the nature and chirality of the side chain(s).


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Probabilities of mutations in telomeres?
Frankly I am a programmer, I've been looking at sites like NCBI and others, but couldn't find what I was looking for so if someone can help:
Can you give me the probabilities of

mutations in Saccharomyces Cerevisiae's telomeres.
Probability of having an insertion
Probability of having a deletion.
Probability of having a substitution.

The reason I need this is that I want to generate true-telomeric data based on, the telomere structure consensus.


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Why does this karyotype start numbering at 11?
Here is some image I found for karyotyping a chromosome:

Why does the band numbering start at 11? When I count other things I usually start with the number one, and in some cases zero. Eleven seems random.

What research have you done before asking it here?

I read the Wikipedia pages on the topics, which are very limited. And I studied a few graphics I'd chromosome bands. I have no background in biology and I did not check any textbooks yet.

@FullDecent It is not exactly my field but I don't quite understand what these numbers and band colours are supposed to mean? Can you please add a link to where you found the picture. It may help me out. I don't really understand the expression "karyotyping a chromosome". Does it mean 'to recognize a chromosome while performing a karyotype' or does it mean 'Figuring out past chromosomal translocation events' or something else?


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Do blurry images cause eye strain? At what point is an image so blurry the eye stops trying to focus it?
I'm a user experience designer concerned about a new trend of blurring screens when showing a lightbox/dialog box over top (see below).
From what I know, blurry images cause the brain to work hard unnecessarily as the eye tries to focus an image. If my team really wants to blur images, perhaps I can give them guidance on how blurry the image needs to be.
Here's an example of a page loading, using the blurry effect:

Other than the dialog box in the foreground, you can see that the rest of the words are blurry but are just clear enough to make out, which makes me fear the eye is trying to focus them.
Whereas something like Apple's iPhone blurs the app icons in the background of its Search feature so much that it looks like a pretty image when you search, and it seems the eye wouldn't focus on that background:

So my questions are,

Does trying to focus a blurry image cause eye strain, cognitive load or any sort of discomfort?
At what point does the eye stop trying to focus and just accept the blur as an abstract image, something that can't be focused, at which time it might relax?  Or is that point subjective and, hence, cannot be measured or put into words?


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what does 'invoking the ghost of competition past" mean? Why is it important for present research on interspecific competition?
Ecological and evolutionairy effects are sometimes difficult to distinguish.

This sounds more like a question about english language, as 'invoking the ghost of competition past' sounds more lyric than scientific. Otherwise, without context there is no real way to answer.

First, the setting for this question is almost always related to explaining some aspect of broadly defined trait differences in extant (currently-living) species. The specific problem at hand is one in which someone is trying to explain what may drive the observed differences among competitors. It is unclear whether such differences are relatively recent (ecological time) or old (evolutionary time).
Consequently, the phrase "invoking the ghost of competition past" implies that someone thinks the observed pattern of differences may have been caused by a process that took place a long time ago, and may not be presently observable/measurable. Anyone performing research on this topic would then have a comparably hard time ascribing causes of differences to ongoing competition, as opposed to past competition.


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Neuron activity on body parts measurable?
Is it possible to measure the neuron activity on body parts like the back or the arm? Or is this done already?
Of course neuron activity can be measured on the scalp using an EEG. I wonder if similar technology could be used to do the same on other parts of the body.
I know there is EMG which measures muscle activity and  that's also easier to measure as the voltages are multiple orders of magnitude higher. But I imagine that one could get much richer data by directly sampling neuron activity.

To meausure single-unit neuron activity you need to use a microelectrode system, but it is very invasive. How useful the information collected depends on what you searching for. If you interest in neurophysilogy its the way to go, if you interested actual outcomes then the average neural response to stimulus is actually more useful

@SciEnt OK, for single neurons one needs (very) invasive sensors. Can you get any statistically stable measurements when you just attach a bunch of sensors and measure all neurons there at once, non-invasively?

(When measuring EEG you don't measure single neurons either, however with multiple sensors one could measure location based somehow, as far as I understood)

yes, after processing you do get a good stable signal. Computational work uses these neural averages as 'the' signal. In the end synchonicity of neurons working together is what really matters. I have found " Theoretical Neuroscience: Computational and Mathematical Modeling of Neural Systems " really useful

@SciEnt Thanks a lot, this very much answers my question! I guess I have an interesting read now ;) (If you like to make an 'official' answer out of it, I would mark it as answered...)

To measure single-unit neuron activity you need to use a microelectrode system, but it is very invasive. How useful the information collected depends on what you searching for. If you interest in studying the neurophysiology of neurons its good way to go. If on the other hand, you are interested actual outcomes stimulation then the average neural response is actually more useful.
Computational work often uses these neural averages as 'the' signal. In the end synchronicity of neurons working together is what really matters in achieving higher order functions.
A good book I have found  " Theoretical Neuroscience: Computational and Mathematical Modeling of Neural Systems " by Dayan P., Abbott, LF., (2005)
really insightful into how brain activity is measured and analyzed. Prior knowledge in Calculus and Statistics will greatly help make sense of the math, but even without it is enlightening.


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Questions about Genetic algorithm paper of Gilman and Ross
I want to reproduce an (old) biochemistry paper of Gilman and Ross, i.e. " Genetic algorithm selecetion  of a regulatory structure that directs flux in a simple metabolic model."  ( The following link leeds to the paper: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1236362/)
I know this is an old paper, but maybe someone here remembers it. I really need the answers of the following questions because the enzymatic model explained in the paper is very important for my master thesis.
First:
The author defines a system of two ODEs but the initial conditions of these ODEs are not printed in the paper. The author just writes: "Initial conditions for the integration are determined by letting the network relax to steady state. " (see p. 1324 on the lower right) . But how is this meant? In this paper the author wants to optimize the mentioned ODEs , so how can I find initial conditions, when there are not all parameters of the ODEs given?
Second:
On the top of page 1324 are two needstate functions defined, called xi_T and xi_F. When I plot xi(F), the plot looks completely different from the one depicted in figure 3b in the paper. So the function defined in figure 3b) must be wrong. Did anyone realize that error and has a workaround for that? Of course I could define my own functions but I want to stay as close to the model in the paper as possible.
Thank you very much for your help.

The first thing, before asking on a random website, would be to see if you can track down the original authors and ask them. It was only published 20 years ago, so there's a good chance they're still alive. First try searching the website of their university, then expand from there. Look up other papers, find old postdocs, see if they know where to find them. Biology is a small world, and people have connections everywhere. With a little earnest work on your part you ought to be able to track them down. Hell, the contact info for Ross is given in the paper, shoot him an email.

@MattDMo Do you really think I didn't already do that?

no offense to you, but given the usual quality of 1-rep "Please do all of my research for me" questions we get, my answer would be yes. If you already have, then congratulations!


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What is the molecule responsible of the yellow color of the Agave americana?
Does anybody know what is the molecule responsible of the yellow color at the edges of this plant?
I noticed also that the new forming yellow part at the begging stage is soft green until it is exposed to light. After the exposition to sun light it change from soft green to yellow(like that of the image bellow).
Does anybody have any explanation?

Xanthophylls, I would guess. These are leaves and all leaves do contain Xanthophylls but the green colour due to chlorophyll dominates. These parts of leaves do not produce chlorophyll.

I think that your explanation is good. But I do not know why this type of  evolutionary adaptation...If there is no chlorophyll but only
Xanthophylls all the yellow parts are useless in therm of photosynthesis, I guess.

Yes. These parts are non-photosynthetic.


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Which is the most extreme thermophilic bacteria known?
Extreme thermophilic bacteria thrive at any temperature above 40/50°C. Thermotoga Maritima seems to be the bacteria that can survive at the highest temperature up to 90°C (reference 1, table 2). I wonder if there is a more exhaustive list of extreme thermophilic bacteria and if there is a known bacteria that can survive at higher temperatures than Thermotoga Maritima.
References:
Ref.1 Front. Microbiol., 05 November 2015 | https://doi.org/10.3389/fmicb.2015.01209
Extremely thermophilic microorganisms as metabolic engineering platforms for production of fuels and industrial chemicals

There is also the bacterium Aquifex pyrophilus which is reported to grow  up to 95°C. I don’t know if this is the most extreme temperature reported for bacteria.

Geogemma barossii, initially designated Strain 121, can survive and reproduce at 121°C, with an optimal growth temperature of 103°C. It's not a bacterium though, but a member of the Archaea domain.

Here is a link to an online lesson covering thermophilic and hyperthermophilic bacterial and archaea. https://courses.lumenlearning.com/boundless-microbiology/chapter/thermophiles/

Methanopyrus kandleri strain 116, another archaeon, is reported to grow up to 122°C with an optimum growth temperature of 105°C. In the paper they also explain that it is difficult to compare this species with others from different studies due to the dependence of growth temperatures on culture conditions.

Is this the same as what grows at Yellowstone's geysers? Because they say "The water can be as hot as 204 degrees and the steam can exceed 300 degrees." That's on the Fahrenheit scale. Converting to Celsius, it's 95.5 and 148.9. https://whyy.org/segments/the-biodiversity-of-heat-loving-bacteria-in-yellowstone-rivals-a-rainforest/


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Easy and cheap antigen/antibody couple
For an application I need to find a cheap antigen and cheap correspondent antibody. The antigen can be literally any molecule that is cheap and potentially easy to produce and with a correspondent antibody that is cheap and easy to produce as well. I imagine this antigen will need to be a molecule that triggers very easily an immune response to result in a easy to produce antibody.
I have never worked in immunology so I don't know what system antigen-antibody to choose. I know pregnancy test are common so probably the antibody for Human chorionic gonadotropin (hCG) is easy and cheap to produce but I don't think hCG is.
 Are bigger molecules better than smaller ones as antigens? Any suggestion is helpful.

I am not experienced in this field but this could be helpful to you.

I think adding how you expect to use this will get you a better answer. For example, there are many protein purification systems that use protein or peptide tags that are recognized by antibodies, but that may not be appropriate for whatever you are planning ...

Really anything. I  like the avidin/biotin system suggested in the link that @trinitrotoulene shared in the comment. Doesn't necessary need to be antigen/antibody but it is preferable. Interesting the protein purification, I'll have a look since those peptide tags and antibody may be common and relatively cheap.

A good choice is the IgG/anti-IgG pair for cheap, easy to demonstrate/work with system. E.g. Goat-IgG coupled with donkey anti-goat IgG.  Just about any antibody supplier will have these.
These type of systems are the basic primary/secondary antibody bindings routinely used in immuno-assays, blotting etc. These may be mouse IgG coupled with a labeled anti-mouse IgG for example.
Reference
Wilson MS, Nie W. Electrochemical multianalyte immunoassays using an array-based sensor. Anal Chem. 2006;78(8):2507-2513. doi:10.1021/ac0518452


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Is biotin a hapten? If so, how does it work as a hapten in the human body?
https://en.wikipedia.org/wiki/Hapten
Hapten's aren't synonymous with allergens. It is defined as a foreign molecule that can bind to an antibody but does not evoke an immune response unless combined with a carrier protein.


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Why and how do red bone marrow concentrations in humans change during traditional aging?
I have found several pictures that suggest this is the case.  As for peer reviewed papers I've found plenty of papers hypothesizing and testing as to the why of changes in populations of HSCs, a few on quantitative changes in MSCs, but none explaining why red bone marrow would become less active hematopoietically in long bones before flat bones.


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evolution or chance?
I was reading my chemistry textbook, when in the chapter on 'solutions', i came across a problem, which calculated the amount of oxygen that can be dissolved in 1cc of water at STP. Then they commented, "this amount is just perfect for aquatic and marine life. Had this been lesser, life in the oceans might not exist at all.' This raised the following question in my mind:
1)aquatic species of flora and fauna evolved over time to adapt to this concentration of dissolved oxygen, and their biological processes were also fine tuned based on the environmental conditions.
2)It really was fate that the dissolved quantity was just enough to support marine life, as the textbook said.
Which of the two is the actual scenario? My personal pick happened to be 1), but I have no proof of it. Can someone explain?

That is not really chance but referred to as the contingency of evolution. Any other oxygen concentration would - observed now, after a long time of evolution - seem to be just as perfectly matching.

Oh my. Do the authors provide any support for this claim? More importantly: what is their affiliation with creationist organizations? Well, back to science.
First, a note about your question. It might seem that you have sketched out two scenarios, but for the biologist, they are equivalent. We know two things: life exists, and life adapts. Yes, the specific circumstances on Earth have made life possible, and subsequently, life has adapted and fine-tuned itself to those circumstances.
Now to answer your question.
I really like the visual representation of the Life Timeline on Wikipedia. 4.1 billion years ago, earliest life appeared on Earth. At that time, all oxygen on the Earth's surface was bound in chemicals like CO2, iron oxide, etc. We are unsure whether the earliest life-forms originiated in the ocean, but we know they ended up there one time or another. The absence of athmosphetic and water-dissolved oxygen of course meant those first life-forms were anaerobes (lived without oxygen). In fact, oxygen was extremely poisonous for our teragrandparents. (We are the ~ 10^12th generation of life.)
So, aquatic life has existed without oxygen, and still exists, whether the solvabily of oxygen is 'perfect' or not.
Another fun fact debunking your chemistry authors statement: water oxygen saturation doesn't reach 100% at all times (linked article provides lots of great information about dissolved oxygen and life, by the way). Lots of life-forms requiring oxygen hence live in a world where the solvability of oxygen is even more than perfect. Furthermore, life exists (but doesn't thrive) in low-oxygen conditions (e.g. pubmed:9510533).

The claim is strange since many bacteria don't use oxygen, and since oxygen is indeed a by-product of early life (thus not using it. Oppositely, oxygen is indeed a poison for cells that they had hard time to protect against, then get able to have some use).
Moreover the amount of dissolved oxygen varies with places, depth, temperature, and along geological times.
So, answer 1.

It was quite clearly answering 1. I made it explicit :-) .


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do cancer cells respond to EM fields?
Do cancer cells respond to electromagnetic fields? If so, can someone please provide reliable information as to how they behave in such fields? Do you suppose the growth rate to be affected in any way ?

I guess you are talking about low energetic EM fields, right? Do you have any special treatment in mind?

Can you be more specific about what kind(s) of cancer you are interested in? Cancer is not one thing at the cellular level. Cancers come in all types.

@Chris, if cancer cells are basically due to uncontrolled growth, we can try to control them using different frequencies and intensities of EM fields. After all, neural signals are electromagnetic in nature. If those EM signals can control the body and its growth, maybe we can use some to inhibit growth as well.

@kmm, suppose i take a lump of gastric cancer cells and expose them to EM fields(variable or constant). Will any significant effect be observed?

Most likely not. There is an approved therapy for brain tumors called tumor therapy fields, but there is little (if any) proof, that this works. Additionally, neural signals are a little bit more complicated than just being a field.


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Are there public records of results with laetrile treatment against cancer?
I'm looking for what the title says. This is based on the book by Edward Griffins. Is laetrile actually fatal because of its cyanide content? Or can it really help in this fight?

Yes, there are several articles describing experimental data from animals and clinical trials in humans. The results clearly show that laetrile is not effective for cancer treatment, and the drive for laetrile as a cancer drug is widely considered to be a quack. See for example this NCI summary or this article.
Laetrile is a modified form of Amygdalin, a toxic plant product found in some seeds and nuts, for example bitter almonds. The compound contains a cyanide moiety and can cause cyanide poisoning. It was labeled "Vitamin B17" by Ernst Krebs in an attempt to get the compound classified as a nutritional supplement rather than a pharmaceutial (to escape FDA regulations), but this is misleading; it is not a vitamin.


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What is significance of opsonization?
Wikipedia says

Antibody opsonization is the process by which a pathogen is marked for ingestion and eliminated by a phagocyte. Opsonization involves the binding of an opsonin, e.g., antibody, to an epitope on an antigen. After opsonin binds to the membrane, phagocytes are attracted to the pathogen.

But why is it necessary for pathogen to bind with opsonin? Can't phagocytes attracted towards pathogen without opsonization? Simply I want to know what is significance of opsonization?

In this process a number of pathogens are already inactivated due to the antibody (the most common opsonin) binding. This is highly important for substances which occur only in very small amounts, but still have a great effect as the tetanus toxin. Here the protective effect of the vaccination comes from highly specific antibodies. The toxin in an infection acts not as a immunogen, since its concentration is too low for that - but enough for the toxic effect.


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What is the function of multiple nuclei in syncytial cells?
What is the function of multiple nuclei in syncytial cells specially in protists with cilia? Is multiple nuclei a special characteristics of only ciliated cells?

A mononucleate's size is limited by its nucleocytoplasmic ratio, and protozoa like being big.
The solution? Multiple copies of the same genes in huge nuclei, or multiple individual nuclei.
Multiple nuclei are common in any large, complex cell. There is nothing specific to the presence of cilia that require multiple nuclei, and ciliates are not the only multinucleate protozoa (the amoeboid Chaos genus can contain up to a thousand). The reason large, complex cells require this is simply because they are so big. Such a huge size requires, in addition to more complex nuclear regulation, a high total protein turnover, which in turn requires a high transcription rate. Even with mRNA being translated by numerous ribosomes, the amplification factor is still limited. Having multiple nuclei increases the rate of mRNA production, which increases the total synthetic capacity of the organism. When only a specific gene is required to be transcribed at a high rate, that individual gene may be duplicated many times. This is often seen in the nucleolus, which contains many copies of the same genetic material required to create the huge amount rRNA needed for ribosome biosynthesis:

Many protozoa are large because they are packing as much complexity into a single cell as they can, even to the point of having a backbone-like structure or simple photosensitive "eyes" (though not all protozoa are large). Many adaptions are required to allow single-celled organisms to grow to this size, such as a more complex cytoskeleton, a dedicated feeding apparatus, a contractile vacuole, etc. Multiple copies of genetic material is just another required adaptation. This adaption can manifest itself in various ways. Some organisms have multiple copies of the same nucleus. Others fuse these nuclei into a single, large nucleus (a macronucleus), keeping a limited number of micronuclei around for sexual reproduction:

Multicellular organisms tend to have multiple nuclei in specific cells for the same reason. Many types of cells, for example, require an extremely high rate of protein turnover and are very large (such as skeletal muscles), so they have multiple nuclei. This occurs when a single nucleus is no longer sufficient, even at peak capacity.
I would like to point out that what you are describing is a coenocyte. A syncytium is a multinucleated cell which has arisen from the fusion of multiple cells and their constituent nuclei (karyogamy), whereas a coenocyte is a cell which had undergone multiple rounds of nuclear division, without accompanying cytokinesis.

Regarding your second question:
Multiple nuclei in a single "cell" is not exclusive to ciliated cells.
Muscle fibers of animals or placenta of mammals undergo cell fusion, resulting in multiple nuclei in one "cell".
Embryos of some animals start with nuclei division without cell division, also resulting (temporarily) in multiple nuclei in one "cell".
Other examples are provided here: https://en.wikipedia.org/wiki/Syncytium


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Can viruses pass through sweat pores?
I have read somewhere that viruses and other microbes can not penetrate skin but what about sweat pores? Can viruses pass through these pores?

How would you expect that it would be determined that viruses cannot penetrate skin? Some theoretical method, performed by pipe-smoking tweed-suited academics at a blackboard, or by testing whether viruses can infect via skin?

'Pore' is a confusing term. Sweat is produced in sweat glands, and subsequently excreted through a duct, as indicated in the image below (sudoriferous ~).
In short, viruses cannot enter the body through these glands because the glands don't really open up into the body, but instead the inside of the sweat gland is lined with sweat-producing cells (fig 2 and 3).
A passive protection mechanism preventing infection is similar to the mechanism by which the bladder is guarded from infection through the urethra: even if some malignant agent were to enter the sweat duct, it is simply pushed out by the excreted sweat.

Figure one: Sweat glands in skin. Source: wikimedia commons.

(source: uwa.edu.au)
Figure two: Slide of sweat gland. Tightly packed secretory cells dump sweat into the lumen through exocytosis (see fig 3). Source: University of Western Australia.

Figure three: Exocytosis. The lining of the sweat gland contains cells producing sweat through exocytosis. Viruses and other pathogens cannot simply enter these cells, and also cannot 'slip in between' the cells. Source: wikimedia commons.

It would be great, if you can at least add the sources for the images. Additionally references for further reading would also be good.

Thanks for the feedback. I had the sources in figure alt-text, but this is much better. Will look at further reading later


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Why similarities among organisms led scientists to believe that organisms are evolved?
Theory of evolution states that organisms are evolved into other more advanced ones over time because there are some traits in modern organisms resemble with organisms existing before (from fossil record). But it might be possible that each organism has created independently of each other. why similarities mean evolutionary relationship?

Theory of evolution states that organisms are evolved into other more advanced ones over time  Nope that's not what the theory of evolution is stating, mainly because the expression "more advanced" does not mean much and also is a loaded expression. You might want to start with an intro course to evolutionary biology to understand what the theory of evolution says. Understanding Evolution is a very introductory course you might like.

@Remi.b Alright I will have a look at what theory of evolution states but the basic thing is humans are thought to have evolved from chimpanzees. What I want to know is chimpanzees might resemble to humans but why chimpanzees are considered ancestor of humans? It might be possible that humans and chimpanzees created individually?

I answered this second comment in answer form as comments were too short for what I wanted to say

Approaching the question from the other direction, we understand how evolution could happen (similar mechanisms are used in e.g. computer genetic algorithms), and see some examples of ongoing evolution, like antibiotic resistance in bacteria.  But we don't see new creatures being created ab initio, and have no evidence for any mechanism by which they could be created.

I see you are new to stack exchange. If an answer states "not an answer" it might be a good idea not to mark it as best answer :) Nice question though!

@AksaK chimpanzee are NOT considered the ancestors of humans, they SHARE a common ancestor with humans, kind of how you and your cousin share an common ancestor. That ancestor is believed to look more like chimpanzee than us humans, but does not mean much.

@Clangorous Chimera: OTOH, there are some people here who mark perfectly good answers as "not an answer".

I will answer by explaining some misconceptions in your original question:

Theory of evolution states that organisms are evolved into other more advanced ones over time

Nope that's not what the theory of evolution is stating, mainly because the expression "more advanced" does not mean much and also is a loaded expression. You might want to start with an intro course to evolutionary biology to understand what the theory of evolution says. Understanding Evolution is a very introductory course you might like

@Remi.b Alright I will have a look at what theory of evolution states but the basic thing is humans are thought to have evolved from chimpanzees. What I want to know is chimpanzees might resemble to humans but why chimpanzees are considered ancestor of humans? It might be possible that humans and chimpanzees created individually?

No, the theory of evolution does not state that humans evolved from chimpanzees. It says that humans and chimpanzees / bonobos have a common ancestor (about 6 millions years ago) that was not a human, nor was it a chimpanzee or a bonobo.
You can find an introduction to phylogenetics in this post and you can find online tools to visualize the tree of life in this post.
Philosophical issue in your question
The theory of evolution makes predictions that have been tested and demonstrated correct. You are asking why would creationism would not lead to the same predictions. For this purpose, one need to know what predictions would creationism make but this is very much undefined. If you can point to specific predictions that creationism would make, then we could tell you whether we have a counter evidence. The issue is that there is always a way to say, everything has been designed so that it looks like evolution is at play even if species were created anew. But this is not falsifiable.
So, maybe you might want to make specific predictions, that in your opinion, would be congruent with creationism but not with the theory of evolution and then we can tell you if we have evidence to support this prediction.
Related posts
While it does not directly answer your question (because IMO, for semantic issue, the question is unanswerable), you might want to have a look at Is evolution a fact? and Demonstrable and repeatable examples of evolution

The main reason organisms not believed to be created independently, (besides no evidence for a creator to do creating) is that organisms do not just share similarities but they share similarities in a predictable pattern. Similarities are not random but follow a pattern that only makes sense if it is due to small changes over long periods of time in an ancestors/descendants branching tree of relationships. Two similar creatures will be equally similar to a third, and those three will be equally similar to a fourth and so on ans so forth in a nested pattern, not just a random assortment.
Humans might happen to be very similar to chimpanzees and vice versa by chance alone, but the chance of both humans and chimps also being very similar to gorilla is much less likely, them being similar in the same ways is even less likely, and the chance of all three also each being very similar to orangutan is even less likely, ect and so forth through the entirety of life. The chances of this arrangement of traits and genes happening by chance (aka without any actual relatedness or common origin) is so astronomically small it is difficult for us to even conceive of events that uniquely unlikely. There is a better chance of all your atoms happening to sync up so you fall/phase through your chair and plummet to the center of the earth in the next few minutes. In fact the entire field of Cladistics is about testing and mapping these relationships, and one of the things they constantly test against is a the possibility of an random or convergent assortment of trait.
This pattern also mirrors the pattern of human driven evolution (artificial selection) in which organisms are bred from other ancestral organisms through small changes by encouraging individuals with certain traits to reproduce and discouraging others, which at the time was far more well understood, which is how they recognized it. It is also why three chapters of Darwin's book was about show pigeon breeding.
And all that is before you get into things like the mathematical predictability of evolution, the fossil record, or directly observed evolution.

Another factor is that when we do see distantly-related organisms having a very similar appearance, we can often identify the evolutionary pressures that would lead to that similarity.  E.g. dolphins and ichthyosaurs look much the same because of hydrodynamics.


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How harmless bacteria on skin defence against harmful bacteria?
I have read that there are some harmless bacteria live on skin and they also have role in protecting body against some harmful bacteria but how do they do so? I mean how these bacteria are able to resist other bacteria which are harmful?

Another way to look at this is, you have a limited amount of skin. "Good" bacteria competes for space on the skin with "bad" bacteria. They kind of strike a balance where harmless bacteria are more common. That protects you in that say you have a microabrasion on your skin; it's less likely to be invaded by harmful bacteria than not as-pathogenic bacteria.

Relations between organisms in complex ecosystems are various, so I won't give an exhaustive answer, only keys to understanding.
First, you need to consider that a bacterium harmful to humans is not necessary harmul to other bacteria. So there is no reason why our skin microbiota will only target/resist to human pathogens.
What's more, microbes are not inherently harmful to us. Their dangerosity also depends on the capacity of the skin to block them 1.
Then, microbial defence mechanisms depend on the kind of relation they have to the potential pathogen: competition, parasitism, predation, etc.
The article cited below will give you a nice overview on the topic.

1 Cogen, A. L.; Nizet, V.; Gallo, R. L. (2008) Skin microbiota: a source of disease or defence? British journal of dermatology, 158, 3, 442-455; doi: 10.1111/j.1365-2133.2008.08437.x


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What fraction of embryos fail to be born? And why that high?
In the book Developmental Biology by Scott F. Gilbert and Michael J. Barresi, it says:

Most human embryos die before being born. You survived.

So how come is that true???
And what percentage of pregnant women lose their unborn child(ren)?

How can we possibly know without knowing with certainty that a woman is pregnant? Many are lost only days after implantation.

What attempt have you made to answer this question on your own?

Is the fastet sperm always the best?

It's a tougher question than it looks; estimates vary pretty widely https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5443340/#__sec2title


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Which fish species is it?
Today we found this kind of fish on the shore of Baltic Sea near Gdansk (PL). It is a very thin "fish" with some kind of a needle in place of nose. It was about 5 cm long and very lively. What is the name of the species?

PS. Kids caught it into a bucket just to take a pic - we released the creature just after the photo session :)

I am super super sure it is a straightnose pipefish which is usually found in the baltic

Yes, but are such long needle noses common in that species?

This looks like a pipefish, possibly a straightnose pipefish.
See also. But the size suggests a juvenile?

Thank you @alan-boyd for your answer. The one you suggest has however much shorter "needle" than the one on my photo, at least compared to the photos over the web. Could it be Syngnathus typhle perhaps?

Agreed, that looks like a possible match, but size is still a problem. Mine was a quick-and-dirty answer - I assumed that a Baltic pipefish expert would be along to clarify. Without a better image you may never know exactly what species it was.

Hi. I also found Microphis brachyurus aculeatus on the web, which looks at most similar to the one we found. However, according to the sources, it does not appear in Baltic Sea , only in Senegal, Angola, etc...