To which ungulate species does this tooth remainder belong? Found on the beach in Çanakkale, Turkey.
I have found a lot of these, but this is the first one that has parts like long teeth. My other findings have sometimes 4, sometimes 6 tubes. Very solid, stone-like objects. Is this from a marine animal or is it a non-living formation, I wonder.
Below image is for scale in centimeters.

View from top and bottom

Other similar findings without teeth-like parts

Its definitely not a marine mammal, just based on size and general configuration.
those convoluted ever growing teeth are pretty diagnostic of non-cetacean ungulates.
Just based on the pattern I would say bovidae, but that does not narrow it down much in turkey, the H shaped central portion is fairly diagnostic of bovidae. However you have several antelope species not to mention domesticated animals that each would fit that category.
I suggest changing the title to ask for ungulate tooth identification. You need someone specialized in mammalian teeth to narrow it down to species. if you can add more shots of the tooth crown (the complex ends like those below) that is the part most useful for identification. See the examples below. The more you have the better.

Source

Sheep or goats teeth.
As it was found at the edge of water and may be from drowning, I would predict that it is much more likely to be from a sheep, as goats are so very much safer around water.

Image from:
"Enamel hypoplasia in molars of sheep and goats, and its relationship to the pattern of tooth crown growth"
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403278/
But really I know because I was a farmboy.


Difference between water and tea My friend heard that tea is worse for drinking than water because "cells have a special membrane and tea has special supplements and membrane doesn't let tea pass and this is why skin is dry even when you hydrate with tea a lot", something about "lipid bilayer".

Is there is some nice scientific article on water andd tea difference to human organism?

Your question is very awkward.

Let's define Tea as boiling leaves in water. At the end, you remove the leaves and drink the flavoured water.

At this point, the "tea" is still very much water - as in tea is water with dissolved chemicals from the leaves. Note, the word chemicals is not to be interpreted in a negative way because everything (including water) is a chemical.

So, the difference between tea and water are the chemicals that dissolve. What are these chemicals? The answer to that depends very much on the tea. Another difference is the temperature - tea is typically hot.

You can look at this article about chemicals in green tea and their associated health benefits. You can do further searches for other tea types and for each of those chemicals.

In short, no you do not get dehydrated because of tea vs. water. Dry skin can be caused by a lot of different reasons. Oh and no, caffeine doesn't cause any significant amount of dehydration as far as I know.

Depends on the tea, but most tea (unless herbal) contains caffeine, which is a diuretic. This means it dehydrates, and why one might experience drier skin. However, this is not a direct relationship and the actual reason why one's skin might be dry is a lot more complex. However, for a basic answer, caffeine is your culprit.


How many ATP molecules are formed? What is the number of ATP molecules formed during the photosynthetic processes which consume 8 molecules of $\text{H}_2\text{O}$ due to noncyclic electron transport and subsequent photophosphorylation?

Assume that quinone cycle facilitates the transfer 4H+ to the lumen of thylakoid membrane for every two electrons passing through electron transport system and one ATP is formed for every 3H+ moving down the proton gradient by the mediation of F0F1-ATPase

MY ATTEMPT: In the lumen, due to hydrolysis 16 H+ are formed. Due to quinone cycle 32 H+ are taken from stroma and transferred to the lumen and NADP+ takes 48 H+ so in stroma there is deficiency of 80 and there are only 48 H+ in the lumen. If I assume that if there were initially hundred H+ on both sides then after non cyclic transport inside the lumen there are 148 H+ and in stroma there are 20 H+ so to have equilibrium then there should be 84 H+ on both side so total 64 H+ should travel then I am getting 64/3 ATP which is wrong. Where I am going wrong?

Screenshot of question paper

Sorry for the poor quality of the image, but its just as a reference for my answer.

You have made the question too complex. From the figure, we find that 1 H2O gives 2 H+ and 2 e-. 2 e-, through quinone cycle, provide 4 H+ i.e. total 6 H+ which form 6/3 = 2 ATP i.e.

1 H2O => 6 H+ => 2 ATP

Multiply this equation by 8 and you get:

8 H2O => 48 H+ => 16 ATP

So, 16 ATP should be the answer.

Reference:

Pradeep's: A textbook of Biology for Class XI, 2015, Vol. II, page IV/106

ACCORDING TO ME THE ANSWER IS 24 ATP THAT IS BECAUSE
8H+ IS PRODUCE DE TO PHOTOLYSIS.
16 H+ WILL BE TRANSFERRED INTO LUMEN.
SO 8 ATP WILL BE PRODUCE BY ATPASE {TOTAL 24 H+]
4 NADPH2 WILL PRODUCE 12 ATP
4 ATP WILL BE RELEASED FROM ELECTRON WHILE MOVING IN PS1.
SO TOTAL 8+12+4 = 24 ATP.


By what physiological mechanism do we not feel microbes (bacteria, etc.) living on our skin? Background
I know our bodies have a handful of ways to threshold our awareness of sensory stimuli:

Neural density

Sensory acuity
I assume really tiny stimuli could fit between receptors

e.g., Oaklander (2001) found nociceptor densities of 2-4000/mm2

Impacts summative abilities to surpass postsynaptic impulse thresholds

Varying thresholds of individual receptors.

Dubin & Patapoutian (2010), for example, show variations in classes of neurons based on their temperature (°C) and mechanical force (milli-newtons) thresholds (see thresholds listed in Tables 1 and 2).

Reticular formation involvement in regulating what we are consciously aware of

My question:

Which of the above physiological mechanism(s) are primarily responsible for our lack of sensation (or lack of conscious awareness) regarding microbes on our skin?

Update: My question is explicitly about physiology. Regardless of the impacts, benefits, evolution ,etc. of not feeling them, they're there. But even though we're covered in microbes, we don't sense them -- how not? I want to know by what physiological mechanism(s) we don't feel microbes on our skin.

Ask yourself, what benefit would it have?

Keep in mind you will always bee covered in them, this is the state you evolved in. Thus sensing them would serve no purpose, and sensory organs are expensive in terms of resources so why would we evolve a useless sense?


Why has our nose evolved with the nostrils facing down? For most animals, the whole bottom of their face sticks out and they have a snout with a mouth and nose at the end.  But humans have a flat face and just a nose that sticks out.  We used to have the whole face sticking out, but our jaws got smaller and smaller.  Because our noses still needed space to do their job, they had to stay sticking out.  People who come from very cold areas have bigger noses than people from where it is hot, so they can warm the air up more.

Why has our nose evolved with the nostrils facing down? Is it because we were water animals, and that would help with water coming in?

I have not been able to find any studies that look specifically at the genetic mechanism for nose development. I certainly do not know but I'll offer up two hypotheses.

My first hypothesis is that the elongated nose is a remnant of the elongated lower face of our ancestral species, as you note in your answer. Take a look at this brief YouTube video (1:17 long, the part relevant to this answer begins at 33 seconds) of a time-lapse composite showing the develop of the human face. Our face develops as two separate halves that meet together in the middle. That's what creates the philtrum under our nose.

Watch the especially carefully from the 54 second mark to 1 minute mark. Note that our nostrils are pointing directly forward and the overall region looks somewhat like a pig snout. The mouth is vertical aligned with the front of the nose. The overall face is much more rectangular and the eyes are on the sides of the face.

Then, the face begins to become rounder and flatten. The eyes move to the front of the face and the recesses our our eye sockets recede. The lower face below the nose recedes, becoming flatter. The only part that does not recede is the nose area. The flattening of the lower face may actually cause the nostrils to turn downward.  Our nose does not develop outward from a flat face but instead is left behind as the rest of the face flattens.  This would be my initial thought as the primary reason for the shape of the nose and direction of the nostrils.

My second hypothesis (and honestly independent of the comment by @Remib) is related to our sense of smell and taste. Although our ability to detect flavors is a complex process, the primary sense involved is smell (Shepherd 2006). Therefore, downward-pointing nostrils are located directly above the mouth so we get a good smell of the food just before it enters the mouth, perhaps enhancing our flavor-sensing ability.

  Shephered, G.M. 2006. Smell images and the flavour system in the human brain. Nature 444: 316-321.

Note that these two hypotheses are not mutually exclusive. The downward pointing nostrils may be a remnant of our facial development but provides an (adaptive?) advantage for flavour perception.

Ive found that the study of this feature, the nose is far from complete.Although we see the evolution of other mammals and their faces has a great deal to do with there ability to survive different enviornments I believe it , our snozz is a genetic mutation in which allows us the ability to go from nonaquatic to aquatic with out needing a snorkel. ?.by defying why we have this thing on our face......some so large some so small I dont believe to have much to do with ancestial deviation of the jaw but the defying feature of the human race.....thank you


When does BLAST fail to align 2 DNA sequences? This is an assignment that had confused me for a long time.  So I think you guys who study computational biology might be interested. The original question is:

  Find the two most similar DNA sequences of length 20 that Blast using a word length of 5 will fail to align.

BLAST works by finding a perfect match between sequences of a length equal to this "word length" and then enlarging it in a standard way -- yet there will be no alignment without this perfectly matched word.

So in your case, you must look for two 20bp sequences with no common 5bp sub-sequence; for instance:

AAAAAAAAAAAAAAAAAAAA

and

AAAACAAAACAAAACAAAAC

I am not sure I understand BLAST correctly.

When using BLAST in DNA and protein, they are different. There is a threshold T in protein "seeding" step, which means the seeding sequence is not perfectly matched. However, it seems there is no T in seeding step and we are looking for perfect match and extend them to neighbouring sequence.

So, if there is no word length 5 exact match between these 2 sequence, BLAST will fail.


Does it make sense to make my own DNA copy (kind of backup) while I am young? As I understand, when I am getting older DNA becomes more and more damaged in my body.

Does it make sense to make my own DNA copy (kind of backup) while I am young (38 years old or for my kids) in case that in future there will be the technology which will make possible to restore damaged DNA from this copy and make me younger?

Or it does not make sense, because original not damaged DNA always can be found in some places of my body?

If it makes sense, what is the best way to do this DNA backup? Cut a piece of hair or nails or freeze a piece of saliva?

While your DNA gets damaged, not every single cell will have the same damage.  Your consensus DNA sequence will not change.

No, it does not make sense. When you ask: "in future there will be the technology which will make possible to restore damaged DNA from this copy and make me younger?" I can confidently say that there won't be such technology, for the following reasons.

1) DNA is only one component of your body's cells; important of course, but not really the 'master regulator' of everything about you (in fact, practically all cellular functions are performed by proteins and other molecules, not DNA). This belief (that DNA can determine every aspect of life) is called 'genetic determinism', and it is known to not hold even in trivial cases.

2) Your environment (diet, air, sun, family, friends, society, random events) plays a major role in who you are and how you age. Even if you were to repair all DNA damage as soon as it occurred (which, by the way, your cells do quite efficiently anyway), you could still not control for all there is outside of you, and thence you could not really 'rejuvenate' with the magic DNA pill. Most people tend to ignore this when fantasizing about DNA's healing powers: there is a world outside.

3) DNA is not something you drink or take as a 'medicine', not now, not in the future. The technology needed to rejuvenate all of your cells will likely not include 'DNA repair'. It might have to do more with metabolism than anything else (also, mutations occur all the time and not all of them are bad, so in fact 'repairing' DNA with your 'juvenile' DNA might not even be good long term).

4) It might make sense to freeze some of your cells for other applications (like tissue regeneration for you/your children), but it is quite expensive at the moment and usually requires a sample of your umbilical cord. I presume the technology to de-differentiate adult cells to totipotential cells is quite feasible, so in the future this application might be accessible, buy still unrelated to rejuvenation (unless there is something like 'whole body' tissue replacement).

As for the previous answer, "Your consensus DNA sequence will not change" makes no scientific sense. Your DNA sequences (of all of your cells) change all the time, and there is no 'average', or 'consensus' inside of you (the term consensus is simply a convention used in molecular biology for simplification).


Deciding between chi square and t test I am always so confused whether to do a chi square test or a t test in the sums given by my biostats teacher. Does anyone have a simple rule to decide this?

This is a very subtle question and I encourage you to read the Wikipedia articles on these different subjects (t-test, chi-squared test, p-value, etc) because the authors worked hard to combat common misconceptions about these commonly used statistical tests. Here is a rather oversimplified rule-of-thumb for these different tests:

t-test: Used when you are looking at the means of different populations. For example, you might want to determine whether the difference in the mean gene expression level between treated and untreated cells is different, or if the gene expression level of cells in a certain environment differs from what you would expect in a null hypothesis. Assumptions: You are assuming that the populations you are looking at are normally distributed. The variance of the populations is not known (that would be a Z-test), but it is assumed that the variance of each population is the same. Finally, for the t-test to work, the samples of the data from the two populations are assumed to be independent.
$\chi^2$ test: Several possibilities for this. The most common in biology is the Pearson $\chi^2$ test, which is used when you are looking at categorical data, like the number of pea plants with white or purple flowers and round or wrinkled seeds, and trying to see whether the number of individuals in each category is consistent with some null hypothesis (such as the number in each category you'd expect if the genes for flower color and seed shape are not linked). Assumptions: The data points were randomly and independently gathered from the population, and you have a reasonably large number of samples.

I'd hate to have made a huge mistake, so please edit my answer and/or contribute your own if you think I am completely misrepresenting these topics!

Its true that T-test are used when your dependent variable is Numeric and Chi-Square test is used when you are analysis categrical variable. But how about this:

You have a categorical response (0,1) to a campaign. 1 who bought the product and 0 who did not. If you sum up the responses in your Test group and Control group and devide them by thier respective population size, lets say you get something like this - .23% response rate in Test Group and .01% response rate in Control Group.

Can't you use T-Test to see if these reponse rates are different? If yes, then let me remind that these variables were categorical (0,1) but we still used them as numeric.

All I want to say is that if we are comparing response rates or percentages, then T-Tests can be used irrespective if the dependent variable is character or numeric.

Sachin


Biology Intuition and Origin of the "facts" I am a graduate physics student but also taking biology classes. I am new to the field of bio. Most of what we do in class seem like memorizations and stating-facts. I am wondering:

How can I develop intuition for biology? (Aside from memorizing and practicing.) I am not even sure what intuition would be like in the case of biology?
Where are all the known facts in biology (and chemistry) come from? Have to be from EXPERIMENTS though, I hope to understand the origins of the I-was-being-told-this-way facts such as the composition of DNA and the types of bonding. By understanding, I don't necessarily mean the exact experimental procedure, but the general idea of how everything came about. (I am mainly interested in molecular and cell bio).
Much appreciation for any input!

Googling "landmark experiments in biology" came up with a lot of hits, what was wrong with the experiments cited in any of those works?  Mendel's pea experiments should be easy enough to understand.

Honestly I don't see how it will benefit you to know the organic chemistry work that went into determining the chemical structure of adenine.

Famous experiments roughly chronological:

1400's they gave elephants wine in the tower of london and belived in 4 elements and blood letting.

Human and animal dissections
Observation of oxygen generated by plants in light
Observation of red blood cells and micro-organisms
First notions of the Cells, cell theory
First microscopes at the same time as first telescopes
Major experimental biology for inheritance of flower colors by Mendel
Advanced medecine and use of electricity on corpses
Theory of evolution using many specimens and case studies
Methodical ecology treaties and reports for many animals by Fabre
Methodical reports of ocean fossils and sea life, fossil biology
First scientific reports of antisceptics
Measures of plant O2 production as a function of light color and temperature
Discovery of vaccines
Discovery of penicillin and antibiotics
Synthesis and measure of soil chemistry
First precise measurements of pH
Discovery of cell nucleus
Discovery of virii
Discovery of DNA
First electron microscopes
Beginning of centrifuge, spectroscopy,

Consider the diversity of animal species and cosmic bodies.

In cosmology you have 10-15 Clades of cosmic bodies, 50 of fundamental particles, 4 forces. There are only 100 common elements.

In biology, 80,000,000 species, 1,000,000 Clades of animals/plants/funghi, 100,000,000 different Enzymes and Proteins which are all invisible, and that beat supercomputers since 2003, 1000,000,000 different organic chemicals.

Microbiology flourished in tandem with Astronomy with the development of dutch lenses used for navigation. Cell theory is a biological equivalent to cosmology.

Biology has 3.9 billion years of cumulative encoding and additive development, as in that every being is like an SHA64 algorythm, that cumulative complexity is arranged into a tree.

Physics doesn't have friends and foes, cumulative memory, encryption, computation ability, 1 billion chemicals, cell walls and cells, number of legs, appendages, reproduduction, division, child rearing, it's a completely different recipe.

Physics is simpler. It's the same as being stuck inside one single protein, where the edge of the protein is the cosmological boundary, and being able to gather masses of data about the contents of that boundary and the nature of the physical universe. The maths formula to represent every protein is probably as big as the universe, there's no size and time boundary in either, except that we are seeing inwards that complexity.

biology is reined by chaos, so the maths of it has many billion degrees, you are talking about an equation with a,b,c,d,e,f,g,h,i,j,k, etc with billions of variables, and the maths formulas are billions of lines long. how are biologists supposed to deal with that?

Physicists are stunned by schrodinger's cat, probability issue.

What is the probablity of predicting where an animal will be on the same time on 2 different days? If you can write equations for that, then physics and biology will be the same. Biologists are not even going to try to write an equation for that kind of thing! they just have to use statistics all the time.

The maths of Biology are the biggest chaos system that man has ever peered into.

They are so incredibly confusing and unfathomable.

Try to write some equations in biology to predict movements of elements. you can't equate a bird like a photon, they are more chaotic and complex.

Biology has trees. Where do trees exist in physics? The biology tree has 80 million known branches.


How having sickle cell trait would provide resistance to malarial parasites? It's mentioned in my textbook that subjects with sickle cell trait develop resistance to malaria. I've read a few research papers predisposing involvement of macrophages and papers asserting involvement of the heme oxygenase system rendering me confused; so what actually causes this resistance. And is this resistance also present in the subjects with sickle cell anemia? Also some African tribes are generally mutated to provide malaria resistance. See this https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3499995/

I would say that there are at least 2 explanations:

Higher levels of free heme in the blood of individuals with sickle cell anaemia/sickle cell anaemia trait. Free heme is toxic to Plasmodium.sp Science. 1981 Nov 6;214(4521):667-9., detailed mechanism is described here: J Mol Med (Berl). 2008 Oct;86(10):1097-111. This effect is also observed in people with other diseases affecting stability of erythrocyte's membrane, such as thalasemia or spherocytosis.
It is also possible that, when erythrocyte's membrane is prone to disruption, Plasmodium.sp  antigenes are present in higher concentrations and may be faster presented to the immune cells.

Sickle cell anaemia is where the red blood cells become sickle shaped hence since Plasmodium infests itself in the red blood cell for oxygen, it doesn't survive because sickle celled RBCs carry less volumes of oxygen.


Can plants suffer from CO2 poisoning? Is there a point where too much CO2 is bad for a plant? Basically when there is too much CO2 in the air can a plant get sick?

Since plants photosynthesize and need CO2 to generate glucose and store starch, and since chemical reactions are pushed toward their end product when the reagent concentrations are increased, one would expect that more CO2 would be better, at least lead to increased growth and survival rates.

Is there a ceiling where CO2 gets toxic?

Short answer
It has been shown that plants may already suffer from doubling the atmospheric CO2 concentration from 340 to 610 ppm, something that might happen during the next hundred years or so based on current emissions.

Background
A popular science website tells us that an excess of carbon dioxide (CO2) reduces the rate of transpiration of some plants. This is so because the stomata, which are the openings of the leaves (Mansfield & Majernik, 1970) and used for exchanging gases as well as water vapor (transpiration) will close when there is too much CO2 in the air, or other polutants such as SO2. As transpiration drops, the water flow from the soil to the leaves also drops, causing a runoff of water.This in turn stalls nutrient uptake. Indeed, doubling the present-day CO2 concentration to 610 ppm does not necessarily lead to increased growth and may in fact inhibit growth due to excess starch formation in the leaves, indicating it's simply stored as backup energy, nothing else (Coviella & Trumble, 1999). It is believed that plants might be near their saturation point and cannot eliminate CO2 faster than they are doing right now.

Somehow plants also become more susceptible to insect foraging when CO2 concentration increases.

Note however, that CO2 tolerances are species dependent. Most research in this arena has focused on common crops. CO2 tolerance in for example cotton plants is low, and starch buildup has been observed in the entire plant, but especially in the root systems and the stem (Hendrix et al., 1994). Other species, such as wheat and rice are less prone to effects of elevated CO2 (source: Nature).

References
- Coviella & Trumble,  Conservation Biology (1999); 13(4): 700–12
- Hendrix et al., Agricult Forest Meteorol (18994); 70(1–4): 153-62
- Mansfield & Majernik, Environmental Pollution (1970); 1(2): 149-54

Source
- Earth untouched

Since you need water to live, seem you would be peachy dropped on the bottom of the ocean ;)

Organisms usually adapt to specific conditions. In particular, plants need oxygen to actually consume the glucose produced in the process of which oxygen is a byproduct.
Is it possible to imagine an organism adapted to not having oxygen, by storing its own oxygen for reuse later? It sure is, and it might have been what originally happened in the original oxygen-free atmosphere.
But as a matter of fact, in the current oxygen-rich atmosphere this ability would be completely useless, just as it would be for you to bring everywhere a backpack full of air to breathe. As a consequence, no mayor plant does it; and it would take centuries of evolutionary pressure to develop it.


Why don't all male animals kill a rejecting female? If a male animal is sure that the female animal will not reproduce with it, wouldn't it be mathematically optimal for the male to kill the female? (To ensure that no alleles of the "overreact-to-rejection" gene in other males can make use of the female as a reproductive resource)

I might be missing something very obvious here, but I can't seem to see why a gene for "kill-rejecting-potential-mate" wouldn't spread through the gene-pool.

The simple answer is most animals females can fight back. Its similar to the reason male to male fighting often evolves to become more and more ritualized. Fighting is risky, and the closer in size and capabilities the fighters are, the riskier it becomes. Behavior that tends to get you injured for little to no benefit tend not to get passed on. and there is little to no benefit in killing females for a male. Plus a female who is alive can change her mind later, so there is a direct benefit to the male for not harming her.

Now there are animals where a female will be bullied into mating to the point of risking injury or death. Those animals are very rare and have high dimorphism, they have males that are MUCH larger and more dangerous than the females, to the point the female is incapable of being a significant threat to the male. It is most common in animals that express harem polygyny. It also tends to carry the risk of inbreeding.

One horrifying example is hamadryas baboons. Males maintain a harem and threaten any female that even strays too far from the male. They even bite disobedient females.

There's natural selection for males that do what ever they can to stop a female mate they already have from having an affair because if she has an affair, she might produce an offspring that's not his own so they can't get as much food to rear as many of his own offspring. Although killing her makes her unable to have an affair, it's not selected for because she can't produce a kid that is his own either if she's killed. If she deserts him in addition to rejecting him, there's no evolutionary advantage in him killing her because she won't stop him from finding another mate that will produce a kid with him. It would however be an evolutionary advantage for a male to reduce his options and do something to make it so that he will be unable to not kill his mate if she rejects him. Females who did not reject males that reduced their options in that way would be selected for and then in response to that change, males that reduce their options in that way would be selected for. If after that, a mutant male that could make it look like they reduced their options when they didn't arose, it would outcompete the males who actually reduced their options and then females who rejected a male would stop being selected against and maybe it some cases be selected for.


Molecular animations of, say, protein synthesis, are simplified, but how exactly? In several animations of biological processes (eg protein synthesis (go to frame 1.20mins), DNA replication, etc), molecules such as amino acids are shown heading straight to the replicating protein as if drawn by a magnet. As far as I know they move randomly. But still, translation occurs at a rate of about 15 amino acids/second and 75 ATP/second, so the rate of gobbling shown in the video clip is not off the mark.

I can think of two explanations:

1) The microscopic world is counter-intuitive. It is so frenetic that normal diffusion is enough to supply the hungry protein. The video simply doesn't show all the input molecules in order not to clutter the picture but essentially it is correct. However, amino acids are not small, and they are attached to the much larger tRNA, so they must be moving relatively slowly by Brownian motion.

2) There are additional helper proteins that concentrate or channel amino acids and ATPs in the vicinity of the ribosome or replicator. Never heard of these.

What is the real explanation?

Edit: To clarify, the question is not about the simulation side of things as such, such as how hard it is to actually make a true simulation. Most simulations, including weather prediction, involve a certain degree of approximations and simplifications. But in this case, there is something definitely untrue in the video clip, namely the molecules being attracted to the ribosome. As explained by a moderator, this means that it is not a true simulation but a "cartoon". So the question is: what would an ideal "non-cartoon" true simulation look like? Would the tRNA be diffusing in at a very fast rate, or are there helper proteins that, for example, tether tRNA in the vicinity of the ribosome? The moderators seem to indicate that diffusion is enough, but I would like to see a reasoned out answer with numbers that show this is the case.

tldr:

Making these things accurate representations is really hard
Accurate representations can be hard to look at anyway, so aren't always good to convey understanding

Molecular dynamics simulations that span long periods can be really expensive because of how computationally demanding they are, and they rely on accurate structural information about all of the molecules involved which isn't always available. The animation you linked might not be an actual simulation for that reason, but you'd have to check for yourself. Really fine grained accuracy probably isn't a priority for making a cool teaching tool like this one, you just want people to understand the just of it and the Brownian motion there might be a stylistic choice. Again, you'd have to chase it up for this specific example, I just want to give you something generalizable to other animations.

To make macromolecules like this actually interpretable by humans it's important to simplify them. One of these simplifications is normally called a 'cartoon', I don't think they guy in your comments was taking a dig at credibility of the video. It's also important to hide all the water molecules because they get in the way of you and seeing what's going on, so that's another way in which it's been simplified.

If you haven't already, have a look at some proteins in the PDB on the structure viewers and switch the mode from the cartoon/ribbons to other models like ball and stick. Ribbons are a useful way to simplify the structure representation so that you can see what the backbone is doing.

Here's one that I like:
https://www.rcsb.org/3d-view/4KEY/1

And you're right, at the systems level of something like protein synthesis, lots of stuff is involved and it's not practical to show all of it. For something like that it's easier to show these processes a a graph (term for connected nodes), check out the KEGG database for examples:

https://www.genome.jp/kegg/pathway.html#cellular

Hope this helps

The good explanation is the second part of your question which you never heard of.

Actually for every movement in the cell, proteins play important role rather than nature of solvent (hydrophobicity, hydrophilicity or other forces) play any significant role. Brownian movement is also insignificant as you know AA (Amino Acids) can be more polar or less polar. Also they can't guide themselves to the desired location in the cell. Proteins which relocated them, cause their faster efficient and direction movement (may be due to formation of gradient or some sort of pulling pushing force due to interaction with other proteins.)

[UPDATE]

Exploring more into this, I came to know that the movement of anything is dependent on a gradient (May be concentration, electrochemical, pH etc...). So everything inside the cell is well planned and well documented inside the genome.


How to estimate a genome's size? The genome size of human is 3.000.000.000 bp and for Arabidopsis it is 255.000.000 bp. I know these numbers because their genomes have been published. Which methods are used by scientists to estimate the genome size before they sequence that genome?

Gel electrophoresis is a basic lab method to get size info about nucleotide fragments, although one might need to chop up larger DNA to be able to apply this method. The wikipedia page covers the topic well, thus I'd suggest reading it. I'll just give a short outline:

Nucleotide fragments are loaded into a gel (agarose or acrylamide).
The gel is put into a static electric field
Nucleotide fragment move to the positive end, because they have negative charge
larger fragments migrate slower than smaller fragments
standardized DNA ladder can be used to get approx size.

UV fluorescent dye is used to stain the fragments.

Another way, is to check closely related species. Among closely related species it is a fair assumption that they have similar genome size. You can also hybridize the unknown DNA to a DNA of such close relative to see how much of them are similar and you can also make estimates based on the size of the hybridized regions.

I guess you could estimate the length various ways. Pulse field electrophoresis could show DNA length, but you need a standard.
When you combine Karyogram and FISH, you would could make a map. By genetical approaches, you could estimate distance on the map by centimorgan. Then you could know how many centimorgan chromosomes are. One centimorgan would be 1 million base pairs.

Oh, I forgot the simplest way. For example, take 1 million cells and estimate how many grams of DNA there.


What is the name of this sea creature? I found this creature on the beach in San Diego. It is 8cm long and the end to the right is the mouth. The underside is exactly the same as what is visible. What is the name of this species.

This animal is a sea cucumber. It is probably a "sweet potato" sea cucumber (Molpadia arenicola). Here is a useful link describing this animal with pictures quite similar to yours:
https://mexican-fish.com/sweet-potato-sea-cucumber/


What is the actual storage form of energy in muscles? ATP or Glycogen? I was asked this question in my latest exam. I think the answer is Glycogen because ATP doesn't store energy for a long time so it isn't the ACTUAL storage of energy. Some classmates argue that in muscles there are other substances, not only glycogen, that are used to produce ATP. In the process of contraction ATP is required so, they say, the question needs the answer to be ATP. Could someone please clarify this discrepancy?

This is a typical MCQ which in order to answer you have to have been at somebody’s lectures or be able to read his mind. The antithesis of education! Cells don’t store energy like car batteries.

Glycogen in muscle is a store of carbohydrate. It can be used to generate ATP if it is broken down to glucose and the glucose glycolysed. I wouldn’t have chosen this as an answer.

The concentration of free ATP in the muscle cell is not sufficient for it to act as store of a high group-transfer potential compound (which is presumably what the question means by energy). This is definitely not the right answer.

However if creatine phosphate (a.k.a. phosphocreatine) was a choice on your MCQ, that was probably the answer expected as it is used in muscle as a storage molecule which can be rapidly converted by creatine kinase creatine and ATP.

PS

As you say in your comment that the only choices were ATP or glycogen, then glycogen is what is expected.

What is the storage form of ATP?
Answer: Creatinine phosphate


Stomata during night (respiration) How does carbon dioxide from respiration diffuse out of the leaf during the night?

Do stomata close completely during night?

Leaves have no need to 'exhale' carbon dioxide - it gets consumed by photosynthesis.

Elsewhere in the plant, metabolic processes produce carbon dioxide. This escapes via inter-cellular gas channels that, in woody plants, terminate as lenticels (little pores) on the stem surface. Oxygen for metabolism diffuses into the plant in the same inter-cellular spaces as carbon dioxide diffuses out.

With roots, the oxygen necessary for metabolic processes is dissolved in water.

If you've meant to ask about leaf adsorption of carbon dioxide and when stomata close, it depends on what carbon fixation scheme the plant exhibits, CAM, C4, or C3.

You might want to also consult an  answer I gave to a similar question previously posed here.

Stomata closes and opens partially for efficient gas exchange to occur,and losses prevents dehydration in leaves. Carbon dioxide diffuses from plant as a from of starch because plants only respire oxygen but they take in carbon dioxide.


Are male and female brains physically different from birth? Male and female brains are wired differently according to this article:

  Maps of neural circuitry showed that on average women's brains were highly connected across the left and right hemispheres, in contrast to men's brains, where the connections were typically stronger between the front and back regions.

But since learning in the brain is associated with changes of connection
strengths between neurons, this could be or not the result of learning.
What about physical differences from birth? Are there differences in size, regions, chemical composition, etc. from birth?

Short answer
Yes, men and women's brains are different before birth.

Background
First off, learning effects versus genetic differences is the familiar nature versus nurture issue. Several genes on the Y-chromosome, unique to males, are expressed in the pre-natal brain. In fact, about a third of the genes on the Y-chromosome are expressed in the male prenatal brain (Reinius & Jazin, 2009). Hence, there are substantial genetic differences between male and female brains.

Importantly, the male testes start producing testosterone in the developing fetus. The female hormones have opposing effects on the brain as testosterone. In neural regions with appropriate receptors, testosterone influences patterns of cell death and survival, neural connectivity and neurochemical composition. In turn, while recognizing post-natal behavior is subject to parenting influences and others, prenatal testosterone may affect play behaviors between males and females, whereas influences on sexual orientation appear to be less dramatic (Hines, 2006).

The question is quite broad and I would start with the cited review articles below, or if need be, the wikipedia page on the Neuroscience of sex differences.

References
- Hines, Eur J Endocrinol (2006); 155: S115-21
- Reinius & Jazin, Molecular Psychiatry (2009); 14: 988–9

One point of view you rarely see is the perspective of sex differences from an evolutionary standpoint. Never mind that this is the reason why the differences exist in the first place if they do at all.

But the short answer is that Human Male and Female brains are unquestionably selected to be different (whether this means they are actually different requires a modern side by side comparison). But to build on this point, think of male and females in terms of evolution. Male and females inherently fill different roles in history and prehistory (If you want to argue that men and women didn't or don't have different roles then show me the man who can give birth to a baby). Given that there were different biological pressures behind the evolution and success of each sex, the brain has been selected (as have other parts of human physiology) to better accommodate the demands of its respective sex as it pertains to one's own reproduction and survival. This much is beyond any reasonable dispute.

Unfortunately this fact cant be used as definitive evidence of sex differences, because even though we can prove that for all of human existence the sexes have done different things what we really need is a side by side comparison of how they are today to come to any conclusion. And given that the current political climate is ridiculously politically correct, it is unlikely any study will be brave enough to publish anything anti PC or else lose funding.

Ref: (Just random references)
https://pdfs.semanticscholar.org/4510/e98234d30ea146f523039ba353520a04be3a.pdf

http://www.annualreviews.org/doi/abs/10.1146/annurev.an.15.100186.000325?journalCode=anthro

https://www.eurekalert.org/pub_releases/2015-10/nuos-wam100715.php

https://stanmed.stanford.edu/2017spring/how-mens-and-womens-brains-are-different.html

Edit:

This extension to address '@Elise van Looij' comment that this is a circular argument.

This is history. I have often heard the 'circular argument' position used to try and defend against evolution, aka which came first the chicken or the egg, but it is a logical fallacy. So for the sake of flushing out the position a bit better lets go through the points.

  This appears to be a circular argument. Males and females have inherited different roles and therefor they have evolved differently
  to fill those different roles. How come they 'inherently' have
  different roles? Because they have evolved that way.

(1) Males and females have inherited different roles? I don't think this is true. Males and females have inherited different potential roles (and maybe an inclination for, or biology best suited for those roles). However no one personally has to fulfill any role. And the roles evolution selects for (namely what is best suited for reproduction) changes over time and between environments. However it is true that those that excel at certain roles best suited for reproduction and survival, will possess traits that will propagate to the larger population by virtue of exponential growth of those genes in the population.

(2) We have evolved differently [solely] because of these roles? No. We have evolved only to reproduce effectively. And this statement isn't limited to just things that reproduce sexually. Biological "roles" are a consequence of the environment. Right now we are still the product of ancient environments because not enough time has passed between then and now for that biological legacy to have been erased. And this is why I put forth the position that the pressures human populations faced for millions(?) of years which unquestionably shaped our biology, can be used in the modern day to make educated hypothesis about our modern (still relatively ancient) physiology.

(3) How come they 'inherently' have different roles? Because in each generation the creatures that did those 'roles' made more babies than the ones that didn't. This is simple math now. 2 A and 2B. 2A reproduce and make 4A. 2B make 1 baby B. Old generation dies, new generation is now 4A 1B. Repeat until B = 0.  Now if you want to go all the way back to when there were no roles, you can do that. Go back in history until we reproduced asexually, were hermaphrodites, or no life existed, or some other condition was met. There is no circular-ness in my opinion because you can follow the path back until all starting conditions are different (and thus the circle ends).

But to reiterate the important point because it might be buried in the rest of the text. We have evolved to be a certain way. This way may change in the future and is probably changing right now. But as we exist right now, we are the product of time in the distance past. That passed has shaped us to be a certain way. And we haven't evolved to be radically different from that way yet because not enough time has passed since then for our fundamental makeup to have changed. Think about it; when did the social roles of Male and Female change? 50 years ago? 100 years ago? 1000 years ago? 10,000 years ago? We took millions of years to evolve into this variant of ape that we are. Our ancestral legacy is still strong with us.

But this turned into a discussion of evolution. Instead of what we can learn from evolution. Which was the real purpose of this post.


Can you explain the behavior of this snake? I just saw this video in which a snake is swallowing grapes.
 ("Whip snake eating grapes").
In the video, the snake just doesn't eat but goes on to swallow 2-3 grapes.
I did some research on the internet and in "bio stack exchange" but only to find that "snakes are obligate carnivores", which simply means they don't have the body mechanism to digest a vegetarian diet.
My guess is that it mistook the grapes for a prey due to the smell coming from the grapes, which may be left there by a rodent or any other organism the snake feeds on.
Can you provide a possible explanation for this snake's behavior? Regards

You're right, snakes rely on scent to capture their prey. The fact that snakes are carnivores may be the one constant among all snake species; absolutely none feed even partially on plant matter. So if plant matter is found in their feces, it must have gotten there accidentally.

Here, check out this post, which answers your question perfectly:

  In most instances, these have been attributed to accidental ingestion, perhaps eaten with a prey item or mistaken for prey by scent...One interesting case was discovered by Harvey Lillywhite in a study published in the journal BioScience in 2008. Studying the scavenging behavior of pitvipers in the intertidal zone, Lillywhite observed cottomouth droppings that were composed almost entirely of seaweed. This was too much plant material to have been eaten secondarily or by accident, and he suspected that there was some other cause for the snakes to be eating it (it certainly wasn't for energy as the seaweed was passing through completely undigested. Lillywhite wondered if it was possible the snakes were feeding on seaweed simply because it smelled like fish. An interesting laboratory experiment proved their hypothesis correct; they offered various plants to cottonmouths, some with fish and others without. The plants without fish were investigated by the snakes, but ultimately left uneaten. Those that did contain fish were quickly devoured. Even when the fish was removed, the snakes ate the remaining seaweed simply because it smelled like their prey!

I've seen a deer eating a live bird so a snake eating grapes doesn't surprise me.
My philosophy is that animals know better than us what they are doing, so if someone is mistaking it's probably us.

Anyway, my answer would be that this snake needs a substance (perhaps the acid since it's unrip) contained in those grapes, if it's not for feeding then it's for healing.


How increased potassium intake increases sodium excretion? "K+ antagonises the biological effects of Na+". I have been reading the same many times without any explanation. How actually (mechanism) K+ helps excretion of Na+?, their interactions? And eventually lowers blood pressure?

That's because cell membrane could have a protein, called Na/K pump who's able to regulate the level of Sodium/Calcium using the energy gained by the hydrolysis of a phosphate bond from ATP.


How is ligand binding modeled? I have the following exercise to solve:

To be honest, for both parts, my only idea so far would be to divide the rate expression by the sphere area and multiply by the new available areas (that of a circle for part a and that of many circles for part b). But if I do this, I will have an "a" parameter always, which makes no sense because it is representative only of the sphere.
Any ideas on how to approach this?
All help is greatly appreciated.

don't use the perfect square model. You will keep getting Pi but it's not a real life formulae only used for theory. Try to use a Cartesian graph but three dimensions to take into account curve flexibility. Integral calculus is similar too or better.


Is it possible for a person to become "reinfected" with the same strain of a virus? If a person contracts a virus, viral conjunctivitis for example, is it possible for the individual to become "reinfected" with the exact same strain of the virus once the person has it treated and the symptoms have gone away? I am a nursing student and am fascinated with virology, but my basic microbiology class did not go very in-depth on the subject.

The nature of infectious agents is that they transmit between organisms. This means that they have reservoirs outside a single host, and hence of course encountering the exact same strain twice is possible if this strain leaves the body and at a later stage is carried back to it. This could typically happen for example with influenza or common cold viruses, spreading from one child to other children at school and later being carried back to the original child through them.

The reason why the child will not develop another illness when being exposed to the same virus again is the adaptive immune response: After the first infection, immune cells specific to a pathogen will proliferate and differentiate both into effector cells to destroy the pathogen, and into memory cells. These can mount a much stronger immune response much faster when they come in contact with the same (or a structurally very similar) pathogen, meaning that a secondary exposure usually does not result in a proper infection and illness. Of course, this mechanism doesn't work properly for anyone with a compromised immune system.

In most cases where a viral disease develops repeatedly, this is due to evasion mechanisms. For example in some viruses, those antigens which tend to be targeted by immune systems have high mutation rates. In this case the "same" virus is actually a mutated strain which causes the same illness, but "looks" different to the immune system, and so the memory cells don't respond. Again, influenza is a great example. The reason why we get flu again winter after winter, is because this virus tends to mutate over the year with relatively low infection prevalence. Then during the winter, when the conditions are favourable for flu infections, typically only a small number of strains cause epidemics - because we were maybe immune to last year's influenza, but this year's has mutated antigens which our immune systems do not recognise yet.

Viruses that mutate quickly (particularly notorious are respiratory viruses such as the flu and common cold) quickly produce new "strains" within the same virus family. While most people should be familiar with the terms "influenza A" and "influenza B", those are merely blanket terms for a large family of viruses with thousands of strains (by surface structure). Immunity against a given strain is no guarantee of immunity to a different strain.

In the general case, reinfection with an exact same strain previously recovered from is possible if the immune system "forgets" the pathogen (which happens with some infections, hence the need for periodic booster shots) or if the person becomes immunodeficient.


Is there any evidence for sperm parameters being connected to fitness of the offspring produced by that sperm? In most (if not all) sexually procreating species the amount of offsprings a male can produce is limited not by the amount of sperm he can produce, but by the amount of eggs his sperm can fertilize (with rare individual exceptions).
Because of that the optimal strategy would be to fertilize eggs with the best sperm.
Therefore it is reasonable to assume that there would be adaptations making sperm with deficient genes less likely to fertilize an egg.
But is there any evidence of this happening? E.g. would fertilizing eggs with less motile sperm (potentially with IVF) produce a less genetically fit offspring or result in a miscarriage?

The only way that natural selection can act on genes is when they're expressed, there's no mechanism for reading and assessing the "quality" of a gene in a sperm. Obviously the genes that effect the quality of the sperm will be selected for/against.


Is there any biological basis for the emphasis on the value of the firstborn son? Is the firstborn son biologically different in any way from the sons that follow?

Perhaps his epigenome is different? I have heard that a man's testosterone levels decrease when he becomes a father -- could this then have implications for the epigenetics of subsequent sons?

There are lots of cases reported now that suggest that overall the firstborn child is usually more intelligent. The articles supporting this are based on behavioural and economic study though, so the biological basis is a little lacking.
It's also not clear if this is nature or nurture. The firstborn may benefit from their parents undivided attention disproportionately.
Here's the press release for it. And the coverage from the Independent
and Forbes
I read somewhere that the firstborn is more likely to be overweight too, but I can't find the article now. Other people may know other traits that are supposed to differ between children.

I remember reading/hearing something about the effect of older brothers on the chances of people becoming certain types of people.

It went something like the oldest was most likely to be a pilot/doctor/CEO etc.

The second was most likely to be a teacher/middle management etc.

There's plenty of blogs that suggest the more older brothers a man has, the more likely they are to be homosexual. But this obviously doesn't look at whether or not Biological influences lead to this "birth order effect", or cultural influences.

I remember a suggestion that it was to do with antibodies (or some other substance) that builds up in the mother's womb after having son's. But again I can't find any evidence for that, so it might be pure speculation.

NB. I don't subscribe to this theory, but if you're really interested, it might be worth looking at the science behind it.


Theoretically, is domestication of (virtually) any animal possible? Looking at ones that manage well alongside us human animals, such as dogs and cats, we see that this is possible for evolved, distant animals to have heritable, preferable traits around people. However, when especially looking at lions and the like, it doesn't seem to work out as well.

Some people have tigers as pets, but in general it is believed that they are more "wild" and not as tame and domesticated as other animals (such as dogs and cats).

Is it possible to selectively breed and enable any animal to be more like dogs and cats? Even sharks? Tigers? Alligators?

If domestication worked so well with dogs and cats, such as them living (for the most part) peacefully and well with people, wouldn't the process be beneficial for other animals so we could all live better side-by-side?

In short, can you theoretically get any animal to have heritable traits?

As the previous answers clarify, all organisms have heritable traits that may be manipulated through selective breeding. It is the pragmatics that can be prohibitively challenging. From an (zoo)archaeological point of view, few animals have actually been domesticated, and only recently in our species' history. The dog is an unusual case, perhaps domesticated 14,000 years ago; most domesticated animals only show skeletal changes within the last 10,000 years. Cats, compared to livestock's total dependence on humans, are 'barely' domesticated--they got used to humans while camping out in Egyptian storehouses where all the mice were, perhaps around 4,000 years ago, but even today a fluffy house cat will revert to a feral state if abandoned.

Many animals are behaviourally unsuitable for domestication. If an animal is dangerously aggressive, for example, they cannot be penned and isolated--so the many controlled generations it takes to reduce their baseline aggression cannot occur. Humans also tend to co-opt pre-existing social structures in a species, such as becoming the 'alpha' in a dog pack or the head 'ram' of a sheep herd. Species without a hierarchy or herd mentality are difficult to control and keep track of, and so do not lend themselves to human care.

You mentioned tigers in your question. Tigers have little to offer people (other than pelts), they're massive/aggressive, and they're jungle loners. You can't raise a herd of tigers; they'll kill each other and the survivor will kill you. That they're carnivores is also challenging, since a carnivore is much more expensive to feed than a bunch of grass-munching sheep. Altogether, there was never a situation in prehistory that would have turned tigers into giant house cats. House cats eat unwanted mice; tigers eat your cattle (and children). The occasional tiger 'pet' won't change that.

Domestication, outside of recent experiments (like the Russian foxes mentioned above), has always been a protracted, indirect process. People started interfering with animals that were already useful in some way(s). Dogs offer warmth, hunting aid, defence, transport, and (in a pinch) food. Alligators, tigers, and sharks are not useful enough to make the danger and cost of raising them worthwhile. Even if you did eventually produce a 'human-friendly' shark, there would still be a 'wild' population ready to eat you--and your complacent pet sharks, too!

For a very readable explanation, try the chapter on domestication in Jared Diamond's (1997) Guns, Germs, and Steel.

No and yes.

What you perceive as domestication has a lot to do with intelligence or even social intelligence of animals.

Common fish is too stupid (from our point of view), to have any social bond with humans. Mammals are usually much closer and have similar structure of intelligence and patterns of behaviour.

That only if you consider domestication as something more and not just human utilization as with breeding fish for food, spiders and snakes for fun (or even snakes for rat-catching, as some African tribes did according to wiki).

So not all animals could be domesticated, they need certain qualities, mostly connected (or we are connecting them) with intelligence.

However, once you look at mammals, which usually have enough social intelligence, you could breed them into domestic animals. It would be hard, there would usually be no other purpose than "We can, so we do", but you could. There were various experiments. One is famous Russian experiment with foxes, another is infamous Hitler's experiment with cows (experiment with bringing back Aurochs, Heck cattle, cows were "undomesticated"). There, in controlled environment, true genetic plasticity of behaviour were showed.

Note that as other posters wrote, this is theoretical. In nature and by natural means, domestication was always hindered by immediate usefulness (not even potential future usefulness). Most of domesticated animals are highly social in their natural form and not very aggressive. Even big cats are quite close. Tigers not as much as cheetahs, which were traditionally bred (or kept as pet) from ancient times.

  In short, can you theoretically get any animal to have heritable traits?

All animals have heritable traits. That's genetics.


Brain regeneration - book recommendation Searching for an up-to-date book on regenerative brain medicine with a focus on stem cell therapy.
Also interesting in genetic engineering of neuronal stem cells for this purpose.

Alternatively, a comprehensive review article is welcomed too.

Neural regeneration is addressed broadly in this chapter from a book published in 2013 (though I would say for a topic such as this, you're probably going to want to read primary literature or recent, less comprehensive reviews in addition to any book chapters published in the few years):

Neural Regeneration by Melissa M. Steward, Akshayalakshmi Sridhar, Jason S. Meyer, published in New Perspectives in Regeneration.

The chapter includes two sections on stem cell therapy and one section on reprogramming of somatic cells to neural lineages.

Regeneration... What a lovely word since 2010
You could start with This text published on 2010 which shows how P21 and it's controller(P53 gene) could regulate regeneration of mammalians' body parts and within them is neurons too.

Regeneration of a hole on ear of MRL mouse or p21 knockout one
This event was accidentally observed ten years before the text get published.
They just couldn't find the ear tagged mice, because there was no hole on their ear anymore.

And you could continue with this text which explains:
p53-Independent Cyclin G Expression in a Group of Mature Neurons and Its Enhanced Expression during Nerve Regeneration

Google Scholar is full of texts, experiments and their results which you need to gadder your information about pathways just by studying and comparing them.
But the most interesting one of them for me was p21 knocked out mice.

As physics helps computation world(Quantum Computers) to do biophysical calculations faster and faster, watching how these proteins and genes play with each other in a 3D simulated human cell like software, will not be a dream anymore.

hope it helps


How long can I store autoclaved disposables and reagents? I want to stock up on autoclaved disposables, such as Eppendorf tubes, pasteur pipettes etc., and some buffers.

If I don't open the container after autoclaving, how long can I store autoclaved materials and consider them still sterile? Does it make a difference if the material is dry or if it is a liquid?

Not really an answer I know, but too long for the comments...

This is still too broad a question.  a well sealed, sterile plastic usually has a use by date, but can probably be used more than a year after you receive it.  But these cases are not usually the issue.

Its sterile medium and chemicals, each of which needs to have their own due date.  LB can be used months after autoclaving, but antibiotics break down chemically in weeks (ampicillin 1000x stocks lose their potency in a month).  Even in the refrigerator Agar plates show colonies after a couple of months and dry out quickly.

So more details would be necessary and the case by case policy is the rule.

added in response to comments

Its really a matter of how well they are sealed. An autoclaved bottle will stay sterile forever, until something gets into the bottle - it depends on how well you have sealed things up and the storage conditions.  For stuff sterilized in lab I would tend to use it within a couple of months. For eppendorfs we'd tend to sterilize a few hundred in a beaker and not worry about them...

Our experiments were working with purified protein were only medium sensitive to bio-contamination; they would be done in a few hours and then sterile filtered again.  If you were purifying RNA for instance you would be much more paranoid I'm sure.

If you start to see contamination I would lower the use date and or improve your protocol.

Plastics that come sterilized and sealed by the manufacturer in 3-5 mil plastic bags have really long use by dates and I've used them for up to a year after we received them.

If you work in a lab, there must be a SOP(Standard Operating Procedure) and you can (You should...) follow that. Each lab will have different standard so providing a single definitive answer here may not be beneficial.


Is there any danger in putting a magnet in your ear (next to your brain) I recently bought some wireless earbuds that fit right in my ear, so they're very small.
But the method it uses for charging is magnetic, so it has magnets built into the earbud.

I was wondering if there's any danger in keeping a magnet in your ear for many hours every day? I'm not sure if it would affect things in your skull/brain.

Every pair of earbuds/headphones have magnets in them, as of now there's no solid evidence that proves that they are harmful or harmless to humans. Keep in mind that, what may be harmful to lab rats may not be harmful to humans as we are more resilient to radiation, etc. (In reference to a study done on truly wireless earbuds.)


How does common cold START? When I searched for the causes of common cold, I found out that it's only cause is the spreading of virus and that it's a myth that you get cold when you get wet. If that is true then how does the virus start to spread if no one else is having cold? Or Simply, Can you get cold by yourself without the virus?

No, only virus or bacteria can cause you cold .Cold weather  causes increase in the spread of virus. Flu virus spread quickly in cold weather. Cold feet can slow down your immune system making you prone for virus attack.Means ,if you are wet you are susceptible to a viral  infection but the cause of cold then would be a virus not the cold weather itself.

Influenza isn't the same virus as the common cold.

Rhinovirus ("nose" virus) is the main cause of the common cold. This is a virus that exists in the nasal passages of all humans. It replicates, like all viruses, by piggy-backing off the metabolism of the host cells (yours). It's present in us, a normal part of the microbiome, but harmless most of the time -- it gets ahead when you are immune compromised, exposed to temperature challenges or chemical challenges, or are infected with some other microbe.

The virus reproduces by making your cells build virus proteins, copy the virus genome, and then build the virus particles that are released to infect more cells. The ideal temperature that human Rhinovirus proteins fold up and work best is slightly below human body temperature. This limits the virus to the cooler part of your respiratory passage -- your nose.

When you are exposed to cooling -- being caught in the rain for example -- your nose and upper respiratory are cooled. This results in the virus replicating at an accelerated rate.

The new viruses leaving the host cells they were made in and invading into nearby cells causes an irritation. Your body tries to dislodge this irritant -- you make excess mucus and you the urge to sneeze

Sniffing or snorting will introduce this mass of viruses deeper into your respiratory tract. They aren't able to replicate here because of the temperature being too high, but they can irritate and invade into your cells. Your body detects this challenge and responds with inflammation, swelling, and as a side effect, pain. Your sore throat.

Ironically, the activity of the immune system responding to this actually harmless virus will compromise the tissues of your throat, and any opportunistic pathogen is more able to invade.

https://en.wikipedia.org/wiki/Rhinovirus this the wiki of the rhinovirus


Are there differences between the activation proteins of Eukaryotes and those of Prokaryotes I'm in BIO 203 (for reference to my skill level), and I noticed the textbook makes a whole section out of transcriptional activator proteins, their function and applications in eukaryotes, but in prokaryotes the term "activator protein" is used only once when mentioning the lac operon.

Are they the same type of activator proteins? Do they employ the same mechanisms?

In general transcription activators are transcription factors. These are very different in eukaryotes although some families share similar domains (e.g. two component signalization). I recommend you read through these two chapters to get a more complete overview on the differences.

https://www.ncbi.nlm.nih.gov/books/NBK21683/

https://www.ncbi.nlm.nih.gov/books/NBK21572/


Proteome patterns between treated and control cells We did 4 experiments to compare the amount of certain proteins in treated and untreated cells. Each experiment was done separately. Because of the high cost of experiment, we were able to perform only one pair (one treated and one untreated) sample for each experiment. We want to see which proteins are differentially expressed (minimum 1.5 fold up/down).

First approach: We have compared protein levels of all 4 treated (as a group) with the 4 untreated (as a second group). There is of course variability between all experiments, because of the nature of the cells. We have a list of the proteins that are differentially expressed as a result of the treatment, however this list is not very long.

My question is (second approach): Can we compare the proteins levels pairwise for each experiment (treated vs its respective control) and make 4 corresponding lists, and then compare these four list using a statistical tool and find which proteins are consistently up- or down-regulated? DO you think that these two different approach will generate different lists of the affected proteins?

If I understand you did a treatment to some cells and compared them with non-treated ones. Instead of running the four experiments at the same time, you did one treated and one untreated at a time. Then you did proteomics for each sample. Is the treatment the same in all four experiments?

Edit after the further comments of the OP: So, since the four treated samples are the same and the four untreated also (same conditions except from the treatment and the treatment is the same), then the way to go is as what your collaborator did.

Identification and quantification of the detected proteins is one thing and every sample of the four are replicates. Comparison between the two conditions is another thing.
The software he uses for ID can combine the same samples and already perform the statistical analysis, so the list you have now has higher credibility in terms of the proteins it includes and their levels for your cells when they are treated or not.

Using only one of your replicates, although it might give you different number of detected proteins or different amounts of each, has lower credibility, because it's only one sample out of four. In plain words, the presence or absence or the amount of a protein might be an artifact or insignificant.

What has to be clear is that the comparison between treated and untreated conditions is done after you have received the statistically correct list of detected proteins.

Thus, and in accordance to what I had said before the edit, if you take the list for each treated sample and compare them with any of the lists of the untreated ones, it will lead to conclusions that won't be as statistically significant as when you combine all treated together and all untreated together (as your colleague did). In plain words, your conclusions will have a higher chance to be wrong.

Every statistical analysis you do yourself for each sample should eventually lead to a similar consensus as your colleague got using the statistical analysis of his software.

As a sidenote, considering how many types of proteins are in a cell, now that you have a quite short list might not be a bad thing at all and you can proceed by:

Concluding that the treatment had minor effect in the proteins that you expected it would affect (if they are not present in your lists as significant different)
Trying to understand, identify and hypothesize on the role of the proteins that made it in your comparison threshold, as they have a much higher probability of being indeed different between the two conditions.

Splitting the samples in your analysis might have a point if the conditions of the experiment were not exactly the same or the treatment level is different etc. In that case you could split the samples accordingly, but that would definitely reduce your certainty level for your conclusions.


Evolutionarily, why do male rats and horses lack nipples? Developmentally male rats don't have nipples because (reddit)

  Testosterone release in the fetal male rat happens before the stage of mammogenesis where the teat is formed whereas other species halt that same process after the teat is formed.

According to the same page, male rats and horses (and mice) are unique among non-monotreme mammals in not having nipples.

Male humans have nipples because there's no evolutionary pressure for them not to. (Why do men have nipples?) Then, why was there selection for males to lack nipples in the case of mice, rats, and horses?

(Apparently, male horses lack nipples because "female horses have their nipples between their hind legs, and in males, that real estate is used for other purposes". (Straight Dope))

Evolutionarily, why do male rats and horses lack nipples?

Male mice lack nipples too. Mice are frequently used for embryonic research as they are small and reproduce quickly. It is thought that male mice do develop nipples, but that they regress during development (Wysolmerski, 1998).

In general, it is thought that mammalian organisms develop as females by default when there is no male (Y) chromosome present (Hughes, 2004). Notably, X_ individuals and XY individuals with certain Y-chromosome deletions also develop as females. Basically, it is testosterone that suppresses female features. Hence, also boys with testosterone production, but without the appropriate receptors also develop as females.

Hence, men have nipples because females do (Simons, 2003).

The development of nipples is a pretty complex process (Wysolmerski, 1998). Disruptions in the process cause regression. Indeed, in mice, the tissues typical for nipples do develop in males during embryogenesis, but degenerate within a few days, leaving no trace of nipples at birth.

Hence, given the mouse example, I think that every mammalian male species develops by default nipples somewhere in development like mice, but that development is halted at various stages across species. The later in development it halts, the more it resembles female nipples. When it is stopped very early after gestation, they regress completely, like in mice.

Why is there a difference between species as to when the nipple development halts? Because the nipple developmental sequence is complex (Wysolmerski, 1998), and because evolution typically prefers losing things over gaining them, it is likely that by happenstance one of many crucial genes was lost in males, but selective pressure was simply too small to be of any significant advantage over males with slightly better-developed nipples. But from here on, it is guessing.

References
- Hughes, N Engl J Med (2004); 351(8): 248-50
- Lawrence, Nature News, August 1999
- Simons, Sci Am, September 2003
- Wysolmerski et al., Development (1998); 125: 1285-94

Stallions/Geldings don't have nipples because a mares "udder" ,so to speak, is underneath her flank area. A stallion's/Gelding's penis is also as well underneath their flank. Their evolutionary genes keep male horses/donkeys/zebras from having these nipples.


Cheap enzyme assay for a high school lab At the moment, I'm designing an experiment for a high school lab with no financial resources. I need to assess the impact of a variety of factors on a specific enzyme's reaction with its respective substrate and determine the rate of reaction. Normally this would require some combination of an assay kit and a plate reader. Though cheaper versions of the former are within my budget, the latter is not.

What are the cheapest ways you can think of to:

1) Get access to enzymes and the substrate;

2) Make them react in a controlled manner;

and 3) Assess the rate of reaction from the resultant substance?

There is the classic potato starch/iodine/amylase experiment:
http://dailynexus.com/2016-08-31/chemistry-101-the-classic-potato-iodine-blueblack-experiment-finally-has-an-explanation/

From memory, when you add iodine to a small piece of potato, the potato starch reacts to produce a dark blue/black colour.  The amylase enzyme in human saliva can break down the starch and remove the colour, which is effected by spitting into the test tube.

You might need to try titrations to work out how to do number 3.

Catalase from blood. Prick your finger,  collect a small amount of blood. Add some hydrogen peroxide to the blood, it will foam as the catalase decomposes the hydrogen peroxide. Obviously there are biohazard considerations when dealing with human blood. Some plants, notable horseradish also contain peroxidase if you wish to avoid pinpricks.


Can anyone identify this species of spider? These spiders are all over everything on my padio in New Hampshire. Can anyone help me identify what they are?

Based on your area and this pest control site I believe that the bugs in your picture are not spiders, they are clover mites. I have found that some clover mites are a darker brown color and also slightly larger. This image gives a better view of the features of a clover mite, including the longer pair of front legs and oval shaped body:  Clover mites don't pose a threat to people or animals as they live off of either plants or fungi, but smashing them can leave stains on furniture and clothing.


Is there a specific word for bacterial death? What do you call it when a bacterium dies? Cellular death is apoptosis, necrosis, and bacterial is ...? I don't simply want to write in a paper that it - well dies!

Death is appropriate. Using this word to describe both unicellular and multicellular organisms places them in the same hierarchy. This hierarchy is the domain of life.

Both prokaryotes and eukaryotes have unicellular and multicellular species.

If you choose another word for death I would suggest not using it exclusively for bacteria. If a reader finds the idea of bacterial death esoteric, they may be inspired to dig deeper into the subject. Encouraging an informed reader would seem to be an effective device in a paper for communicating scientific information.

You could qualify the word 'death' to be more precise. Senescence is the natural process of deterioration of life with age.

Google has a great tool for tracking word popularity. Here's a Google graph for 'senescence'.

The word bacteriocidal is commonly used when describing agents that kill them, as opposed to agents that slow their growth which are said to be  bacteriostatic.


Why does deamination in the lagging strand lead to an increase in the relative number of guanine and thymine to cytosine and adenine? My question arose from this article on Wikipedia on the GC-skew in bacterial genomes: https://en.wikipedia.org/wiki/GC_skew
As far as I understood, the lagging strand (the template strand), during replication, is more often single stranded than the leading strand (template), so it is more prone to mutations like deamination. Therefore, on the lagging strand (here, the one being the template to the strand formed by Okazaki fragments), one should expect more Ts and fewer Cs. Conversely, the strand synthesised by Okazaki fragments should have an enrichment of As and a depletion of Gs. Why does the Wikipedia article mention a increase in the ratio of (G+T)/(C+A)? I would expect an increase in the ratio of (T)/(C). I don't get the link with Gs and As.

I think you are referring to this sentence from your wikipedia link:

  There is a richness of guanine over cytosine and thymine over adenine in the leading strand and vice versa for the lagging strand.

Note that this is not saying (G+T) > (C+A). It is instead saying (G)>(C) and (T)>(A). I think that those are not the same as saying (G+T) > (C+A), though that is also true, probably?

So I think that there is no contradiction there- it is just, as you say, more Ts (relative to expected equality with As) and fewer Cs (relative to expected equality with Gs).

If I understand correctly, the importance of the GC skew, and the reason that it is interesting, is that it acts as a deviation from Chargaff's parity rules (as explained in the article). These rules state that for any given hunk of DNA, (G)~(C) and (T)~(A), which is the expected composition for (for example) double-stranded DNA, because of base-pairing.

Edit: for more information on Chargaff's rules, see this other question which I have (through pure coincidence) answered here. Note that the second parity "rule" is a statistical phenomenon, rather than a logically required rule. The wikipedia page on Chargaff's rules is also informative.

Hope that helps.


How much of my ancestry comes from each grandparent? Three of my grandparents were Eastern European, back at least several generations. I recently discovered that I am less than 25% Eastern European, the rest being Western European and other. How likely is this?

On average, 25%, because you have 4 grandparents, and all of your genetic material came from them as a collective. Of course it's possible to be more genetically similar to a particular grandparent by random assortment of chromosomes, but the average will be 25%.

Genetic tests can't tell you what your ancestry is (companies implying this are probably misleading you on purpose). At best, they can tell you how correlated certain features of your genome are with people from a certain geography. Even people who are currently live in Eastern Europe will not test as "100% Eastern European." There is far too much mobility and breeding of populations across geography and far too much variation within populations.

[English is not my native language]

I know a girl (say, Natalia) who took a DNA-test at National Geographic, while her half-brother (say, Sam) took one at 23andMe. They were both told that they had one-eighth of Ashkenazi origins. And in fact, they share an Ashkenazi great-grandparent.
So, I conclude that they have one-eighth of this great-grandparent, and the precision was so great that I am inclined to believe that there is a high probability that it is the same for everyone : one-half of each parent, and one-fourth of each grandparent.


Are there nerves in the umbilical cord? I have always imagined that cutting the umbilical cord after birth might be painful. But I have always been confused about who would feel the pain and why. It occurred to me that the mother or the infant could only feel pain if they had nerves connected to the umbilical cord.

Do either mother or infant have nerves running into the umbilical cord that carry nociceptive information?
If not, is there a reason why no pain receptors are present?

Short answer
There are no functional nociceptors present in the umbilical cord.

Background
Having had the opportunity to cut the umbilical cord of one of my kids, I can anecdotally confirm neither newborn nor mother gave any sign of pain during the procedure. That is, when cutting the umbilical after the birth of a full-term baby. The only person clenching his teeth was dad :)

In fetuses at gestational age of 18-36 weeks no stress response was noted after puncturing the umbilical (Teixeira et al., 1996), indicative of the absence of pain receptors connected to the baby's brain.

I couldn't find information about pain in the mother, but I cannot imagine that the maternal central pain centers are being connected to the umbilical, which would be pretty extraordinary. This, because long-distance neural connections are rarely, if ever, established in adult humans. Also, I haven't heard any reference to the mother feeling pain because of injury to the umbilical cord. For example, knots in the umbilical cord, or cords wrapped around the fetus' neck due to excessive movements of the fetus are never noticed by the mother, and are only revealed during ultrasounds.

Note, however, that the umbilical cord is innervated by cholinergic neurons that are thought to be involved in the control of blood transfusion to the fetus, but presumably do not carry sensory information to either fetus or mother (Ellison, 1971).

References
- Ellison, Am J Anat (1971); 132: 53-60
- Teixeira et al., The Lancet (1996), 347: 624

Yes there are

THE placenta and foetal membranes are usually described as being devoid of neural elements1,2. In other descriptions, the possibility of an innervation is not considered3,4. Nevertheless, reports of the presence of nerve elements in these foetal tissues continue to appear in the European literature5–7.

https://www.nature.com/articles/214103a0

They are especially small


what happens when you put enhancer and caat box in prokaryotes what happens when you put enhancer and caat box in prokaryotes

I do not think that enchancers do anything in procaryotes since there is no
chromatin spatial organization of DNA involved.


Where is pollenkitt secreted? Where is the pollenkitt material secreted? I think the tapetum would be a good candidate, since it provides nutrition to the pollen grains.

The correct name of the coating is "pollenkitt", not "pollen kit" (I edited your question accordingly).

From the book "Biology of pollen" (Shukla, Vijayaraghavan and Chaudhry, 1998):

  The term pollenkitt is used for the oily, pigmented and sticky coating deposited on the pollen grain surface during the final stages of maturation. (emphasis mine)

That may explain why you and others struggled to find an answer in Google/Google Scholar.

Back to your question: there are two types of adhesive coats in pollen grains:

Pollenkitt
Tryphine

Pollenkit is the most common one and, as tryphine, it is secreted by the tapetum.

According to Pacini and Hesse (2005):

  Two types of sticky pollen coat material exist in angiosperms, both produced by the anther tapetum. Pollenkitt is the most common adhesive material present around pollen grains of almost all angiosperms pollinated by animals, whereas tryphine seems to be restricted only to Brassicaceae. (emphasis mine)

Sources:

Pacini, E. and Hesse, M. (2005). Pollenkitt – its composition, forms and functions. Flora - Morphology, Distribution, Functional Ecology of Plants, 200(5), pp.399-415.
Shukla, A., Vijayaraghavan, M. and Chaudhry, B. (1998). Biology of pollen. New Dehli: APH Publ. Corp.

Yes it's Tapetum.Pollen Kit is made up of Hydrophobic pollen attractant and tryphine(A mixture of hydrophilic substances)


How do roots absorb water instead of presence of waxy - material suberin in the form of casparian strips on the wall of endodermis? I found that in the endodermis, the tangential and radial walls have deposition of the waxy, and hence water-impermeable, material suberin in the form of casparian strips. The endodermis comes before the vascular bundle so how is water absorbed in roots?

The plants do  have waxy walls and stuff, the plants use "Suction Method" to suck the water from the ground. Due to transpiration plants loose water from the top or aerial region of the plant and since water is absent in that region there is vacuum present so it sucks water from the ground. This is how plants absorb water.

[Reference--- https://en.wikipedia.org/wiki/Xylem ]

[Ref. Wiki Images and text part and cross check for better understanding]


Which fish did modern tetrapods descend from? Did modern tetrapods descend from Tiktaalik or Ichthyostega? While I understand that in terms of all tetrapods, the lineages of Tiktaalik and Ichthyostega both would be included, but I want to know if their lineages have continued to the modern day. Since they also have 10 million years between them, it's possible that both of their lineages have not continued to the modern day. It's also possible that neither of them have continued to the modern day and it was a later fish species altogether whose lineage has continued to this day in the form of currently living tetrapods even though Tiktaalik and Ichthyostega were the first vertebrates on land. I'm especially interested in knowing which fish pecies have humans descended from. I'd be grateful if anyone is able to shed any sorta light on this.

Your question cannot be answered.
One of the effects of how incomplete the fossil record is, is that it is impossible to say if a species was a member of a direct line or a side branch. we just do not have the resolution in the vast majority of the fossil record to tell. The answer could be both, neither or one or the other and we would not be able to tell. All we can say is it is likely they were closely related to or part of our ancestral line. But the working assumption is always that you have a related sister species and not the ancestor unless you can show extremely good evidence otherwise, (which is so rare you can assume it is impossible in extinct vertebrates).
Tiktaalik and Ichthyostega only give us a rough idea of what our ancestors would have been like. It is impossible to say with any certainty if either was a direct ancestor or merely a sister species to them. This is part of the reason cladograms are constructed the way they are, so that no fossil is ever put on the direct line.
Source.
Source 2
Note: Tiktaalik probably did not live on land, more likely it was a shallow water air breather.
Also whatever species was the ancestor of tetrapods, all living tetrapods would be its descendants. One aspect of population genetics is for a specific individual in an ancestral population, past a certain point in a linage  either every descendant is your descendant or you have no descendants.

Technically they descended both from the tiktaalik and Ichthyostega because Ichthyostega was later, but in the same family and evolutionary line as tiktaalik.


Pressure change in atria Background:It is said that during the phase of isovolumetric contraction , due to sharp rise in the ventricular pressure, there occurs bulging of AV valves into the atria producing a small but sharp rise in the intra-atrial pressure called c-wave.( in the second cycle of diagram).

Question: I am unable to understand why is then pressure in atria falling after the end of isovolumetric phase, even though the pressure in the ventricles is rising, so this should further bulge the AV valve or atleast( due to action of papillary muscles) have same pressure, So why is pressure falling?

The curve you are talking about is JVPJuglar Venous Pressure Curve.
You are talking avoit x-decent after c pulse.
The downward deflections of x decent is produced by the atrium relaxation and the downward movement tricuspid valve.
This causes decrease in atrial pressure.
A new fascinating question could be why x-decent is greater than y-decent.
Good luck.


Suitable writings for self-study in general biology/chemistry I have recently commenced a graduate education in mathematics. Since I am currently attending extra classes in programming, which are not included in my education, my institution will not let me attend further courses in biology. Hereby, my question is simple:

What are suitable writings for self-study in general biology/chemistry? By general, I mean somewhat of an university-level introduction of mentioned fields.

My level of knowledge is slightly above "advanced" high school chemistry/biology.

(I apologize for my bad english, I'm Norwegian.)

My personal favorite intro biology book is Campbell Biology. The new edition is a little pricy, but you can probably find one of the older editions for pretty cheap--my intro class used 9th edition, and I don't think much has changed other than some of the taxon names.

I'm not sure what branch of Bio you're interested in, but Campbell covers all of introductory cell biology, organismal/evolutionary and ecology. The "concept check" questions at the end of each chapter are fantastic open-ended responses, and I believe most (if not all) have answers in the back of the book

I'm not as solid in general chemistry, but some good ones I remember are Brown, Lemay, and Burston which got me through AP Chem, and Zumdhal which my university uses and I haven't heard any complaints. The Brown text is a pretty good intro though. It provides good information and I thought it was pretty enjoyable to read.

I recommend any Schaums Outline book on the matter. I've read several of them and, although there are books that are better and more specific in many instances, they follow a very easy to grasp format that is common to all other Schaums Outline books.
Therefore, they are a great start for self-studying any subject. The main good point is that, as they are not too dense, the chances you'll leave the book half-through, and stop studying in general, decrease a lot. They will increase your curiosity and understanding, so after reading them you should be ready to read more dense books later on.
I want to clarify that they are not equivalent to "for dummies" books at all. Although they are not dense, they are written assuming you are not dumb and under the principle of being able to make you pass your tests without attending classes. So they are serious books made for practical purposes; no pretence whatsoever.
Particularly on Biology, there are several books:
Schaum's Outline of Biochemistry
Schaum's Outline of Biology
Schaum's Outline of Microbiology
Schaums Outline Of Genetics
Etc. You can learn about any science with them, really.
I'll leave a link with more details on the one in Biology:
https://bookstore.lsue.edu/schaums-outline-biology
They have books on many other sciences. They are designed for self-study.


Why do redheads tend to sunburn more easily? Reading Marion Roach's book on redheads she mentions visiting Rees lab where he shines UV light on her skin. Apparently this is an ongoing experiment of his regarding the propensity of redheads to sunburn more easily, but the book doesn't adequately explain why.

Why do redheads sunburn more easily?

You should have a look at wikipedia > melanin.

  Melanin is a broad term for a group of natural pigments found in most organisms. [..] Melanin is an effective absorber of light; the pigment is able to dissipate over 99.9% of absorbed UV radiation.1 Because of this property, melanin is thought to protect skin cells from UVB radiation damage, reducing the risk of cancer. Furthermore, though exposure to UV radiation is associated with increased risk of malignant melanoma, a cancer of the melanocytes, studies have shown a lower incidence for skin cancer in individuals with more concentrated melanin, i.e. darker skin tone. Nonetheless, the relationship between skin pigmentation and photoprotection is still being clarified.

Most of the variation in skin color among humans is caused by differential levels of melanism. People with red hair have a low level of melanism (almost by definition) and therefore suffers more from sunburn than people with more pigmented skin.

The more important thing is that Melanin is formed through evolution due to Darwinism. If you lived in places which didn't get much sun you went whiter and sunnier places darker. Over generations of darkening the skin took on a darker pigment to protect itself by production of structures within the cell that was compatible with those energies to prevent deterioration and provide a medium to equalize the energy flow from the sun (Basically one of the many ways evolution was proved by sequencing ecoli strains and exposing them to synthetic sweeteners so that we could sequence the DNA structure during the evolution process). Basically the stronger you are and more adapted you are to the environment the more likely you will reproduce and propogate your characteristics. If you are whiter you required more Electromagnetic energy absorbtion for other processes so you gained characteristics that would enable that flow of energy.