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Why aren't leaves black?
I s'pose this is a variant of the age-old question, "Why are leaves green?"  It's fairly easy to ask teh internets and find plenty of answers for that one.
I have a different but related question: why aren't leaves black?  That is, chlorophyll varieties in leaves' cells mostly absorb red and blue wavelengths.  Why isn't there a pigment in photosynthesis that absorbs green?
Instead, the green gets reflected back to the atmosphere.  Its energy is otherwise lost to the plant.  Nature is awfully well optimized to so many niches; why would this band of light be wasted?
There are some plants that do absorb green (and have dark leaves).  These pigments -- such as anthocyanins, betalains, and carotenoids -- don't have any role in photosynthesis, and play other roles (such as protection against extreme temperature, or acting as an anti-oxidant).  Am I missing some pigment in my list that is green-absorbing and participates in photosynthesis?  If there were such a plant with a pigment like that, why wouldn't these plants dominate?  Is there a large cost to producing the green-absorbing pigment that mostly negates the advantage of the extra energy gained?
After a little more searching on SO, I found the top answer to this question.  In slightly different words, it says that light arrives in quanta, the chemistry in photosynthesis is driven by a certain threshold of energy, and any excess energy from a photon goes to waste heat (that tends to denature some of the proteins involved).  The answer points to another answer with similar reasoning.  However, their explanations don't account for the fact that chlorophylls strongly absorb blue in addition to red, where blue photons have nearly twice the energy of red ones.
Moreover, the answer goes on to say:

Of course, this is still no explanation why leaves are not simply black — absorbing all light is surely even more effective, no? I don't know enough about organic chemistry, but my guess would be that there are no organic substances with such a broad absorption spectrum and adding another kind of pigment might not pay off.

Are there nothing other than educated guesses at an answer?  And why not use a combination of pigments, instead of a single, broad-spectrum absorbing pigment?  For example, some metabolic pathways use parallel processes.  Quoth the Wackypedia:

Sometimes more than one enzyme can catalyze the same reaction in parallel; this can allow more complex regulation: with, for example, a low constant activity provided by one enzyme but an inducible high activity from a second enzyme.

It appears bacteriorhodopsin has a somewhat complementary absorption spectrum to that of chlorophylls: https://biology.stackexchange.com/q/58572/48437

Does this answer your question? Why do plants have green leaves and not red?

Evolutionary answer: I like to go one step before green plants and consider the humble alga. Algae were historically classified as green, red, and brown, based on the wavelengths that their characteristic pigments absorbed. It is believed that land plants evolved from a common ancestor of algae, so you might wonder why we don't have similar broad categories of green, red, and brown plants.
Our best guess is that the organisms we call "plants" came from a single evolutionary event and share a common ancestor with green algae, rather than a different group. These green plant-like beings were probably the first big land organisms to try photosynthesis and happened to do well enough to out-compete any other plant-like being that might arise in their environment. Being green was "good enough" to for photosynthesis, allowing these organisms to survive and thrive.
Meta-answer: "Why" questions in biology often have probabilistic (and intuitively unsatisfying) answers. It's very hard to collect data that can "prove" why certain things evolved the way they did. Plus, evolution is not an engineering or design process. It leaves dead ends and doesn't always find the right solution. Founder effects can be very strong. But organisms which last long enough for us to study tend to be "good enough" at what they do. Here, the most parsimonious explanation for why leaves aren't black is that land plants came from green algae and didn't need to produce more of other pigments to take over the world.
Biochemical side-note: Plants can suffer from photooxidative stress when exposed to intense light due to the generation of reactive oxygen species, which disrupt metabolism. Therefore, some non-green pigments, like xanthophylls, are actually responsible for quenching chlorophyll and dissipating energy away from light-harvesting complexes. More energy is not always a good thing.

Thanks!  If I can restate in my own words, it's two things.  (1) Absorbing only red and blue light is good enough to dominate; why bother expending extra effort that isn't necessary (or if it ain't broke, don't fix it).  And (2) green light is used for other purposes such as quenching chlorophyll (regulation) and fueling anti-oxidants.  Neat!  TIL carotenoids play both roles.  The xanthophylls you mention assist quenching.  Carotenes absorb shorter wavelength light, scatter longer wavelengths, and transmit what they do absorb to chlorophyll (to provide extra energy to the photosystem).

Another intriguing hypothesis is that the first successful photosynthesizer was purple (absorbed abundant green and reflected red and blue).  The green algae then exploited a niche by doing the reverse (reflecting green and absorbing red and blue).  Eventually the second comers out-competed the first movers, and began to dominate.  There was never a need to re-adapt once dominant and absorb green.  See this answer: https://biology.stackexchange.com/a/45335

Circling back to this a loooong time later, here's another piece of the puzzle: it's hypothesized that eukaryotes engulfed cyanobacteria -- becoming chloroplasts -- and this event only happened once in all of evolution.  (That is, no convergent evolution at play among all plants and algae.)  All descendants of that common ancestor all have the same green appearance.

In addition to the points mentioned in the other answer, there is also this paper highlighting the importance of a steady energy flow compared to simply optimising energy capture. See this article in Quanta Magazine for a summary.
From the Quanta article:

Gabor and his team developed a model for the light-harvesting systems of plants and applied it to the solar spectrum measured below a canopy of leaves. Their work made it clear why what works for nanotube solar cells doesn’t work for plants: It might be highly efficient to specialize in collecting just the peak energy in green light, but that would be detrimental for plants because, when the sunlight flickered, the noise from the input signal would fluctuate too wildly for the complex to regulate the energy flow.
Instead, for a safe, steady energy output, the pigments of the photosystem had to be very finely tuned in a certain way. The pigments needed to absorb light at similar wavelengths to reduce the internal noise. But they also needed to absorb light at different rates to buffer against the external noise caused by swings in light intensity. The best light for the pigments to absorb, then, was in the steepest parts of the intensity curve for the solar spectrum — the red and blue parts of the spectrum.

Thanks for the addition. We ask that answers not simply link to outside info in case such links later die. Leave the links but either quote or summarize the main points in your post please. Thanks!

Leaves are usually dark green meaning they actually do absorb some green light and convert it to useful energy, they just reflect more green light than any of the other wavelengths that we can see, thus giving them a green color.
Also, not all plants have green leaves, cactuses for example, have more like green stems with no leaves at all.  And in fact, many desert plants have a very strong white tinge to them because of all the white light they reflect in an effort to not overheat and kill themselves by absorbing such absurd amounts of light.  Many have evolved reflective wax coatings or tiny hairs that provide shade.  The conclusion from this seems to be that the limiting factor for many plants growth is not how much radiation they can absorb per area of leaf, and therefore, there isn't an evolutionary pressure to increase their energy absorption by evolving black pigments.
Note: I disagree with the other answer stating that it is the result of all plants being descendant from a common ancestor that used green pigments.  While it is true that all plants are descendant from a common ancestor, I haven't seen compelling evidence that black plants have never evolved or never had the opportunity to evolve.  Far more likely in my mind is that they are perfectly possible and don't evolve simply because there is no advantage to doing so.  Which I think is incredible; and very surprising.  But, I think that's the answer with the most evidence.

Hmm.  I'm not buying the excess heat thing.  Cacti are the exception, not the rule, when it comes to leaf shape.  Most leaves are thin: the have an extraordinary amount of surface area relative to volume.  Heat transfer to the surrounding fluid seems more than adequate.  I say "fluid" because some plants live in air, but others in water.  Which brings me to: they evolved in water, and water provides an enormous heat sink.  How could heat be a concern for those first-evolvers?

yeah, you're right i think.  I don't have much evidence, so this is mostly conjecture.  To conjecture, I'd say that forestecol provides a compelling overview of what selection pressures the "first-evolvers" were dealing with.  However, to change my answer from above, the most intense limiting factor with the "heat" is probably at the molecule level and substructure level, so it doesn't matter how much water the leaf is, because the clustered pigments and proteins will heat up faster than they can transfer their energy to the surrounding water.


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Acid splashing beetle | Germany | Middle Europe
I found a beetle trapped in the bottom of a staircase. When I tried to put it on a paper, it turned and splashed something like acid in my face. I saw drops on my glasses and it begun to burn on my forhead. It escaped then through the drain grate.
It was about 4 cm long and probably brown (not sure about the colour). All I found were the Brachinus beetles but they seem to be smaller and I heard no explosion.
Does anybody know what kind of beetle this could have been?

@SonicSplasher where I live? Germany, Middle Europe (as written in the title)

oops , didn't really read the location in the title

source: Stack Exchange

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How do scientists know what part of DNA does what?
There are many genetically engineered foods and animals and I was wondering, how do scientists know which part of a DNA to cut in order to produce the desired result. For example I want to make a tomato more durable and to do that I cut the durability part of the DNA of something long lasting and put in the tomato. I'm not sure, but I guess that's not how things work. If I wanted to make a human with tiger arms, I'll just cut the arms DNA part of the tiger and put it in the human DNA, no? I'm sure it's much much more complicated than that.
P.S - I'm just 16 and interested in biology, I do not posses any university/professional academic knowledge.

This is a tough question (scientifically)! Generally speaking, it's impossible to look at a DNA sequence and predict what function it might have. It's easier to go backwards: identify a function/trait of interest, figure out what proteins are necessary for that function, and then deduce the sequence.
I'll describe one strategy to go from protein to gene, and name some techniques which you can read up on if you want to learn more.
To find the amino acid sequence of a protein, you can chop it up using proteolytic enzymes. This gives you fragments of varying lengths, since the enzymes will cut semi-randomly at different sites in the protein. Run these fragments on chromatographic paper. You can deduce the amino acid sequence from the pattern, because larger fragments will move slower. This is the same idea behind Sanger sequencing (aka chain termination sequencing) of DNA, and was invented by the same guy.
If you know what the amino acid sequence is, you now know the mRNA sequence, since protein is translated from mRNA. However, in eukaryotes, you don't know the DNA sequence, since we have introns - i.e. bits of the sequence which get cut out between transcription and translation. We need a way to get from mRNA (protein precursor) to DNA (gene).
To do this, purify mRNA from a cell and generate a library of complementary DNA (cDNA) using reverse transcriptase. Then, sequence the cDNA library to generate expressed sequence tags (ESTs), which are subsets of the full cDNA sequence. Because the ESTs are subsets of the sequence instead of the full transcript, it's possible to "CTRL+F" the organism's genome and find the gene which contains the EST.
Scientists have been doing this for decades, so nowadays you can search a gene/protein database and instantly know which sequence is responsible for, say, a specific channel protein.
To go in the other direction from gene to protein to function/trait, you have to do a fair bit of legwork as well. In very, very simplistic terms, you "cut" some DNA, put it into a package, and deliver the package to your favorite organism. As you said, it's a bit more complicated than that. :)
For complex, polygenic traits, it's harder to (1) identify the genes responsible and (2) successfully engineer an organism to have all of those new genes. You're unlikely to see a human with tiger legs any time soon. It's much easier to give an organism a few genes that confer very specific traits. Look at this list of genetic modifications to crops and click on one of the traits; usually only 1-3 genes have been introduced.

This answer feels incomplete and pretty much skips over the very important work in genetics done in lower organims like yeast to identify the function of genes.

@Cell thank you for pointing this out. I felt this particular user was looking for a simple explanation that they could visualize, so I chose to describe one specific approach. In fact, I started writing this answer in response to a different question that the user asked shortly after this one, but the other question was so broad that my answer was better broken into pieces. I'll edit my response today to give a brief sketch of yeast genetics and am welcome to further suggestions.

I will name one classical methodology to associate genetic variation in population to phenotypic variation.
We can figure out functions of specific sequence thorugh correlation analyses. We sample a number of individuals from the population, sequence them (or genotype them) and measure a phenotype of interest. Then, we screen through their genome and for each locus (locus = position in the genome) we investigate whether there is a correlation between the genetic variation at this locus and the phenotypic variation. It is classic to represent these correlation tests throughout the genome with a Manhattan plot

, where the Y axis is the negative of the log of the P.value and the X axis is the position in the genome. From the above plot, one can tell that several loci at the end of the 19th chromosome are associated with the phenotype of interest. There is therefore likely at least one SNP over there that affects this phenotype.
This type of analysis are called Genome-Wide Association analyseS (GWAS; pronounced G-wass).

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Do epigenetics determine the proteins a cell produces and therefore it's function?
I'm having trouble understanding what epigenetics is in a simple sense.
How I imagine it is that if we had 2 twins with identical DNA and we let them live we will see that they'll develop differently. Their DNA will stay the same (unless the DNA gains mutations, which could lead to cancer...) but their epigenetic tags will differ. These epigenetics tags determine the execution of parts of the DNA and the way the twins live their lives determine how the tags will be distributed. It's hard for me to find an example.
Another way I think of epigenetics is for example the cells in the muscles have a specific epigenetic tags to produce the specific proteins needed to create the muscle and the cells in the skin for example have different tags, produce different proteins which produce the skin.
Is my understanding of epigenetics anywhere close to the truth?

Short answer: Yes, epigenetics play a role in determining gene expression, therefore protein expression and function.
Lifestyle factors like diet, smoking, alcohol consumption, and stress can change one's epigenome. A historical example of this might be the Dutch Hunger Winter of 1944-45; there is evidence that after the parents' generation suffered during World War II, the children who were conceived during this time and exposed in utero to famine had different epigenetic marks than their siblings who were conceived not during the famine.
Epigenetic regulation is also essential for cell differentiation in vivo and in vitro. Embryonic stem cells undergo many changes to their epigenome in order to become mature cells. One interesting example for further reading is the transcription factor NeuroD1, which binds to targets in the DNA to cause widespread changes in gene expression that are specific to neurons, and commits cells to a neuronal fate. It doesn't bind to thousands of neuronal genes; instead, it causes a "ripple effect" thanks to epigenetic mechanisms.
Longer answer: Epigenetic marks are added to the genome for many reasons, including the two you just listed, and I think it is helpful to understand what happens at a molecular level in order to understand "why" we have them and to better visualize what the epigenetic marks ("tags") are. This might help you to think of better examples on your own.
DNA spends most of its time wrapped around proteins called histones. A complex of DNA and histones is called a nucleosome. DNA-in-nucleosomes is called chromatin. Chromatin can then either be "loose" (called euchromatin) or "compact" (called heterochromatin). There are more detailed ways to define how accessible chromatin is, but this is the basic idea. Intuitively, loose chromatin is more easily accessible and the genes there can be transcribed actively. Compact chromatin is less active.
The looseness of chromatin is determined by how closely the nucleosomes interact, which is controlled by the histones' molecular properties. Whether or not the histone proteins interact to make the chromatin compact, or repel each other to make the chromatin loose, depends on what modifications they possess. These modifications are added by histone-modifying enzymes.
Histone-modifying enzymes are regulated by transcription factors (i.e. during the process of differentiation) as well as signals generated by extrinsic factors (i.e. during the organism's lifetime). The balance of activating and silencing activity is what adds and removes these marks to give a cell its individual epigenome.
So, in simple terms, epigenetic marks determine how accessible different parts of the DNA are, and a whole lot of factors (like cell identity and lifestyle) can determine where those epigenetic marks are.

The question makes no mention of epigenetic marks. It is very clearly put — has two parts, neither of which mentions epigenetic marks, and neither of which you answer, although you say the answer is yes. It isn’t.

@David, although the answer uses "marks" and the question uses "tags", the two are both used for epigenetic modifications, I believe synonymously.

@mgkrebbs — You miss the point. The poster gives two examples of what he thinks epigenetics may mean. One, for which he states he knows no examples is dangerous anti-science. I will put this in an answer when I get home.

@David - I added some references to support the two examples. I still think that it's very hard for a beginner student to think of examples of epigenetics without having a physical picture of epigenetic modifications, which is why I chose to explain epigenetic marks (tags).


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Effects of horizontal vs. vertical motion on human body
I want to know if moving along a vertical plane in a circle differs in its effects on the human body from moving horizontally in a circle. Imagine a ferris wheel with a diameter of 50 metres. If a person on it was travelling at 10miles an hours, would they get less dizzy than a person travelling on a roundabout or carousel with a diameter of 50 metres travelling at 10mph?

The inner part of your ear contains fluids that controls how dizzy you feel, with no consideration for direction. I believe astronauts feel dizzy for the initial day or so, before their body adjusts to liquids, if that helps you visualize it. However, on earth, I’d be inclined to say that horizontal would be better due to gravity and the direction the normal force of the fluids is pointing, but I could totally be wrong. Hope that helps.

Accelerations are sensed by your vestibular system located in your inner ear, more specifically the otoliths for linear accelerations. Your question is not very clear because you do not specify how exactly people would be moving, but let me try to answer anyway. First, in theory the otoliths detect accelerations only, so as long as you move at a constant speed in a constant direction you do not perceive your own movement (thanks, otherwise you wouldn't be able to stand being in a car, train or plane). Second, if you move in a circle horizontally it's different, and how different depends on your orientation. If you always look in the same direction, your acceleration will be a cosine function in the orientation of you head, and a sine orthogonal to your orientation (so you perceive the same as if you were on a sledge that moves back and forth and right and left, obviously as such a sledge would therefore be moving in a circle). But if you look in a direction tangent to the circle, then you are back to the case of constant acceleration and don't even perceive your own motion. Third, vertically it's even more different because of gravity. Gravity  is a constant acceleration toward the earth. So you always perceive it (that's why you know the orientation of you head even with your eyes closed and even if you are not moving). So this is similar to a horizontal circle, except that it would add up to the constant pull from earth gravity. Finally in space there would be no difference between the 2 cases.
That might sound complicated, but take the example of rotations (rotational accelerations are processed by the semi-circular canal but lets neglect that). If you spin at a constant speed horizontally (alongside the vertical axis), you wouldn't be able to tell you are spinning because your acceleration would be constant. But if you spin vertically (alongside a horizontal axis), then you would always perceive you are spinning because you would always be able to perceive earth gravity (as it is an acceleration) and you would presumably get very nauseous. And again, in space there would be no difference.


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How can the same transcription factor be both an activator and suppressor of the same gene?
For example, hunchback in moderate concentrations is an activator of kruppel, but a suppressor of kruppel in large concentrations.
From what I've seen in literature, that's because the kruppel's enhancer has several binding sites for hunchback: some responsible for activation, while others for suppression. But why would hunchback in moderate concentrations bind only to activation sites, and why would higher concentration "change its preferences"? What chemical mechanism is responsible for this preference?
P.S. I provide hunchback and kruppel as an example, but this is a general question: how could the same transcription factor be both an activator and suppressor of the same gene?

It could be due to higher affinity for the activation sequence than the repression sequence and/or higher avidity for activation sequences mediated by cooperative binding. Consider that the weaker something the binds, the more of it you need to ensure that a significant portion is binding. This paper looks promising in addressing your specific example, though I haven’t read it. You may also be interested in this answer.


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Why biologic systems tends to become more complex?
From elements, chemical compounds, cells, multicellular organisms, society evolves and with each step possibilities increase and things get complex. We are builing structures like ribosome builds polypeptide chains.
So my question is why humans keeps continue to live, does our brain is unconsciously tries to get our society to get bigger, why life has a tendency to get complex with time?

Why was this question received so poorly? Even if the assumption does not seem to hold, it is a question asked by many, and the (already existing) answers are quite useful.

I disagree with the assumption that biological systems have evolved to become more complex.
A clear example of the contrary is found in the Rickettsia species of bacteria which live inside the cells of its host (obligated intracellular parasites). Their genomes contain split genes, gene remnants and pseudogenes that may represent steps of a genome degradation process.
Here you can find more information about  Rickettsia evolution.
Here you can find an essay about complexity as a driving force in evolution.

This is an old and interesting question: how do we explain apparent trends in evolution without falling into the trap of teleology or goal-directed evolution, the idea that evolution is working toward a particular end point?
I don't know the answer, and I don't know if anyone knows the answer, but at least two books have tackled the question in a serious way.

John Tyler Bonner argued in a 1988 book that complexity tends to increase because of the correlations between organismal size and complexity. Cosma Shalizi's summmary of his idea is that:

... [f]illing a previously empty niche does wonders for the reproductive success of an organism; variations which increase size make new niches available, and so are favorably selected. But, owing to constraints imposed by basic physics and chemistry, larger organisms must be more specialized internally, i.e. more complex, to be as efficient as smaller ones, or even just to survive, so the selection is especially favorable for larger and more complex organisms. Because of the way developmental processes work, this complexity will probably be retained even by later, smaller organisms in other niches. Voila: the evolution of complexity, by means of natural selection.

Bonner's argument might or might not work at the level of cultural evolution.

In contrast, McShea and Brandon argued in a 2010 book that random variation by itself should tend to increase complexity. McShea's summary:

even when forces and constraints are present, a tendency for complexity to increase is always present. The rationale is simply that when selection is absent, the parts of an organism should tend spontaneously to accumulate variation, and therefore to become more different from each other ... A consequence of the [Zero-Force Evolutionary Law ] is that we do not need natural selection to explain complex tissues and organ in organisms.

Part of the problem lies in measuring - or even defining - complexity in evolutionary terms.  An example I read about (though I can't vouch for it) is the difference between amphibian and mammalian reproduction.  Amphibians simply lay their eggs outside - which means their genes must be prepared to handle a wide range of environments and still produce an adult frog or salamander.  Mammals keep their embryos inside, in a tightly-regulated environment.  And then there's metamorphosis - are the different stages of a butterfly less complex than mammalian growth?

fair enough, but from a very broad perspective there are reasonable ways to define this that will distinguish bacteria from (say) kangaroos - number of cell types, variety of biochemical pathways, genome size, ...

@BenBolker Number of cell types is probably a good indicator / proxy for organisms, but it's hard to judge, because so far we have estimates for model organisms at best. Genome size is not correlated with organism complexity unless prokaryotes vs eukaryotes is all you care about. I would also be surprised if the number of actual biochemical (i.e. metabolic) pathways an organism has correlates with complexity, since higher eukaryotes are outsourcing a lot here; number of genetical pathways/circuits might again be viable though.


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Why proximal muscle weakness is seen earlier than distal muscle weakness in Dermatomyositis?
It is said that in dermatomyositis(DM) , proximal muscle weakness is seen earlier than distal muscle weakness. It is also said that , DM is due to damage to small blood vessels contributing to muscle injury.( from Robbin's textbook of pathology pg.no: 1238-1239, 10e)

Shouldn't the distal group of muscles being smaller show weakness earlier? Why inclusion body myositis does not follow the pattern as in DM?

Usefull links:
https://www.mda.org/disease/dermatomyositis/causes-inheritance
https://emedicine.medscape.com/article/332783-overview#a1
My hypothesis are
1) Since skin, is commonly involved in sunexposed areas, may be enviornmental factors do play a major role. So, Proximal Muscles are more used in day to day work, so are more favourable site for drugs, autoantibodies to act upon.
2)May be, in case of due to drugs or vaccines, proximal muscles may be are preferrential site of action of these, making these group of muscle more suceptible.
By the way correct answer would be: Its under research.


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What jellyfish is this?

I saw this jellyfish at Brighton Beach, Victoria, Australia. I have searched jellyfish images but there is nothing similar. It is round with a diameter of approximately 80cm and the blue part looks like hundreds of thin tassels.

Please copy the picture to your post directly using the edit button and then pasting the link into the photo uploader. Thanks

diameter of 80 cm! are you sure you haven't done a typo

https://jellywatch.org/

Looks like Pseudorhiza haeckeli. Based on cross motif, and long tail. Grows over a metre across. There is a photo at https://www.abc.net.au/science/photos/2012/01/11/3406019.htm?xml=3406019.mediarss.xml#bigpicturepos
but dont copy it here - copyright.


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In adverse effects of Heparin, why is bleeding from deeper organs more common?
The reason given in my book is that it i because it interferes with the secondary hemostasis..but i did not understand how that implies that bleeding from deeper organs is more common..

Skin is extraordinarily tough compared to much of our internal tissues; it has to be to protect us. To bleed, skin integrity must be breached, which usually involves sharp objects.
Think for a moment that most splenic or hepatic injuries (even complete ruptures) occur from blunt force trauma without breaking the overlying skin. For a more common example, if someone hits your thigh with a baseball bat, you will get a large bruise, maybe even a broken bone, but the skin will usually remain intact (if badly bruised) from blood vessel damage beneath and within the skin.
Many organs are delicate, and damage within them is not rare. Bleeding within/from some bodily organs is fairly common: runners bleed from their kidneys, and many, many people bleed from somewhere in their GI tract. High blood pressure may cause bleeding in the brain (a stroke) but it won't cause bleeding from the skin.
Just add to all the above the effect of anticoagulation (what heparin does.) I hope that explains things. If it doesn't, please leave a comment.

Thank you very much for the explanation. To clarify further, i wanted to know whether bleeding from deeper organs probably happens (normally) also due to pressure from surrounding tissues?

@Curious - Not necessarily pressure from surrounding tissues, no. Our bodies are well designed with things to minimize the effects of normal pressure.

Ok so..why exactly does bleeding occur more from deeper organs or delicate structures? Why is it 'delicate'?

Tissues are more delicate than skin because they serve a different function than skin, which is protective. They need protection: the brain needs the skull, the lungs, heart, liver, pancreas and spleen need the rib cage. We have minor internal injuries all the time: we damage our liver, we erode a part of the lining of our GI tract, we weaken blood vessels or break small ones, etc. Internal tissue isn't tough, it's tissue. Muscle is probably an exception, and bone is pretty tough, but even most broken bones occur without skin being damaged.

Skin is just built to be tough. I could go into histological reasons (what you'd see in a microscope) but that would be outside the range of this question.


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A study found that the hepatitis C virus can live on surfaces for six weeks. Did they end the study before the seventh week began?
A study once found that the hepatitis C virus (HCV) can remain infective for six weeks on ordinary household surfaces. You can see the free full text, or a summary for busy clinicians.
What happened in the seventh week? Did the virus cease to remain viable, or did the study just end suddenly?
From part B of this figure, it looks to me like the study just ended suddenly. But I'm not a biologist, so I'd like to hear your opinion.

The place to find this information would be the Methods section of the paper.

We spotted 33 µL of plasma spiked with HCVcc on the 24-well plates. They were either immediately tested for viable virus or stored at 4°C, 22°C, and 37°C for up to 6 weeks before testing.

They tested their samples for (up to) 6 weeks. At the time of the 6th week they still found infectious virus. They did not test samples beyond 6 weeks so they can't say anything about infection past that time.

I appreciate your answer! ❧ I've now asked a follow-up question: "We know that the hepatitis C virus can live on surfaces for at least six weeks. Maybe longer. The infectivity study ended after just six weeks; why?"


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How to grow a spirulina biofilm on a carbon/graphite cylindrical cathode?
I am trying to grow a spirulina biofilm on my cathode for a fuel cell but it doesn't seem to be sticking to the cathode. I have a culture of spirulina  and I've submerged a few cathodes in it to try and develop a biofilm. This is not working. Is there anything I can do to promote spirulina growth on my cathode like coating it in glucose or something?

I keep finding articles that say Spirulina Platensis actually inhibits biofilms. Research is underway to use this property of Spriulina Platensis to disrupt the biofilms that protect pathogenic bacteria from antibiotics.


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Frog identification - two different frogs seen in New Zealand
Me and my friends saw these two frogs in man-made ponds in an area which is undergoing development for residential use. Anyone able to identify these beauties?
Also would be interested as to how these frogs got there, as the pond wouldn't have existed 2-3 years ago and there are none nearby.
Location these were found can be seen in the following link:
https://www.pic2map.com/yibrir.html

the first frog(the green one) resemble GREEN AND GOLDEN BELL FROG - Litoria Aurea

Description of the frog -

Have golden-bronze colored spots
Have a black line from the eye to the nostrils
Found in northern Island

And coming to the second frog it resembles Southern Bell Frog - Litoria Raniformis

**Description of the frog - **

Have a distinctive black line running through their back
Found almost everywhere in new Zealand
They have black-brown patches on their skin (can increase in blackness based on the surrounding environment)

Coming to your question , the golden bell frog seems to stay in small temporary water ponds even puddles
On the contrary the southern bell frog lives permanently in a pond so probably it lives somewhere nearby
That'll be it


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What is the biological name of this plant?

The plant was observed in a rural area near Digha.

This is Ageratum conyzoides, a flower of Asteraceae family.
The common Bengali name of this plant is Uchunti.
Other than this purple colour a white colour of this flower is also observed.

@Ayandip If the question has been correctly addressed you can accept the answer by clicking on the tick under the downvote arrow.Also you can  upvote it.


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We know that the hepatitis C virus can live on surfaces for at least six weeks. Maybe longer. The infectivity study ended after just six weeks; why?
Background
A paper has found that the hepatitis C virus (HCV) can remain infective for at least six weeks on ordinary household surfaces. You can see the free full text, or a summary for busy clinicians.
Elsewhere, Brian Krause has added:
"They tested their samples for (up to) 6 weeks.  At the time of the 6th week they still found infectious virus.  They did not test samples beyond 6 weeks, so they can't say anything about infection past that time."
My question
So, at six weeks, they saw that the virus was still infective. Why might they have ended the study right away instead of continuing it for a few more months?

I removed the postscript as it had nothing to do with the question. If you pose a question it will stand alone and people will answer it or ignore it as and in the way they think fit. If they have the reputation and think the question is subjective in a way that does not fit with SE Biology they will vote to close regardless.  I would vote to close this question as of little general interest, but am happy to leave it to die of neglect.

They ran out of samples
Their test is destructive, they can't test the same sample twice. They planned out a number of samples to test for each time period and tested them. At the end of six weeks, they were done.
It doesn't really matter
The point of the paper is that HCV is infectious long-term on surfaces when not cleaned properly, indicating there is a risk of fomite transmission long after an infected patient leaves the area.
They also show that if surfaces are cleaned, the virus is killed effectively. The authors are not advocating to quarantine a hospital room until any residual HCV dies from air exposure, they are advocating being sure to appropriately clean hospital surfaces to prevent potential disease.
It isn't typical (in fact, it is impossible) for a single scientific study to answer all open questions in one shot. If someone wants to put an upper bound on the duration that HCV remains infectious in the world they can do a new study with longer time points.


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Is there any difference between fascia and skin ?Are both the different names of the same thing?
Skin is the outermost layer of the body ,and it consists of two layers; epidermis and the second layer the dermis .There is another layer the (third layer) beneath the dermis called superficial fascia or subcutaneous tissue. I want to know that is superficial facia  a part of skin.?Can we say that fascia is another name of skin?

The superficial fascia is the lowermost layer of the skin found in nearly all parts of the body and it usually blends with the reticular region of the dermis. But that doesn't mean it's a part of the dermis. The subcutaneous tissue/hypodermis/superficial fascia is NOT part of the skin but lies beneath the  dermis of the skin. Therefore, it can't be used as an alternative name for the skin.

Fascia is made up of sheets of connective tissue located below the cutaneous layer. These fibrous tissues attach, stabilize & separate muscles, maintain vessel patency, and enclose different organs.
Fascia can be classified as superficial, deep, visceral, or parietal.
Superficial: Superficial fascia is found directly under the skin and superficial adipose tissue layers. It can sometimes include muscle fibers; for example: platysma muscle in the neck, the external anal sphincter, and the dartos fascia in the scrotum.
Deep: This one surrounds bones, muscles, nerves, and blood vessels. It is commonly has a more fibrous consistency and rich in hyaluronan as compared to the other subtypes. Deep fascia tends to be highly vascularized and contains well developed lymphatics. It is further divided into 2 subtypes:

Aponeurotic fascia
It forms into sheets of pearly-white fibrous tissue to attach muscles needing a wide area of attachment. Aponeurosis can thin into a tendon and become a point of origin or insertion for other muscles. Some examples of aponeurotic fascia include the fascia of the face, limbs, thoracolumbar fascia, and rectus sheath.
Epimysial fascia
Also known as the epimysium, this is the connective tissue sheath surrounding skeletal muscle and can, in some cases, connect directly to the periosteum of bones.

Visceral: Visceral fascia surrounds organs in cavities like the abdomen, lung (pleura), and heart (pericardium).
Parietal: Parietal fascia is a general term for tissues that line the wall of a body cavity just outside of the parietal layer of serosa. The most commonly known parietal fascia is found in the pelvis.


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Observed to Expected CpG
Observed to Expected CpG is calculated as below :
Obs/Exp CpG = Number of CpG * N / (Number of C * Number of G)   where N = length of sequence.

I also don't understand the expected CpG which is:
Expected =  (Number of C * Number of G)/ N

Can someone give an example or intuition for the above formula ?

First, count the number of each nucleotide in the sequence, and divide that by the total number of all four nucleotides in the sequence.  For the C. elegans genome these frequencies will be approximately:
A = 0.32
C = 0.18
G = 0.18
T = 0.32
These frequencies should sum to 1.00.
If you select one nucleotide at random from that DNA sequence then those frequencies become the probabilities for selecting a specific nucleotide at that site.  So very roughly you would be twice as likely to get back an A or a T (compared to a G or a C).
Next count the number of each of the 16 possible dinucleotides (e.g., AA, AC . . . TG, TT) in that DNA sequence and divide the numbers by the total number of nucleotides in the sequence.  That will give you the observed frequencies of the dinucleotides. CG (or CpG in your post) is one of these.  If CG occurs proportionally to the frequencies of C and G then if you picked a random dinucleotide from the sequence you would expect the probability to be 0.18 * 0.18.  You can do this same calculation for all of the dinucleotides in a genomic sequence and compare the observed frequencies to the expected frequencies.
If every site is truly random in the sequence then the observed dinucleotide frequencies should be identical to the expected frequencies, and this would be a zero order Markov chain.  In fact, genomic DNA is usually not accurately modeled as a zero order Markov chain.

According to you explanation, shouldn't  there be N^2 in the denominator for expected CG ?

Technically, I believe the denominator should be THE TOTAL number of dinucleotides that can be formed by the genomic sequence.  For the purposes of this example that number is not very different from the total number of nucleotides in the sequence.  There is no component of the calculation that  requires squaring the total size of the genome (that would be a very large number).


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Finding intensity of selection against dominant homozygotes
I was looking at some Olympiad questions and came across the following:

If the frequency of a completely recessive allele is $0.2$ and it remains unchanged from generation to generation due to superior fitness of heterozygotes, then find the intensity of selection against the dominant homozygotes.

As far as I know, selection intensity is a quantitative measure of the superiority of the individuals selected for breeding. However, I am not really aware of how to compute its numerical value.
The best I could do was to assume that the frequency would be a ratio of the selection coefficient of recessive homozygotes ($s$) to that of the sum of selection coefficients of both recessive ($s$)and dominant homozygotes ($t$), i.e. $\frac{s}{s+t}$, but that doesn't seem to lead me anywhere. Also, I can't think of a concrete reason as to why the frequency would be of this form if it is actually.
Any suggestions/pointers would be much appreciated.


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Is it possible in modern biology to make any person's identical twin (or genetical clone) using his DNA?
I was told by a Biotech professor (who came in our college for a guest lecture) that Bio Technology has now become so advanced that if we want to make an identical twin (or Genetical DNA Twin) of a person then we can now be able to it using his DNA. I am a Mathematics Student so I don't know much about it. I just attended the lecture because I found it interesting. I am sorry, I know I should have asked this very simple question in Quora but, I wanted a precise answer which could be believed. So I asked here, where I will get answers only from the very experts. I apologize again Thank You So Much in advance
Edit 1 :- I am satisfied with @Remi.b 's answer, @Bryan 's explanation and @anongoodnurse ' references. I should also have mentioned genetical DNA Clone in the place of identical twin. Now I've added.

I will assume that by "identical twin", you refer to "clones". Individuals who share the same genetics but of course do not necessarily share the same womb. I won't pay much attention in detail epigenetic modification nor in the length of telomeres.
While it has never been done for ethical reasons, we would probably be quite able to make a clone of a human being. We can take a cell from an individual, make it totipotent again, like a zygote and then, insert this zygote into a woman's uterus. The resulting individual is a clone and therefore have identical genetics, just like two identical twins. Similar technics have been used to clone Dolly the sheep.
We cannot, however, modify the DNA in all cells of a living individual to make this individual a perfect cone of another one.

Can you add resources to we would probably be quite able to make a clone of a human being? The wikipedia pages do provide useful resources to the terminology, but the answer itself seems unsupported. (I don't question the answer in itself - you're totally right).

Has any organism been cloned by the method you described?

Isn't Dolly the sheep a bad example? If I remember correctly the sheep displayed a lot of age-related abnormalities. Take into account the age difference between it and the original then you have two sheep that would not likely pass as "identical" twins. Basically the question is if turning a differentiated cell totipotent again undoes all gene silencing?

@Cell Fair point. You are going into the details of what one might want to mean by an identical twin. I don't think these semantic details are so much the point of the question. I assumed the main point was to understand, we can clone but we can't modify the genetics of all cells in a living organism.

I am quite satisfied with @Remi.b 's answer. I apologize, I used the wrong term i.e. Identical Twin , while I should have used clone in that place. I'll try to explain clearly, what I meant by my question by giving an example; e.g. If I am an adult and I want my child to be 100% like me. Then, is it possible to get it done by Biotech?
As you said we'll make it totipotent and insert it into a woman's uterus. Will the resultant baby have characters from that woman? I was unable to understand Cell 's point & your answer on that also. People who commented here, please upvote my question. ty

Sorry, I tried you in chat, but no go. https://www.youtube.com/watch?v=meiU6TxysCg. Reminded me of your question on Parenting. See? As natural as can be! ;)

@NavedTHESheikh - They will only share genetic traits. Some behavioral traits as well, but many behavioral traits are a mixture of nature (genetics) and nurture (environment). There have been cloned dogs who were unloved by the owners because while they looked the same, they weren't behaviorally the same, i.s. "She isn't my Molly."

@Remi.b - I agree with Cell; early cloned (and even recent) do not have the vigor and lifespan of the original. Something is missing. But +1 anyway for a good explanation.

Thank you so much @anongoodnurse , your video reference was fun Watching, interesting and gave me full experience what you were trying to explain. I could not understand, what did you want to say by saying Sorry, I tried you in chat, but no go

Yeah I have completely understand. Your example of dogs was great. Thanks again @anongoodnurse

Not to belabour the point, but I don’t believe Dolly was cloned by inserting an induced totipotent cell into a surrogate mother.

@NavedTHESheikh - I'm sorry I wasn't very clear. That video was intended for Remi.b. It's an aside, unrelated to this issue. But it was fun to watch, wasn't it? :D

@canadianer - I thought I was a stickler! :) Technically you're right, of course.

Identical twins share:
A) Near-identical genetics, save mutations introduced after the original zygote splits
B) A womb/developmental environment pre-birth
and often share
C) A similar developmental environment after birth (i.e., in most circumstances identical twin humans would be raised in the same household)
Despite these similarities, 'identical' twins do develop some differences in personality, etc, and are often be physically distinguishable. Raising a newborn individual from an adult's DNA would ensure that at a minimum (B) and (C) are not fulfilled, and (A) could differ more than typical of identical twins if a somatic cell is used that has some mutations (which it almost certainly will) or if the cloning process introduces additional genetic or epigenetic changes.
Given those limitations, yes, such a thing is within the realm of possibilities, but there are technical challenges to doing such a procedure in humans, and there are ethical barriers to working through those technical challenges such that I would say our technology level is there yet we may not yet have the specific technology necessary. I think it is likely the Biotech professor you are referring to is intentionally blurring any distinction between the two.

Thank You So Much for giving your time and knowledge in answering my question. But, as I am not a Biology Student, I couldn't understand some terms that you used here. I also had used the wrong term i.e. Identical Twin while I should have used Clone instead. In other words, someone's offspring is exactly 100% like him. The only difference between them is the age difference, nothing else. Please, could you elaborate your answer towards this point in some simple words? Thanks again.

@NavedTHESheikh - A clone is even less like a twin, as Brian explained. Brian's answer was simple. See my comment above on Remi.b's answer. Genetics are only part of what makes a person unique. Environment - even microenvironment - makes a difference. That's why twins do not have the same fingerprints: because amniotic fluid flow is different for each twin depending on their hand movements.

@NavedTHESheikh An identical twin is a clone, genetically. As anongoodnurse says, I've already said this fairly simply here; we've done this with other mammals but not humans, the barrier to further development is mostly ethical, and a genetic clone is going to be less similar than identical twins are.

@Bryan Krause oh now I've completely understood it. Thank You So Much for further explanation.

@anongoodnurse Thank You So Much, your explanations gave me a very important link towards understanding the answer.


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anyone can help identify this aquatic microganisms?

I extracted from fish excretion and at 400x
At the moment i have yet to try any medication because i don’t know what this is. Can someone who has seen this before share the light? thanks!

It's a Rotifer, commonly called wheel animal It uses the hooks to attach itself to the fish's gills.
https://www.google.com/search?tbm=isch&sa=1&ei=1t4qXJS_Jaiu0gLYppCYBw&q=rotifer+under+microscope&oq=rotifer+&gs_l=img.1.1.0l10.83680.92883..95716...0.0..0.181.993.1j7......0....1..gws-wiz-img.......0i67j0i10i67.8Yg5stvFiH4
https://l450v.alamy.com/450v/k42bdt/rotifer-lapadella-apsida-female-free-swimming-microscope-freshwater-k42bdt.jpg
I hope this helps


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Why do we use different micropipette tips for different volumes?
Isn’t it easier to use a 1000 µl micropipette tip for all volumes? I don’t understand why there are different tips for smaller volumes. Does it affect the accuracy of the pipette for very small (<5µl) samples?

This question is about fluidics and principles of physics rather than that of biology.

The short answer is yes, the accuracy is affected.
Automatic pipettes are most accurate in the middle of their range. The average error on a pipettes is already about 2%, but this is worse at the top end or bottom end of the pipettes minimal and maximal volume.
More subtly, have you ever tried to pipette 1 uL with a 1 mL pipette? Or even 5 uL. The bore of the pipette is too wide for starters, and the expulsion force/pressure to eject the fluid wouldn’t work very well.
On top of that, the surface tension would seriously hamper any ability to actually manipulate the fluid.


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Why did Trilobites evolve armor?
The Trilobite is probably one of the most successful created which evolved in the cambrian explosion.
Though many sources stated the Opabinia has been hunting for Trilobites, this has yet been proven wrong.
Due to my research I haven't found much more animals in the Cambrian age that grow larger than Trilobites or Opabinias - so I do wonder why did Trilobites evolve such a powerful full-body armor when they're have been no clear natural enemies.

predators don't have to be larger than their prey. More importantly Opabinia could not eat them with the armor, but they could easily eat them without the armor, that would be the point of evolving armor.

Your link that says "proven wrong" includes a hypothesis that Opabinia could have eaten trilobites during their molt, simply that it would not be able to eat through their armor (all the better reason to have armor).
The best evidence we are likely to have that trilobites had predators is that they have defenses; the fossil record is incomplete, and just because trilobites are well-preserved does not mean their predators must be. Unless other evidence surfaces for an alternative explanation, the simplest reason for why trilobites evolved armor is that trilobites with armor were protected from something and therefore selected for.
Injuries seen in fossil trilobites are similar to injuries from failed predation of modern related species (see for example Bicknell et al., 2018) and seem to be widely reported (Bicknell et al. 2018 cite a variety of other sources).

Bicknell, R. D., Pates, S., & Botton, M. L. (2018). Abnormal xiphosurids, with possible application to Cambrian trilobites. Palaeontologia Electronica, 21(2), 1-17.

I agree with the hypothesis at first sight. Additionally I must confess I did link an older article because I couldn't find the one I was actually pointing to in time (it was also from wired.com stating that these researchers had actually proven it wasn't possible due to further research).
The fact that there is such a high amount of Trilobite species which can be found all around the world, yet so few predators makes me wonder how an animal evolves a protection. We can agree they had a better success rate, but why would they evolve such a thing if (let's say) there is no predator yet?

Also Opibinia appeared in the middle Cambrian age, while Trilobites had evolved in the early Cambrian already.

@polarlighthouse I'm not an expert in the field, but I thought that the high number of trilobite fossils is simply because they fossilize so well and have been around so long, rather than them being the only animal around. Predators are typically outnumbered quite a bit by the species they prey on. Not having identified a definitive predator does not mean they have none.

I'm neither an expert, but since the Paelozoic age was actually the longest the earth's existence with animal life it's hard to believe there is no evidence of Trilobite predators when we have so many evidences about the amount of Trilobite species. Of course, predators are naturally less amount of their prey. I'm just wondering and it makes no sense to me to evolve something before there is a predator. But thtat's probably what we wonder about the cambrian explosion at all.

There are very few animals that can eat a turtle would you argue a turtles shell is not for protection? If he protection was not effective there would be no reason to have it.

@polarlighthouse Injuries to trilobites (see the edits to my answer) are evidence that they were indeed predated even if the specific organisms doing the predation are not specifically known. You are right that it makes little sense to evolve armor if there are no threats that armor protects against, though armor could also be protective against damage from waves+rocks.

waves/rocks/etc came also to my mind. Thank you for your answer/comments!

@john you clearly didn't understand the essence of my question.

@polarlighthouse You want to know why ammonties have armor when no predators could eat them with the armor. which ignores the alternative could the predators eat them if they did not have the armor.

Predators need not be large, nor do they need to fossilize well.  Consider the lamprey https://en.wikipedia.org/wiki/Lamprey#Fossil_record or even the common tick.


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

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

wikipedia > Cell Division
wikipedia > Fragmentation (reproduction)

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

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


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What is official term for contraction induced muscle "vibration"?
I can activate my tensor tympani muscles at will, it makes me hear rumbling bass sound becose the muscles "shiver / "vibrate" when contracted. Also when I put cleched fist to my ear I can hear it too. I read all muscles make makes this rumbling low frequency sound when contracted.
I wanted to study this thing but I run into the problem becose I dont know how is this muscle vibration officialy called. I dont know what words should I type to get relevant search results. I dont want anything about shivers, tremors or other stuff, I just want to know how is the normal muscle "rumble" called.

you may be able to post an answer to What causes “ear rumbling”?


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Does the DNA stick to surfaces we touch?
In case of robbery, the police visit the robbery scene and collect some samples like foot print or any item suspected to have been touched by the robber. The sample is then taken to laboratory for DNA analysis. Does that mean whatever we hold or touch, our DNA sticks or drops on it?

"Transmittable" might not be the right word, but yes, we deposit DNA on things we use/touch.

By your use of the term "transmittable", your title make it feel like you are talking about parent to offspring transmission of DNA.

@Mallam_Bello, it's inappropriate to say that"DNA" drops on the surface we touch. The cells of the body drop

Yes, we leave DNA on everything we come in contact with. Even simply standing, we shed skin cells and hair (although only the follicle has DNA) etc. DNA may also be transferred from clothes to clothes.
You might be interested to read this article :) http://www.forensicsciencesimplified.org/dna/how.html

Yes, and as DNA technology becomes more sensitive, there is the unfortunate effect where it's very easy to detect the DNA of a person who hasn't personally been in the location, or was a long time ago. The amplification of DNA is incredibly efficient now, theoretically needing a single cell

This is not only a theoretical thing - it is possible to amplify a single cell.


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How to add oxygen to indoor air without opening windows?
I'm not a biologist. I have read that low oxygen levels in the home can have a negative effect on health. I am interested in increasing the amount of oxygen in the air in my home.
To open the windows would be the most effective way but the air outside is cold and measurably polluted (PM2.5 usually greater than 30µg/m3) so I would like to find other ways.
I know that plants add oxygen to the air but I have read that an unrealistically large amount of plants would be needed to make a meaningful difference to the oxygen levels.
I am wondering what other methods I can use and also whether what I have written above is correct.
Please forgive me for my ignorance. If this is the wrong place to ask this question then please help me to find the right place. Also sorry for not knowing what tags to use.

You should not keep so many plants inside a closed room. In addition to the above answers, there is another thing to consider. If you don't open the window there will be no air circulation. In absence of fresh air germs can grow inside the room, which may cause health issues. The indoor air can become more polluted than the out side air. If you really can't open the windows, I would suggest you to install a good quality air purification system, which don’t produce ozone by-product. Even though the air purifier cleans the air, you still need to keep the windows open

You should also have in mind that, meanwhile plants produce oxygen through photosynthesis, they also carry out aerobic respiration. In short, this process requires oxygen which is normally not a problem during daytime as photosynthesis covers the oxygen needed. Nonetheless, during nightime, plants remove oxygen from the atmosphere and do not replenish it. This is why nurses normally remove plants from hospital rooms at night. So if you want to put plants in your room, have in mind that is best to take it outside during the night.
Refer to this link for more information: http://www.saps.org.uk/saps-associates/browse-q-and-a/453-do-house-plants-remove-oxygen

When plants photosynthesize they take carbon dioxide from the air and water from their soil, and using energy from sunlight combine these into sugar. In the process, oxygen gas is released as a waste product
This is pretty much the reverse of what you are doing. You take in oxygen from the air and you use this to break apart fuel, releasing energy and breathing out carbon dioxide and water as waste
Plant
[carbon dioxide + water + sunlihgt -> sugar and oxygen]
You
[sugar + oxygen -> carbon dioxide + water + energy]
Therefore, to add more oxygen you want a photosynthetic plant. this website lists the best ones for adding oxygen and also for cleaning the air. when plants pull gases out of the air, they filter and kill bacteria and spores out of the air too using their leaves.
https://www.bhg.com.au/best-air-cleaning-plants
You want leafy green, fast growing for the best effect.


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Do all commercial ionizers produce harmful ozone?
I'm not a scientist. I have read that negative ions have health benefits. I am interested in increasing the ratio of negative to positive ions in the air in my home.
I see that ionizer machines exist (e.g. https://www.amazon.com/s/ref=nb_sb_noss_2?url=search-alias%3Daps&field-keywords=ionizer).
I have also read that such ionizers produce ozone and that ozone can damage the lungs. Also sorry for not knowing what tags to use.
Do all ionizer machines produce ozone and are the levels produced harmful?
Please forgive me for my ignorance. If this is the wrong place to ask this question then please help me to find the right place.

"Negative ions" in this context having health benefits is complete nonsense pseudoscience.

This seems more to be about the specifications of a commercial product or set of products rather than a specific biology question. To be on-topic, you'd need to ask about ozone concentrations that would be harmful - to perhaps specified tissues of a particular set of creatures - and you'd need to show your research. Finding out if such levels are produced by a commercial machine would be off-topic here.


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Why is ATP hydrolysis to ADP, rather than ADP hydrolysis to AMP, used to drive biochemical reactions?
ADP has two phosphate groups, and can be hydrolysed to AMP in a reaction which involves a similar free energy change to that of hydrolysing ATP to ADP.
Why is the latter reaction, rather than the former reaction, coupled to energetically unfavourable reactions to provide an overall reaction with a negative change in Gibbs Free Energy?

I have edited the question to change it from one of fact (that the poster could have checked) to one of evolutionary biochemistry, which I think is more interesting.

Ah sorry, in my original question I wasn’t implying that ADP->AMP wasn’t as energetic as ATP->ADP, I was asking about the evolutionary biochem question to which you corrected it! Thanks!

The larger molecule (ATP) is easier to handle in biological systems.

Summary
The original question was edited — with the approval of the poster — so that in brief it now asks:

Why is ATP hydrolysis to ADP, rather than ADP hydrolysis to AMP, the
  normal way in which cells drive reactions which alone involve positive changes in Gibbs
  Free Energy?

The scope of this is wider than that originally assumed in the answer from @user1136, but he has also contributed to this answer by his comments, which I have incorporated into my revision.
To my knowledge there is no generally-accepted provable answer to this question (as opposed to listing advantages for the system as it works today). What I shall do is present a hypothesis that could explain this situation. The fundamental idea† of this is that:

The contemporary use of ATP rather than ADP in energy transfer
  reactions evolved from a preference for NTPs, rather than NDPs, as the
  precursors of RNA synthesis. This preference was a result of the fact
  that the conversion of NTPs to NMPs and pyrophosphate could prevent
  the reversal of this (and other) synthetic processes in a way that conversions  liberating phosphate could not.

AMP, ADP and ATP: Standard Free Energies of Hydrolysis

There is general agreement that the values for ∆G°′ (standard free energy change at 37˚C) for the hydrolysis of the terminal phosphate bond of ATP (β-γ) and ADP (α-β) are similar. (The following are from J.L. Jain, et al.:
ATP → ADP + Pi  –7.3 kcal/mol
ADP → AMP + Pi  –7.3 kcal/mol

Hence, there is no intrinsic energetic difference that might explain the preferential use of ATP over ADP as an ‘energy donor’ in biochemical processes, i.e. it is not evident why e.g.:

Glucose + ATP → Glucose 6-phosphate + ADP

and not

Glucose + ADP → Glucose 6-phosphate + AMP

And, as @user1136 mentions, there are examples where the energy of the hydrolysis of ADP to AMP can be used to ‘drive’ other reactions. He mentions polynucleotide phosphorylase, to which I would add  adenylate kinase, as this is not a synthetic process and is pertinent to the energy metabolism of nucleotide phosphates:

ADP + ADP ⇄ AMP + ATP

The introduction of AMP into the discussion raises the question of the value of the ∆G°′ for the following reaction:
ATP → AMP + PPi

Many texts quote a value only slightly greater (ignoring the minus sign) than those for phosphate release (the one cited quotes –7.7 kcal/mol), but a 1995 review of the situation in the Journal of Biochemistry suggests that the difference is actually greater: –10.9 kcal/mol, as opposed to –7.8 kcal/mol for the hydrolysis of ATP to ADP and Pi.
The relevance of this is considered in the next section.
Biosynthetic processes and ATP
It seems to me that the example of polynucleotide phosphorylase is especially pertinent because it is a biosynthetic process in which the nucleotide monophosphate is actually incorporated into the product.

[AMP]n + ADP → [AMP]n+1 + Pi

However this ADP-driven non-template dependent synthesis of polynucleotides is not model for template-dependent RNA synthesis, one reason being that it can also operate in the reverse direction as a phosphorolytic 3ʹ to 5ʹ exoribonuclease reaction:

[AMP]n+1 + Pi → [AMP]n + ADP

Irreversibility is an important feature of template-dependent synthesis of RNA¶, and it is thought that the key to this is that fact that ATP is the substrate and is cleaved between the α and β phosphates liberating pyrophosphate rather than monophosphate.

[NMP]n + NTP → [NMP]n+1 + PPi

The reason generally proposed to explain why this reaction is irreversible is that in the cell pyrophosphatase hydrolyses the pyrophosphate to phosphate in an exothermic reaction. However the problem in evolutionary terms is that pyrophosphatases would have to evolve before this would work. However, if the ∆G°′ for pyrophosphate release has a greater absolute value than that for phosphate release, this in itself would affect the equilibrium of the reaction in a manner favourable to synthesis, albeit at the greater effective cost of an extra ATP. The later evolution of pyrophosphatases would have served to reinforce and enhance the irreversibility.
The Hypothesis
The hypothesis is that nucleoside tri-phosphates developed early in evolution to provide a means of making nucleic acid synthesis essentially irreversible by a mechanism that generated pyrophosphate. As the example of polynucleotide phosphorylase shows, nucleoside di-phosphates do not allow this.
A priori it would seem that there is no reason why ATP rather than ADP should be preferred for coupling biochemical reactions. However, if one accepts the argument that ATP synthesis was required for nucleic acid synthesis, there would seem no reason for having a set of reactions generating ADP for other purposes. The energy of hydrolysis of ATP to ADP in such reactions would, in any case, have to be utilized, otherwise it would represent a net loss. Why go any further?
It may have been that ATP was preceded in evolution by an an earlier ‘energy donor’. However I would suggest that once a mechanism evolved for synthesizing and using ATP (and other NTPs) for synthetic purposes, it was more efficient to use this for metabolic purposes, largely displacing any previous energy donor molecule.
† Footnote 1
I have touched on this very tangentially in my answer to a quite different question about ATP. The common idea, however, is that the purine and pyrimidine rings of NTPs serve no purpose in energy transfer, but are a relic of their requirement in RNA synthesis, where the NTPs are not merely providing energy, but are incorporated into the RNA product.
¶ Footnote 2
RNA and DNA synthesis are not the only synthetic processes in which this strategy for irreversibility is adopted. The tRNA amino-acylation reaction — essential for protein synthesis is as follows:

Amino Acid + ATP → Aminoacyl-AMP + PPi

And the first step in glycogen synthesis is the formation of UDP-glucose:

Glucose 1-phosphate + UTP → UDP-glucose + PPi

@user1136 — Thanks for that — have downloaded the paper and will read it. Sounds the sort of thing that must have been discussed in TIBS at some stage. It is interesting in that it would provide less reversible phosphodiester bond formation without the hydrolysis of pyrophosphate, which one might suppose developed subsequently in evolution to lock things down. I'll revise my answer when I have a moment.

This is amazing, exactly what I was wondering!

Just updated as promised. To try to make the argument easier to follow I relegated certain points to footnotes. Happy to be informed of any typos or mistakes.

It can, and a very famous example is polynucleotide phosphorylase, an enzyme of great historical importance in the elucidation of the genetic code.
That said, it is very uncommon, and polynucleotide phosphorylase is the only example that I know of (but other users may be able to provide additional examples).
There is certainly no thermodynamic reason why the 'high-energy' bond of ADP cannot be used as a source of free energy.
Polynucleotide phosphorylase was discovered in Ochoa's laboratory by Mairanna Grunberg-Manago. The story goes (from memory) that Ochoa was very dismissive when Grunberg-Manago told him that the enzyme uses dinucleotide phosphates, rather than trinucleotide phosphates, and he told her that her conclusion was impossible. He later realized his mistake and apologized, and the biosynthetic activity of the enzyme provided a simple and elegant method for making short RNAs that were used to unravel the genetic code.
(I do not have the source of the above story 'to hand' (as I am on holiday). Perhaps someone can help me with a more authentic account of the story? Otherwise I'll 'dig out' the original source in the coming days).

Wow, that's really cool! If there is no thermodynamic reason, is it just by chance that life didn't really evolve to use the ADP->AMP pathway that much?

ATP can be hydrolyzed to AMP and pyrophosphate and the pyrophosphate is then subsequently hydrolyzed to phosphate. This is used by some enzymes to ensure the irreversibility of their reactions.

To be clear, I wasn’t critiquing your answer but rather adding some additional information that might be helpful to... someone.

@SullyChen — I don't think so. See my answer. BTW user1136, could you consider changing your name to something more memorable.

ATP -> ADP is easier to break than ADP -> AMP. I dont think i can explain why without invoking third-year chemistry notions of electron orbitals ...
Conceptually, the terminal phosphate link on the triphosphate is more unstable than the terminal one on the dipeptide, and so breaking this bond and liberating this bond energy to do work is easier, and the amount of energy is a small and useful amount. Breaking high energy bonds is harder, and if the energy released is in excess of what is need it can cause undesired side reactions.
Metabolism is step-wise to keep the unit of energy at appropriate level.

Please quote standard Gibbs Free Energies of hydrolysis to support your statement. And perhaps you would like to explain what dipeptides have to do with this.


text:
Polydactyly and its genetics
One of my friend was saying that her aunt (father's sibling sister) was having polydactyly but none of her cousins (her aunt has two daughters) is having it.
What is the chance that my friend's children inherit polydactyly?
(considering that her partner nor anyone in his generation exhibit polydactyly)

if polydactyly is autosomal dominant (Wikipedia), then effectively zero.

Polydactyly can be dominant or recessive. that is

A single copy of the mutation/s involved result in the phenotype
vs
Both copies of the gene must be mutated to result in the phenotype

When two random people who don't have polydactyly nor a family history of polydactyly have a child, there is around 1/548 (0.18%) chance that child will be polydactyly because the parents were carriers without knowing it, and a 1/11.7 (8.54%) chance the child is a carrier of a single copy
If the aunt's polydactyly is Dominant, then your friend's father hasn't inherited it (he isnt polydactyly) and just has the normal population chance of being a carrier.
In the case of Dominant polydactyly, assuming your friend has a partner with no history of polydactyly, your friend and her partner have the same chance as average of a polydactyly child (1/548)
If the aunt's polydactyly is recessive, meaning she has two copies one from each parent (you friend's grandparents), there is a 1/130 (0.76%)chance your friend's child will have polydactyly (4.2 times more likely), and a 1/4.5 (21.4%) chance of being a carrier (2.6 times more likely)
I'll quickly go through the working/
if you're interested:
Given that the grandparents are both carriers (needed for the aunt to have two copies), then your friend's father has a 2/3 chance of being a carrier of a single copy (1/3 chance no copies, 0/3 chance having two copies because he isn't polydactyly).
Your friend's mother has the usual 1/11.7 chance of being a carrier.
The chance of your friend inheriting a single copy is (chance passes from father) + (chance passes from mother) - (chance of getting two copies)
=0.6600/2 + 0.0854/2 - (0.33*0.0427)
=0.3727 - 0.0140
= 0.3586
35.9% chance your friend carries one copy
Your friend has 1/2.8 chance of carrying and 1/5.6 of passing it on
Friend's partner has the 1/11.7 chance of being a carrier and the 1/23.4 chance of passing it on
Therefore their child has
=0.1793*0.0427 (chance friend passes on * chance partner passes on)
=0.0076
=1/130 chance of having two copies, having polydactyly

=0.1793 + 0.0427 -(0.1793*0.0427) (chance any copies - chance two copies)
=0.2143
=1/4.7 chance of one copy a 2.5 times increase risk

That's a really detailed answer. Good one and thanks for simplifying the confusing parts. But can you add any reference? It will help me accept your answer.


text:
Gene vs Protein homology
I am trying to find homologs for some proteins and I am wondering if it is better to find it by comparing the proteins or the coding genes or either is fine.

Think. What is likely to be more conserved — protein sequence or nucleotide sequence?

In most* scenarios you will probably want to look at a comparison of proteins following some additional matching that considers more than a single gene/protein. Luckily, this is a very common problem and one can often look up homologs through existing reference databases such as https://www.ncbi.nlm.nih.gov/homologene
Further, if genes are not present, their documentation will provide a good overview on ways to find homologs in other organisms.
*in some very special scenarios, gene sequences might be more suitable. For instance if one wanted to study similarity of non-coding regions of a gene. However these exceptions would seem beyond the general character of the question.


text:
Can endemic diseases be acute?
Diseases can be classified as :endemic ,or pandemic,...etc.
 An endemic disease is an infectious disease which is generally or constantly found among people in a particular area.
Disease conditions are :

acute: rapid onset , severe symptoms and brief duration.
chronic:gradual onset and long duration

Can an endemic disease be acute? Or is it always chronic ??

Endemic and chronic/acute are unrelated properties of a disease. Endemic is a description of the frequency of a disease in a population or in an area. Chronic/Acute is a description of the state or course of a disease in an individual.
For example, influenza is endemic in North America: the frequency goes up and down, there's always a few people who have it, but most people don't. Periodically the influenza virus mutates, and becomes much more successful at infecting people. The frequency of the disease goes way up, and influenza becomes epidemic. However, regardless of whether the disease is endemic or epidemic, the disease processes is usually acute: it comes on suddenly, it gets worse for a few days, and then it get better (or you die).
Malaria in endemic in much of Africa and SE Asia (it's always around), but the disease can be either acute (you have fever, chills, prostration), or chronic (the parasite lives in your body, and you can be a source of the disease, you don't necessarily have obvious symptoms, but may be suffering long term damage.


text:
Calculating fraction of protein unfolded from spectroscopy data

This is a question from a homework pset of previous year. We are given the absorbance at 222nm of both a wild type and mutant protein at different temperatures. We are then asked to calculate various thermodynamic quantities from these data. The first thing it asked for is the Tm of both wt and mutant. To get the Tm, I need the fraction of protein unfolded, since Tm is defined as the temperature at which fraction unfolded is 0.5. However, I am confused as to how to calculate fraction unfolded. In the answer key, the professor used a equation, f=2*(A222-0.5), without any explanation. Can anyone explain to me where does this equation come from?
Edit: Sorry, I forgot to tell you that f stands for fraction unfolded.
Thank you very much
Zeyuan

I've plotted the data for ease of answering, though it is not necessary if you know what to look for in the data.

As expected, the melting curves are sigmoidal with horizontal asymptotes at approximately 0.5 and 1. You should be able to see this in the raw data as well: the absorbances hover around 0.5 before rising rapidly and then plateauing around 1.
You want the fraction of unfolded protein as a function of absorbance, so you need to normalize this data to the range of [0,1]. There's a straightforward formula for this which, put into the terms of your question, would be:
$f = \frac{A_{222} - min(A_{222})}{max(A_{222}) - min(A_{222})}$
$f = \frac{A_{222} - 0.5}{1 - 0.5}$
$f = \frac{A_{222} - 0.5}{0.5} = 2(A_{222} - 0.5)$
Intuitively, you might think about it as follows: at low temperatures, when the protein is folded, absorbance is 0.5. Consider this a blank or baseline measurement which gives the absorbance of the solution when no protein is unfolded. Since you are only interested in the signal from unfolded protein, you can subtract this value (0.5) from the rest of the data.


text:
How can seedless fruits not be GMO?
Biology is the closest I could find to botany on SE.  Grafting can not occur naturally and so if a fruit does not have seeds there is no way it could reproduce in nature.
That logic makes complete sense to me so I am wondering why seedless fruits claim to not be GMO?
Take for example, Satsuma oranges.
Were they somehow crossed like a mule?  See here.  And then grafted over and over again?
It appears they occur naturally and are then grafted.  See here.
So the deeper question is does grafting create a "clone" of the grafted organism?
And deeper yet, what defines genetically modified ( GMO ) from simple genetic variation?

The production of seedless fruits is quite well described on: https://en.m.wikipedia.org/wiki/Seedless_fruit

The difference between genetic variation and GMO is something better discussed on a religion site.

"GMO" is a tricky concept. The wheat we've been eating has was first genetically modified by humans 8000 years ago, and today you'd laugh at what was called 'corn' 10,000 years ago. When humans make new hybrids, we have genetically modified a species. Something that comes from a genetic mutation is still a genetic modification. I think we're just getting into more sophisticated ways to get what we want (and what we don't intend as well...)

Pick a question, but most of your issues can be answered by asking what is a GMO, because the answer is nobody can agree.

@jamesqf ????? Huh?? Not at all. And in fact, such a question best belongs here on Bio.SE

@anongoodnurse (and John)  It's not too tricky; but rather it's surrounded by a lot of misinformation. The term "GMO" is strictly applied to genetic modifications due to human-mediated transgenic manipulations. The genetic variation that arises from cross-breeding (even if it's "unnatural" in a cultivation setting) is simply a "natural" result of subsequent normal biological processes. Such crossbred crops do not have their genes modified directly by humans and are therefore considered to simply be "crossbred" and not genetically modified.

@theforestecologist - I believe you. That's what I would reserve it for as well. But conceptually... how different is animal husbandry selecting for a particular trait over decades vs. splicing in a few genes associated with that trait and getting it in a couple of years  It's ever more sophisticated manipulatioin of the gene pool. But you'll get no more serious argument from me. I get it. I just think of decline in Monarch butterflies, a totally unconsiderd side effect of GMO corn. (for fighting corn worm borer)

@anongoodnurse I think most scientists in the field would agree that it isn't all that conceptually different which is why any furor about GMO safety is a bit silly, the exception being the economic arguments, though there could also be an argument that the speed at which we are able to make changes makes it more likely that those changes will have unintended side effects.

GMO stands for Genetically Modified Organism.
Grafting a plant to a rootstock of another plant is a form of plant husbandry -- a farming technique -- but this isn't changing the DNA code of either of the plants. Sort of like you receiving a donated organ wouldn't be the same as Genetically Modifying you. When a desired trait arises in a plant this is a way to keep reproducing it without having to wait for cuttings or seeds to grow.
There are some plants such as seedless watermelon that are reliably made by crossing two seed species. You take two species of watermelon, Species 1 and Species 2. Both of these are normal -- they make seeds. When you cross them, you get seeds that grow into AB hybrids, seedless watermelons. These AB are infertile, so you have to cross A and B again each year to get more seeds to plant.
Species 2 has twice the number of chromosomes as 1. They are able to cross and make seeds that grow. But when the [1x2] plants grow and try to form seeds, those cells have an odd number of chromosomes. The process of making seeds and pollen -- meiosis -- has a step when half of the chromosomes go into one cell and half in another. Because there is an odd number, the process never finishes and you get no seeds.
to demonstrate how this doesn't work, lets look as a simple example.
Species 1 has two chromosomes [A and B]. It has two copies of each chromosome in all of its cells (one from each parent), and just one copy in its sex cells
Species 1 Normal Cells [AA BB] and sex cells [A B]
Now, Species 2 has a different set up. It has twice the chromosome number
Its normal cells are [aaaa bbbb] and its sex cells are [aa bb]
this means that when you cross pollen from one with seed from the other, you get
[aaA bbB] or [AAa BBb]
When these crosses try to make seeds, its impossible to halve the triplet chromosomes.
True GM technology is used to do things such as, in olives taking the genes that cause oil production to occur, and copying them many times. This gives you more oil production.
Or, in tomatoes -- when you pick a tomato the cells of the skin start expressing a gene that makes the skin soften and break apart. This facilitates seed dispersal. GM deletes that gene, making the fruit bruise less, reducing need for packaging and quadrupling the shelf life.

The system has flagged you as a new user to me and other list members who help monitor this site. I have noticed quite a few other answers from you which have also been flagged as requiring additional references, so can I point you to the Help on Answering Questions. The reason we ask for supporting references on SE is if you post an answer, how do I or anyone else know it is right? What if someone else disagrees? One may feel: "this is my area" or "I taught this to students for years", but one has to demonstrate one is correct to others.

This is a very good answer, but, as David stated, sources are usually required for this site. Having said this, it's nice to see such a good, detailed, and correct answer.

Starting with your last question: The USDA (United States Department of Agriculture) defines genetic modification as "heritable improvements [...] by genetic engineering or other more traditional methods". The EU defines GMOs as "an organism, in which the genetic material has been altered in a way that does not occur naturally" using DNA altering techniques.
These are rather legal than biological definitions. For example, the EU Court of Justice has recently ruled that organisms produced by mutagenesis are technically GMOs but do not fall under the GMO legislation.
So, let's look into how seedless fruits are produced:
This can be achieved by making a plant, that is able to grow fruits but fail to produce functional seeds due to unsuccessful meiosis. This is done for bananas and water melons by crossing a diploid with a tetraploid plant, which produces a triploid plant where chromosome pairing during meiosis is unlikely (more on this in the wiki article). For oranges this is done by growing genetic clones together. Since they cannot self-fertilize (and identical clones cannot fertilize each other), they don't develop seeds but still grow fruits.
These techniques don't require any genetic modification by targeted manipulation of the DNA. Crossing two plants with different characteristics is also done in conventional breeding, which is also not classified as GM. However, it would be possible to genetically alter plants to block seed production and produce seedless GMOs. It would probably be a legal dispute whether this change is "heritable" when there are no seeds, so classification might depend on country policies.
The problem with seedless fruits is that you need seeds in order to grow new plants. To produce new seedless water melons you always have to cross the parents again. Plants that are able to reproduce vegetatively (parts of the plant can grow new plants), can be propagated by replanting branches. For plants, where this doesn't work very well, grafting is a solution to improve the process (a well growing plant is used as a root). Vegetative propagation in any case produces genetic clones, as you have pointed out correctly. The propagation method is independent of the technique that first produced the seedless plant and does not decide the GMO or non-GMO classification.


text:
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?

Related: https://biology.stackexchange.com/questions/5445/why-does-the-cold-make-us-sick

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.

Got it.. . But then if it's summer and no one has the cold, how does the virus start with 1 human ? Is my real question.@RabikJohn

It doesnot have to be cold outside to catch a cold. If you catch a cold in summer ,it would be exactly like catching a cold in winter .The rhinovirus that causes cold can spread easily in summer as in winter.So it doesn't depend on weather .Second thing ,how it spreads to other person?That's what we call ;contagious disease  (that easily spreads by water droplets when you sneeze )so any one breathing in that air containing your virus can got cold.

Just to get it cleared,  are you saying that the cold has started with the birth of humanity and since then it has never stopped ( as in saying that humans have cold everyday but it just spreads at a higher rate at some occasions)? @RabikJohn

An important detail to add is that virus can survive without a host for some time free in the environment and surfaces. You  dont forcefully catch a cold from a person that has a cold (at least not directly).

Humans donot have cold everyday ,whenever we encounter any virus ,our immune system tries to get rid of it. But sometimes immune system fails to do this so an  infection prevails. As I said earlier ;cold feet can slow down the immune system and  the virus takes an advantage of this.

@AdheshSagar I'm pretty sure we all have a few viruses even when we are healthy. Their amount is not enough to cause infection, but when immune system weakens they can spread. And then infection starts. Why do we have viruses? Well, if we got cold at least once a small portion of viruses probably will be able to survive. I don't know if these viruses can be passed to a child from mother, but I guess it's likely.

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

BTW: There are around 200 viruses that can cause a cold, among them are Rhino-, Adeno- and Coronaviruses just to name the more important. See [wikipedia}(https://en.wikipedia.org/wiki/Common_cold#Viruses) on it.

Why didn't we evolve to leave behind that virus from our nose?

"Rhinovirus...(is) present in us, a normal part of the microbiome," Please source this. From one review article on respiratory illnesses, "up to 27% [not 100%] of asymptomatic healthy children carry multiple respiratory viruses in their nasopharynx at any given time...", "viral presence might indicate a true subclinical infection..." It's not cut and dry yet.

Although there are some minor issues, this answer doesn't deserve a -2. Stephanie, can you please address these issues pointed out in the comments and improve your answer. Also consider the fact that cold air also causes damage to the nasopharygeal mucosa and thereby promotes infection.