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Which is the reference 16S rRNA?
Recently, I've stumbled upon a fact, which hasn't bothered me for many years. The fact is that all universal 16S primers are written as "[FR][0-9]+" (in regex notation), that is they have a position with respect to a reference. I've read through many papers, wherein these primers were introduced, and most of the time the authors say nothing but "E. coli 16S". Anyway, in one case I've found that it is in fact the reference K12 E. coli. But the problem is that it has 7 distinct rRNA operons: rrnA, rrnB, rrnC, rrnD, rrnE, rrnF, rrnG. Do you have a reference showing a particular operon used for the 16S position notation?
Edit

Figure 2. Hypervariable regions within the 16S rRNA gene in Pseudomonas . The plotted line reflects fluctuations in variability amongst aligned 16S rRNA gene sequences of 79 Pseudomonas type strains... (Bodilis et al., 2012)

Are you sure they differ in sequence at the primer? The sequences of the structural parts of the genes are apparently almost identical. Have you checked GenBank?

@David I haven't checked that myself, but here is a relevant reference ... or the same strain may have multiple copies of the 16S rRNA gene that differ by 5% for some regions (such as Escherichia coli K12 [12])... (Nguyen et al., 2016)

@David while the primers are indeed located in short conservative regions between hypervariable regions, the latter are extremely variable. I've added a figure depicting this variation across several Pseudomonas strains. Therefore, it doesn't matter, whether the primers are located in conservative regions or not, what's important is that they target regions that can vary in both sequence and length.

As you correctly point out, designing an optimal primer pair for 16S-rRNA sequencing is a tricky affair because even the less-variable regions are not same between different strains and species. Sambo et al (2018) have even developed a bioinformatics software for optimal design of primers for 16S-rRNA sequencing for multiple bacteria.

We propose here a computational method for optimizing the choice of
  primer sets, based on multi-objective optimization, which
  simultaneously: 1) maximizes efficiency and specificity of target
  amplification; 2) maximizes the number of different bacterial 16S
  sequences matched by at least one primer; 3) minimizes the differences
  in the number of primers matching each bacterial 16S sequence. Our
  algorithm can be applied to any desired amplicon length without
  affecting computational performance.

There is diversity in the 16S-rRNA genes within the same species i.e. the different copies are not exact duplicates (Větrovský & Baldrian, 2013).

Větrovský & Baldrian (2013)

Interestingly, the different rRNA operons in E.coli have different promoters and are even differentially expressed during stress conditions (Kurylo et al., 2018).
However, Kitahara et al. (2012) found that 16S-rRNA genes isolated from soil samples, in place of the original E.coli gene, could support its growth. In other words E.coli is highly robust to mutations in its 16S-rRNA.

After counterselection, ∼200 clones of KT103-derivatives (carrying
  pRB103 whose 16S rRNA gene was substituted with foreign genes) were
  obtained, from which 33 nonredundant 16S rRNA genes (A01–H03) were
  identified. Through multiple alignment of E. coli 16S rRNA and our
  metagenomically retrieved 16S rRNA sequences, it was found that at
  least 628 (40.7%) of the 1,542 nucleotides were variable, indicating
  marked mutational robustness of the 16S rRNA. Strikingly, the
  functional 16S rRNA sequences (except A10 and F02, which were 99.0%
  identical to E. coli 16S rRNA) obtained in this study showed only
  80.9–89.3% identity to E. coli 16S rRNA, which was well below the value reported thus far (Proteus vulgaris 16S rRNA, 94% identity to E.
  coli 16S rRNA)

For your question

But the problem is that it has 7 distinct rRNA operons: rrnA, rrnB,
  rrnC, rrnD, rrnE, rrnF, rrnG. Do you have a reference showing a
  particular operon used for the 16S position notation?

I don't think any one of them is considered the reference. The complete E.coli 16S-rRNA sequence reported in NCBI seems to consider a "consensus" of different reported sequences:

[5], [7] contain updated sequence data for the original work by the
  same laboratory [4]. There were too many discrepancies between [4] and
  [5], [7] to list each revision in our sites table. The sequence shown
  is from [7]. [4], [5], [7] point to a number of cistron
  heterogeneities. There is uncertainty, however, with regard to
  assigning these various heterogeneities to specific cistrons. The RNA
  method used by [4], [5], [7] gives the average of all the cistrons
  present in the cell [7]. The heterogeneities are classified by their
  relative proportions into major, minor and undetermined species. The
  sequence shown corresponds to the major species. The heterogeneities
  were annotated as variations in the sites table. It is not known which
  of the residues 'c' (base 633) or 'a' (base 641) undergoes a deletion,
  giving rise to the minor component 'atctg'. [7] suggests the existence
  of one or two mutated cistrons among the known seven cistrons of
  ribosomal RNA. With the exception of a single base deletion, this
  sequence is identical to the current 16S rDNA sequence for the E.coli
  rRNB gene.

The NCBI page also lists different polymorphisms and base modifications in the 16S-rRNA within and between different strains/"species".
NCBI has several partial sequences as well. When I checked for P.aeruginosa and B.subtilis, I could find only one or two complete sequences (rest were partial). Moreover, each entry indicated the strain that it was obtained from. Therefore I assume there is no single reference sequence.
I guess that people do consider the different variants while doing phylogenetic analysis (or simply just look for conserved "signature" sequences for a given species). I am sure that there are computational algorithms for doing the classification in an optimal manner (see Chatellier et al., 2014). Since, I don't have an expertise in this area I cannot say anything conclusively about the routine practice. In fact there is still ongoing research in improving the analysis (for example, Yang et al., 2016 and Sambo et al., 2018).

While I don't have access to the original paper by Ehresmann et al. (1972) that seems to be the source of that sequence, the preview does suggest that their methodology can only produce a consensus sequence.


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Do mitochondria contain the genes to specify themselves?
My book says :
"Mitochondria contain their own genetic material so when a cell divides, the mitochondria replicate themselves under the control of the nucleus."
The book means that the mitochondria contain the genes which produce the mitochondria right  ?

The answer is a bit more complicated than that. Mitochondria contain their own genome called mitochondrial DNA (mtDNA), encoding 13 proteins that are part of respiratory complexes I, III, IV, and V, 22 transfer RNAs (tRNAs), and two ribosomal RNAs (rRNAs). The separate tRNAs and rRNAs are necessary because the mitochondrial genome uses a slightly different genetic code than the nuclear genome.
So, the mitochondria contain nearly all of the genes necessary to construct the respiratory chain, as well as the machinery to translate the mRNA into protein. However, it does not contain any of the genes necessary to actually replicate the mtDNA (DNA polymerases, etc.) or construct the mitochondrion itself - synthesize the components of the different membranes, arrange the membranes in their required conformation, chaperones to assemble the complexes of the respiratory chain, etc. - these are all encoded in the nuclear DNA.

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What is the smallest difference in light wavelength that the human eye can detect?
Is there a lower limit to the difference in wavelength (colour) our eyes can detect? If so, is this consistent between individuals? Are there any other traits correlated with precise colour vision?

Here is an insane article that suggests that humans can't differentiate colors very well unless there are words for them... https://www.sciencealert.com/humans-didn-t-see-the-colour-blue-until-modern-times-evidence-science

The eye really on can sense 3 colors, or to be more precise it only has three types color sensitive each of which detects a large range of wavelengths with no way to distinguish between them within the same cone. We only determine color by the different levels of activation between the different cone cells. This means we need a lot of light to see color and our ability to detect differences in color really depend greatly on where on the visible spectrum that color falls.

As for more precise color vision. The greater the number of types of cones cells the more color sensitive the eye ,birds and reptiles can see far more colors than use becasue they have 4 types of color sensitive cells as opposed to the human 3. More widely spaces base colors will give greater sensitivity. This is why even among trichromats human color vision is poor becasue two of our base colors are close together and overlap greatly.  That is because humans (and primates) are secondarily trichromats, gaining a third base color from a recent mutation. wiki on the subject

Is there a lower limit to the difference in wavelength (colour) our eyes can detect?

The average human can detect differences in color as low a 1 nm depending on color subject to:

minimum spot size - "Mapping the Perceptual Grain of the Human Retina", by Wolf M. Harmening, William S. Tuten, Austin Roorda and Lawrence C. Sincich in the Journal of Neuroscience 16 April 2014, 34 (16) 5667-5677; DOI: https://doi.org/10.1523/JNEUROSCI.5191-13.2014
background color - "Sensations from a single M-cone depend on the activity of surrounding S-cones", by Brian P. Schmidt, Ramkumar Sabesan, William S. Tuten, Jay Neitz and Austin Roorda in Scientific Reports volume 8, Article number: 8561 (2018) DOI: https://dx.doi.org/10.1038%2Fs41598-018-26754-1
location of cone, proximity to blood vessels - "Selective Stimulation of Penumbral Cones Reveals Perception in the Shadow of Retinal Blood Vessels", by Manuel Spitschan, Geoffrey K. Aguirre, and David H. Brainard, in PLoS ONE 10(4):e0124328 (April 2015) DOI: https://doi.org/10.1371/journal.pone.0124328

The following graph shows the minimum and maximum discrimination values at various frequencies:

Figure 13. Mean wavelength discrimination curve. (From Davson, H., The Eye, vol 2. London, Academic Press, 1962)
Source: Color Perception by Michael Kalloniatis and Charles Luu

Source: Computation of Cone Fundamentals (Color Matching Functions) in Terms of Energy for Various Field Sizes and Ages Based on CIE 170-1, Spreadsheet Prepared By Mark Fairchild (mdf@cis.rit.edu), RIT Munsell Color Science Laboratory (mcsl.rit.edu), from Rochester Institute of Technology, Program of Color Science: Useful Color Data.

If so, is this consistent between individuals?

No.

Individual variations in photopic sensitivity
Results for 52 individuals, based on heterochromatic step by step brightness matching; "The visibility of radiant energy" Gibson, Tyndall and Kasson (1923)
A newer study, "Individual Differences in Scotopic Visual Acuity and Contrast Sensitivity: Genetic and Non-Genetic Influences" (Feb 17 2016), by Alex J. Bartholomew, Eleonora M. Lad, et al., PLoS One. 2016; 11(2): e0148192. DOI: 10.1371/journal.pone.0148192
PMCID: PMC4757445, offers a different variance plot (without nm):

Fig 1. Test-retest assessment. Four data sets are depicted: Visual acuity (left panel) and contrast sensitivity (right panel) at photopic luminance (green triangles, near top left and at scotopic luminance (blue discs, near bottom left). Result of the first test on the abscissa, second test on the ordinate. Grey 45°- line is the identity line, next to it the ± limits of agreement (photopic, dashed; scotopic, dotted). Visual acuity in logMAR units have an inverted scale, and contrast sensitivity is in logCSWeber units, meaning that better performance corresponds to the top right for both graphs. As expected, photopic measures of VA or CS are markedly better than scotopic ones. The 95% limits of agreement are remarkably similar. All in all, there is no marked deviation from a normal
distribution, and the reliability is good for the range measured.

Are there any other traits correlated with precise colour vision?

For your third question, above the one question per post limit, I'll offer these links (I may come back to this as time permits):
The website Handprint has these webpages:

Measuring Perceptual Discrimination
Individual Differences in Color Experience
Color and Language

See also:

"Color naming across languages reflects color use", by Edward Gibson, Richard Futrell, Julian Jara-Ettinger, Kyle Mahowald, Leon Bergen, Sivalogeswaran Ratnasingam, Mitchell Gibson, Steven T. Piantadosi, and Bevil R. Conway in PNAS October 3, 2017 114 (40) 10785-10790; first published September 18, 2017 https://doi.org/10.1073/pnas.1619666114
Human Color Vision
Teach the Correct Color Theory in School

Briefly: Precise color perception is not only the capability of the eye but the training of the brain (seeing different similar colors and having a need to differentiate between them) and the teaching of the vocabulary, the learning of the differences, and learned application of this in practice.

I am unable to answer the first question.
But yes, there is an upper ad lower limit to what frequency of light the human eye can detect. This is why you cannot see microwaves, infra-red, ultraviolet or gamma rays. Given the light cones humans have, the limits is consistent within the species. However given that the exact number of each light cone (red, blue, green) varies between individuals, sensitivity to a particular colour will vary between individuals. So both of us can see blue. But my blue maybe bluer than yours.
Should be noted that there are two variants of the green light cone in the human population. One has a sensitivity that is slighted to the red. And the gene for the green light cone is on the X chromosome. So about 2-3% of the women in the world have both variants and thus better colour discrimination.
https://en.wikipedia.org/wiki/Tetrachromacy
PS: Yes.. there are colour blind people. And if you include colour blind people then there are some people who have a narrower range of colour perception than most of the human population.

The question asked about the smallest difference in wacelength, not about the wavelength bounds of the parts of the EM spectrum visible to humans.

First, it depends a lot of the brightness. And also, of the part of the spectrum: we have high accuracy between red-green (since 2 of the cone have close sensitiveness), and very few in deep red and violet (were mostly a single cone reacts).
As always, you do have differences between individuals. Small ones, + big ones related to the variations in cone peak sensitiveness (or missing or extra cone).
In addition, it seems that there is a cultural factor: some cultures are more trained to pay attention to differences within blues, or reds, or greys.

that is a good point.. I recall reading an about an idea in psychology.. if you have a name, a word for  a thing, you can more easily recognize it and distinguish it. So if your language/cultue has more words for the different shades of blue, you are better able to recognize those shades. (Other examples include types of snow, clouds and  waves)

About 2 nm wavelength difference. The human eye can detect about 150 different hues in a rainbow, which for us consists of a visible light 380-700nm. About 300nm/150hues = 2nm per smallest detectable difference between two hues. I guess that's the answer you were looking for?

Welcome. Can you add sources to your claims?

Yes I can but why should I? There are many sources on the internet claiming the hue discrimination skills of normal and color deficient vision. It's a well known fact. The average is about 2nm in cyan-orange range, while at the ends of the spectrum (violet-blue and orange-red) it starts to decrease toward 10+nm for each hue to be discerned.

Because it's the convention of this site, that's why. -1

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Few deciduous trees in old forest
There is an old forest near me that has lain untouched for at least 150 years and possibly longer. The forest is on a big hill which is surrounded by a marsh.
The great majority of trees in the forest are gigantic hemlocks with aspens a distant second. The aspens are only found in the lower lying areas.
I am puzzled why there are so few deciduous trees in the forest. Deciduous trees are the most common around the town, and hemlocks are relatively rare outside the forest. The only deciduous trees in the forest are maples, and the few maples that are there tend to look sickly.
Why would there be so few deciduous trees? Do the hemlocks kill them off somehow, or would it be due to the soil?

Check out the radio lab podcast on underground network beneath of grow forests, perhaps it could provide you with some possible pointers to your question

Could you clarify what you mean by 'hemlock' in the question? Hemlocks are from the Apiaceae family and they are weedy.. Members of the Tsuga genus are also known as hemlocks but they are a kind of pine tree. A  sentence about the general location and climate may help as well.

150 years is nothing in the live of a forest, trees live for hunderds of years. If the hemlocks were planted 150 years ago it is no surprise that they are still there.

@Micael, Tsuga is really the only things that makes sense here, since poison hemlocks in apiaceae are herbaceous.

please provide the location of this forest

Interesting question, but we need a little more info. Location to start with. Some information on the approximate size and height of the hill. Any information you have of the soil (rocky or not?) and last: a picture would be great.

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Why does an electric shock contract the muscle?
From what I understand, the electrical impulse in our nerve cells is not made of electrons, but of ions that move from different environments with different concentrations, which is totally not related to the electricity we use, which is made of electrons. The electricity we use makes our muscles contract, why? Does it have to do with the fact, that when we put electrodes with electricity in an electrolyte, ions move?

Nice Question! Lets first introduce ourselves to the topic i.e. Electrical Muscle Stimulation.

Electrical muscle stimulation (EMS), also known as neuromuscular electrical stimulation (NMES) or electromyostimulation, is the elicitation of muscle contraction using electric impulses...The impulses mimic the action potential coming from the central nervous system, causing the muscles to contract.

Now, lets come to the main point. Its actually not about flow of electrons or ions, but the change in voltage that plays the pivotal role in muscle stimulation. See this:

Crystallographic structural studies of a potassium channel have shown that, when a potential difference is introduced over the membrane, the associated electric field induces a conformational change in the potassium channel. The conformational change distorts the shape of the channel proteins sufficiently such that the cavity, or channel, opens to allow influx or efflux to occur across the membrane. This movement of ions down their concentration gradients subsequently generates an electric current sufficient to depolarize the cell membrane.

In short, when you touch a wire, you become a part of the circuit i.e. any 2 points on your hand (or your hand and foot, if you're barefeet) act as part of the circuit i.e. there is potential difference between them, which generates an electric field. This electric field causes the voltage-gated channels in neurons/muscles to open which, in turn, generates an action potential and causes the muscle to contract.

References:

Electrical Muscle Stimulation - Wikipedia
Voltage-gated Ion Channel - Wikipedia


text:
How to selectively breed a plant?
Let's say I ordered seeds of a plant online. Then, I plant the seeds and grow a few plants. Then I take the seeds that the plants produced and separate them based on each plant.
Is it possible that I could then use those seeds to continue growing plants that have a desired characteristic? For example, if I wanted to grow taller and taller plants could I just keep planting seeds from the tallest plant? Or would I need to use a different method or technology to do this?

Yes, just planting seeds from the tallest plants would already do great. You could just chose an arbitrary size threshold under which you discard the seeds and above which you plant the seeds. Or you could plant all the seeds of the largest plant, almost all the seeds of the second to largest plant, all the seeds of the third largest plant etc... If plant height is a heritable characteristic (and it certainly is) then you will see a result after a few generations only.
You might want to ensure you understand the definition of heritability and the basics of quantitative genetics by reading the post Why is a heritability coefficient not an index of “how genetic” something is?.
Now instead of picking a random threshold for selection, you could be smarter and make some calculations. If you were to perform too a strong selection pressure (such as growing the seeds of the tallest individual only), then you will very quickly reduce genetic variation for height to zero and therefore remove all heritability. If you are using not a strong enough selection pressure, then you might barely see any changes even if you go on for many generations. Estimating the right type of selection pressure depends on the specific population you are facing (typically population size) and to its evolutionary history (typically previous selection on height or correlated traits and past population size).

Just a quibble: if the seeds are commercial varieties, they may be hybrids, and could be sterile or not capable of breeding true.  Also for commercial or hobby breeding, other techniques such as hybridizing between species or inducing chromosome polyploidy are used.


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Identification of cocoon
Looks like metal and has grown lines around it. Tried to search about it but didn't find results. Hanging on 1 of my plants. Curious to know which insect is inside. Please answe4 if anyone knows

Please answer fast .....want to know

people will answer in their own time, if at all, and requesting that people hurry is not an appropriate use for comments. Improving your question will help to attract an answer. I can think of three things that will help. 1, Correct the spelling errors. 2, include the geographic details of where the cocoon is. 3, add a photo that has the cocoon in focus so that people can identify it.

Are you asking about the thing that is not in focus? Because if you are, then I suggest getting a new photo where it is. Could you add information about where you took the photo, what time of year, and what kind of plant? All of this will be relevant.

In spite of the fuzzy picture, I think it's safe to say the chrysalis is that of the Common Crow Butterfly in its shiny stage.
Here is a sharper picture:

The orientation of the chrysalis is about 180° from yours; however, the various bulges and markings match up, and the host plant looks appropriate (without identification.)

The common crow (Euploea core) is a common butterfly found in South Asia and Australia. In India it is also sometimes referred to as the common Indian crow, and in Australia as the Australian crow. It belongs to the crows and tigers subfamily Danainae (Danaini tribe).

If you want to know how I found it, I used Google Images and searched "gold metallic colored cocoon". it was right on the first page. :)

A nice LMGTFY answer! +1

@James - Teach a man to fish, and all that.


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Interpretation of table on analysis of genetic diversity between groups
I am very confused about how to interpret Table 8.3 in Smith's Evolutionary Genetics.
Is the GST in the table the same as the G,ST (with the comma), which is defined (pg. 156; Box 8.3) as "the probability that two genes drawn at random from the same deme are identical"?  If so, is it not the same as Hs, the probability that two homologous genes from the same deme are identical?  If it is the same, why do they differ?
And why would Hr be larger than Hs?  That is, why would a gene be more likely to be identical with a gene from a different deme than the same deme?  Doesn't this suggest negative assortment?
Thank you very much to anyone who can help!
This is the table:

Welcome to Biology.SE. Can you please just display the figure directly on the post (screenshot the image from the pdf and add the image using the icon dedicated to adding images). Users don't want to click on a link, load a pdf, screen through 362 pages trying to find Table 8.3!

The title is really not informative. You could ask "What is the difference between Hs and Gst". Also, can you please use the > symbol for quotation and indicated where (what page, what column, what paragraph) the quote comes from.

GST or GST' (I've never seen G,ST) is not "the probability that two genes drawn at random from the same deme are identical". This definition matches $H_s$ (as you figured out). $GST = \frac{H_t - H_s}{H_t}$. I have never seen $H_r$. Hopefully, there is a definition of $H_r$ in the text. It could be defined as $H_r = H_t - H_s$ given what you seem to say but please make sure to quote the book on that definition.

I apologize to you.  After zooming in on the text, I found that what I thought was the definition for Hr was actually the definition for Ht.  I did a text search:  that was the only mention of "Hr" in the book.  So, I do not know the definition for Hr.  So by that definition of GST, if GST is positive, does it mean assortment is negative?  Which of these measures would represent "relatedness" in Hamilton's rule?  (Or would there be a combination necessary?)  Thank you!

The link given appears to be to an illegal copy of a book.  I have deleted it and vote to close.

I'm voting to close this question as off-topic because cites pirated text.

The text was cited by an article I am reading.  I am trying to complete a paper (not for school).  I do not currently live near a university library and therefore cannot get it via interlibrary loan.  The cost of the text is prohibitive, since I am only interested in one page of it.  I believe voting to close would be unnecessarily severe.

I would appreciate an answer to my questions.  That would be a productive way of responding.

If it makes a difference, I do not expect to be paid in any way for said paper.

Is Hs equivalent to Hamilton's relatedness?  Thank you.

No $H_S$ is not equivalent to $r$ (relatedness). $r$ comes from the field of quantitative genetics for which you need to consider a phenotype, while $H_S$ comes from classical population genetics and is independent of the phenotype. You can find book recommendation here for a good intro to population genetics.

Remi, I thank you very much and I am very sorry.  I didn't realize I had a response.  I guess we don't receive an email notification.  After asking this question, it occurred to me that Hs would be equivalent to relatedness if one omits intergroup effects?  I have a couple of intro to population genetics texts (the Gillespie text and the Hartl text), but Hs is not in the index of either of them.  Does it go by another term?  I do not understand the distinction you made between considering a phenotype and independent of phenotype.  Can relatedness be calculated from a combination of Hs and GST?

For context, Schonmann, VIcente & Caticha, 2013 says the following, "For these games, the condition for altruism to proliferate is Hamilton’s classical rule...Therefore, in this setting, altruism can only spread when either relatedness is large, or the cost/benefit ratio is low. And since relatedness is often low [28] (Table 8.3), [30], [31] (Tables 6.4 and 6.5), [32], [33](Table 4.9), exceptionally low cost/benefit ratios are required, as observed for instance in [34]."   The measures listed in the citations are:  hr, hs, gst, and fst.  How can relatedness be determined from these measures?


text:
What is this creature? Where can it be found?
I recently received the picture below from a friend and began to worry. Does it really exist? What type of creature is it? What habitat does t live in and what is its range?

A probability always depends on a priori such as typically where do you live, do you often drink from rivers, etc...? You should probably just ask "Is this a real thing?", "what is it?" and "where does it live?" Note that you can  improve the post by removing unnecessary informations such as how many people liked the post or what time it was when you took the screenshot.

Thanks for the comment, I've edited the question and the picture to suit your request.

The creature in the man's hand is a baby eel. Giveaways: it has fish eyes and the flattening of the tail. The lower right picture suggests it's a vertebrate (i.e. not a worm.)

Exactly which eel it is is unclear, but you can read more about it in the linked article. Indeed, your first picture appears in the article.

These transparent wonders are not a species, but rather they are the second stage in the life cycle of a number of eel species in the family Anguillidae. This particular specimen is an American eel, Anguilla rostrata. For the rest of the post I'll focus on the life cycle of this species for simplicity's sake.


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From what stage can you speak of an inflammation?
Imagine you hit your foot at a table leg and it hurts a while or you got a tiny graze. Those injuries aren't an infection but could these things still be called an inflammation?
Is it necessary that in both cases cells are damaged to induce a cascade of hormones? Or with other words, is there always an inflammation when cells are damaged or is needed more?

From PubMed Health:

When a wound swells up, turns red and hurts, it may be a sign of inflammation. Inflammation is – very generally speaking – the body’s immune system’s response to stimulus. This can be bacteria colonizing a wound or a splinter piercing your finger, for example. Inflammation happens when the immune system fights against something that may turn out to be harmful.

So when inflammation occurs, chemicals from the body's white blood cells are released into the blood or affected tissues to protect your body from foreign substances. This release of chemicals increases the blood flow to the area of injury or infection, and may result in redness and warmth. Some of the chemicals cause a leak of fluid into the tissues, resulting in swelling.
Signs of an inflammation :
There are five signs that may indicate an acute inflammation:

Redness
Heat
Swelling
Pain
Loss of function

There is a loss of function, for example, when the inflamed limb can no longer be moved properly or when the sense of smell is worse during a cold.
This means that an inflammation does not start when a wound has been infected by bacteria, festers, or heals poorly, but already as the body is trying to fight against the harmful stimulus or a viral infection.
Not all five signs occur in every inflammation. Some inflammations occur silently and do not cause any symptoms.
So depending on the symptoms we can decide if there is an inflammation or no.

Inflammations are non specific defense reactions instigated on cell injuries.
Inflammation reactions are characterised by certian physical changes that are inturn caused by physiological changes.
The physical changes are:

pain
heat
redness
swelling
loss of function

Here the redness is caused due to vasodilation of the nearby blood vessels (mostly capillaries) which means that the amount of blood passing through the vessel is increased and thus the region appears red. But this doesn't end there, as the vessels dilate their permeability to fluid and leukocytes increase that ooze out into the tissue and cause the region to swell up.
The resident phagocytes (phagocytes present in body tissues including skin) together with these leukocytes  fight against the invading microbes. However microbes that are present all around us, even abundantly on skin get a chance to enter our body through the smallest cut or tissue damage.You can say inflammation is a defense mechanism that the body employs to mitigate any imminent infection.
Now coming to your questions:

Those injuries aren't an infection but could these things still be called an inflammation?

Yes they are inflammations. If they are displaying the classical symptoms then they are inflammations.

Or with other words, is there always an inflammation when cells are damaged or is needed more?

Yes, there's always an inflammation if cells are damaged.

Is it necessary that in both cases cells are damaged to induce a cascade of hormones?

No in none of the cases mentioned by you a cascade of hormones is induced. Rather in both cases; INFECTION and INFLAMMATION a number of immune cells are induced to carry out a cascade of reaction which actually identify the microbes and cause

phagocytosis
neutralisation
agglutinisation or
complement fixation

However an infection can be caused without cell injury, e.g. pathogens entering through nose and mouth.
Note: Phagocytosis etc are complex immune reactions that occur against pathogens and there are chapters dedicated to them in Immunology books . I would suggest you to go through a google search to get a general idea if you are curious enough to know what they are.
Sources:

Kuby Immunology 7th Ed
Wikipedia

DId it help you understand the difference between inflammation and infection?


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Is sperm (spermatozoa) a bacteria?
Is spermatozoa (ie human) technically considered bacteria? I've been told it is and I've been told it isn't. Would it meet the definition? If not what is sperm considered?

A sperm is not a bacterium - a sperm cell is an eukaryotic cell with a haploid set of chromosomes.

The sperm cell is a eukaryotic cell. All bacteria are prokaryotic. (doesn't necessarily mean all prokaryotic cells are bacteria). Whoever told you that it's technically considered a bacteria, must have used it as a figure of speech referring to it's characteristics.. example, the sperm cell has a flagellum, which some bacteria also have.
The sperm cell is neither technically nor literally a bacterium.

Complement: it's not even a real being: it can't reproduce, it's almost not functioning (I'm not even sure than his DNA material is in a transcriptible form. Basically, it's a dedicated half-cell of a multicellular organism, frozen genetic packed content + a flagellum + mitochondria + enough energy to make it beat for a short duration.
As such, we might even find it to share common things with the definition of virus :-)

If you try, you can even find commonalities with a parasite, but it all depends on definitions and perspective. Example, in order for it to "survive" it must break into an ovum and develop into a fetus, while a parasite also can rarely live without a host... It's all about changing an explanation to make it fit something, using the right words, you could even compare a sperm cell with a snake... Both use peristalsis to move.


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Evolution of plants and chloroplasts?
I am considering the evolution of plants, specifically considering the chloroplast. I am getting slightly confused and cannot seem to find the information I need to build a coherent picture in my head. Specifically, I have the following questions:

Is the defining feature of a plant cell that it has, or once had, chloroplasts? Is the group of plants all of the species which came from the single common ancestor eukaryotic cell which first acquired a photosynthesising bacterium as an endosymbiont?
In that case, the plants Alectoria sarmentosa (witch's hair lichen) and Monotropa uniflora (Indian Pipe), which are non-photosynthesising plants and do not have chlorophyll, must have some remanant of a chloroplast inside of them (unless they are not actually plants and are just plant-like fungi). My question here is, are these really plants? If so and it is true that plants are defined as all being descendant from this first photosynthesising eukaryote ancestor, then what is their 'remnant chloroplast'? I.e. what organelle do they have that used to be a chloroplast.
If it is true that there are plants which have organelles that used to be chloroplasts but not longer have chlorophyll and photosynthesise, then it is almost certainly the case that the chloroplasts carry out some function other than photosynthesis that is beneficial to the plant's survival (e.g. I know that remnant mitochondria- hydrogenosomes and mitosomes- are useful for fixing iron although they do not carry out respiration). What are the other functions of chloroplast-like organelles?

Modern biology attempts to group organisms by clades, that is, into groups that contain all descendants of a particular organism and no others.  A clade may be associated with characteristics that most or all members of the clade possess, but those characteristics do not define the clade.  Previously it was common to describe biological groups by particular defining characteristics, but that has been largely abandoned because it often does not reflect true relationships.
"Plants" (or Plantae) is a term that can mean several different things, which are outlined in this Wikipedia table.  In short, it might be (approximately) the clade of "land plants", the clade of "green plants", which includes land plants and green algae, or the clade containing those plus the red algae and the glaucophyte algae.  That last clade, also known as the Archaeplastida, is thought to include all descendant species of the initial organism which initially established the symbiosis leading to chloroplasts (although not some organisms that acquired chloroplasts by secondary ingestion of archaeplastida).  It seems like you are most concerned with that third group.
Alectoria sarmentosa (witch's hair lichen) is not a plant by any of these definitions.  It is a lichen, which are symbioses of a fungi with a cyanobacterium or a green algae.  Green algae of course have chloroplasts.
Monotropa uniflora (Indian Pipe) is a member of the heather family and so is a plant by any of the above three definitions.  It does not have chlorophyll; my guess is that it likely has degenerate chloroplasts.
I think a separate question would be appropriate to inquire about the chloroplast remnants of non-photosynthesizing plants like Monotropa uniflora.

Moreover, even among archaeplastida, the chloroplasts don't seem have the same evolutionary origin. I am not too sure about it though.


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How do I efficiently grow bioluminescent algae?
I have 6 vials of Pyrocystis lunula that I would like to grow. What would be a more suitable container, a tank or a clear jar? Also, I would like to know what kind of nutrient solution to use. Is it possible to get them to reproduce at a rate that eventually there can be a whole tank full of them?

What sort of research have you done to try and answer your own question?

I have no experience with that particular species but dinoflagellates are often slow growing, very tricky to get to high densities and hard to maintain for a long time without proper experience and lab conditions.
If you still want to have a go I would recommend the following. Growth conditions are rather similar for most dinoflagellates: use a rotary shaker (gentle rotation) in a 12:12 day night regime, don't dilute to hard when subculturing and use standard F2 medium (see link for recipe). If you cannot get hold of seawater you can use saltwater aquarium salts such as Instant Ocean.
Most hate temperature changes so best to keep them at 18-21C

So I can just go to the beach and get some sea water from their?

You will have to sterilise it first (autoclave) and add nutrients such as iron, nitrate and phosphate. See the F2 recipe on the link provided


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Research from the early molecular genetics era that supported protein as the primary carrier of genetic information?
I can't seem to find anything on my own. Surely there were experiments performed (possibly using bacteriophages) that managed to come to this conclusion?
Specifically I'm interested in anything pre-Hershey/Chase.

do you want primary literature or just something that talks about the historical aspects? have you tried google?

@VanceLAlbaugh I have tried google, I have also searched my schools' library/journal database (and looked at the genomics shelves in person). I would appreciate primary literature or a historical piece that references primary literatures/goes into more detail than "...molecular geneticists felt that proteins had to be the primary carriers of genetic information because they could be much more differentiated than the 4-base DNA molecule" and the "1 enzyme 1 gene" hypothesis.

This is a wild guess, but have you looked at Schrödinger's What is Life? It's not a primary report on experimental results, but might have useful refs.

It’s difficult to be convincing with a negative answer, but I venture that the answer to your question is that the idea that protein was the genetic material was not supported by any experiments, but was a supposition based on the conventional wisdom that proteins were more complex and therefore more suited to the job.
I suggest that you should be thinking earlier than bacteriophage and Hershey and Chase. Bacteriophages only came into genetic research after the war, and the Hershey/Chase experiment (1952) was only a rigorous confirmation of the conclusion of Avery et al. in 1944 (mentioned in this Scitable article). The system that Avery et al. used (bacterial transformation) went back to Griffiths in 1928 and must have been the first that allowed any sort of experimentation in this area. And I think it was more a question of working out what was happening than devising an experiment to distinguish between protein and DNA as the genetic material.
To my mind this illustrates something about how science progresses. It is often dependent on advances in technology and changes in the conceptual framework in which scientists work. (Sometimes — e.g. Mitchell’s Hypothesis — it needs the experimental results to change that conceptual framework.) Coming back to the Hershey/Chase experiment, this was performed when the balance of scientific thought had already changed to DNA as the genetic material.
Footnote: It’s earlier than you think
I generated the Google ngram below to put the term you use, ‘molecular genetics’ into historical perspective.

This shows that the term ‘molecular genetics’ was hardly in use at the time of the Hershey–Chase experiment and Watson and Crick’s postulate of the structure of DNA in the early 1950s. I think that this reflects the fact that the concept was not current. The more popular term, ‘molecular biology’ gained currency on the basis of the structural work on DNA and proteins, and the name of the journal in which much of the work was published (Journal of Molecular Biology). The question is assuming a state of science that did not actually exist before the 1950s.

If it helps here's the Avery et al. bibliography.

I am relying heavily on Morange's book (quoted below) for what follows.
As pointed out by David, the definitive experiment showing that nucleic acid, rather than protein, is the carrier of genetic information is that of Avery, MacLeod and McCarthy (1944). Their conclusion that DNA is the 'transforming principle' was, however, very reluctantly accepted by the scientific community, in particular by the biochemists (see Cobb, 2014), and it was not until the famous 'Waring blender' experiment of Hershey and Chase (1953), and beyond, that it was accepted that DNA is the hereditary material.
So, to attempt to answer your question, what was the evidence for proteins (in particular enzymes) being the hereditary material?

It was known that proteins are one of the two components of chromosomes (Morange, p 35)
The tetranucleotide hypothesis of Levene, published about 1910, held that DNA was made of a monotonic, tetranucleotide repeating unit, and this gave rise to the idea that DNA had only a non-specific structural rule in the chromosome (Morange, p 34).
By the 1930's, several enzymes (including urease) had been crystallized by
Northrop and Sumner and it was unequivocally established that enzymes are proteins and are macromolecular, thus ushering in the great era of enzymology. Compared to the dynamic world of enzymology, DNA was considered boring.
In 1935, Wendell M. Stanley had isolated TMV virus as "a crystalline protein possessing the properties of Tobacco Mosaic Virus" and had published the results in Science. Crystallization (wrongly) implied purity and it probably understandable that such a high profile result lent weight to hypothesis that genes and proteins are intimately connected. This result was criticized, however.  Bawden & Pirie (1938) in the UK repeated the experiment but (unlike Stanley) found  6% RNA in the final product (Morange, p 65).
Beedle and Tatum (1941) had published the 'one gene one enzyme' hypothesis and (to again quote Morange) [p 35] this "had reinforced the more or less conscious identification of genes with enzymes and proteins". The idea that enzymes must be important in hereditary was further reinforced by the work of Garrod on inborn errors of metabolism, which also associated enzymes (specifically, the lack of them) with hereditary factors (Fruton, p431)
Avery's work was sharply criticized in some quarters, most notably by Alfred E. Mirsky, who pointed out that trace contamination by proteins could not be ruled out as an explanation.  A great account of the controversy with Mirsky and of the reasons why Avery's work was only slowly accepted is given by Cobb, 2014 [pdf]. One interesting stat from this paper: Hershley and Chase did not quote any of Avery's papers and Hershey is quoted  as saying that “I wasn’t too impressed by the results myself”  (Cobb,2014). This despite the fact that the DNA preparation of  Hershey and Chase contained maybe 20% protein, but that of Avery and colleagues contained less than 0.2% (Cobb,2014). A key paper in the controversy (by Mirksy) may be found here [pdf]

J.B.S Haldane stated (in 1942) that "the size of a gene is roughly that of a protein molecule and it is very probable that genes are proteins" (quoted by Fruton, p 430).
So the biochemists, it would seem, felt that proteins were the 'holy grail' of hereditary, and this attitude prevailed in some quarters long after Watson and Crick.  Morange (p 232) points out that Arthur Kornberg discovered DNA polymerase in 1958 and was (jointly) awarded the Nobel prize in 1959.  Watson and Crick, whose seminal paper on DNA was published in 1953, were not so honored until 1962.  That is an interesting, and perhaps very revealing, point.
And speaking of Nobel prizes, Avery did not get one (he died in 1955), perhaps in part due to the controversy with Mirsky (see Cobb).  Erwin Chargaff - he of the A/T and G/C ratios - (who accepted Avery's work as of fundamental at a very early stage) is quoted as saying that Avery's work deserved two Nobel prizes. And, of course, Chargaff himself did not get one, which he surely deserved. As well as the famous ratios, Chargaff was one of the first to suggest that "Differences in the proportions or the sequence of the several nucleotides forming the nucleic acid chain also could be responsible for specific effects" (see Cobb).
Fruton (pp 416-417) quotes Francis Crick as saying about the reception of the double helix. "The reaction of many biochemists, including Joseph Fruton, ranged from coolness to muted hostility. They had long considered the biology of the gene to be based on proteins, not nucleic acids, and thought the problem far too difficult to tackle in the immediate future. It did not help that the structure had been put forward by two people who were not obviously card-carrying biochemists".  Fruton (p 417) rejects this view and points out that in their classic text book (with Sofia Simmonds) the Watson and Crick structure for DNA was readily accepted, and concludes (p 417) that "I can only surmise that Francis, who showed me much kindness during my stay in Cambridge during 1962 - 1963, may have accepted too readily some idle gossip".
All this and more may be found not only in Fruton and Morange, but also in Judson's great book The Eight Day of Creation (which I don't have to hand at the moment).
Edit
After replying to David's comment, I dug out some further quotes by Sydney Brenner from  Biochemistry Strikes Back which are also (somewhat) relevant.
"In years gone by, biochemists viewed most of the rest of biology as a
descriptive science and from the even loftier standpoint of physics,
Rutherford dismissed it as stamp collecting.
The early days of molecular biology were marked by what seemed to
many to be an arrogant cleavage of the new science from biochemistry.
People like myself, whose application for admission to the Cambridge
Department of Biochemistry was ignored and who did not even receive the
attention of a rejection letter, often expressed exaggerated
views of our relationship to biochemistry. However, out argument
was not concerned with the methods of biochemistry but only with
their blindness in ignoring the new field of the chemistry
of information". (Brenner, 2000)
(He goes on to say: "I once made the remark that
two things disappeared in 1990: one was communism and the other
biochemistry and that only one should be allowed back.  Of course
biochemistry never really went away but continued to flourish in
the thousands of unread pages of biochemical journals") (Brenner, 2000) .
Some great references:
Cobb, M (2014) Oswald Avery, DNA, and the transformation of biology
Current Biology, Volume 24, pR55–R60 free pdf
Fruton, J. S. (1999) Proteins, Enzymes, Genes. The Interplay of Chemistry and Biology. Yale University Press.
Judson, H. F. (1996) The Eight Day of Creation. Makers of the Revolution in Biology (25th anniversary edn). Cold Spring Harbor Press.
Morange, Michel (1998) A History of Molecular Biology (translated by Matthew Cobb).  Harvard University Press

A much more complete answer than my tentative contribution.


text:
Iron deficiency anemia
It is said that iron deficiency anemia is characterised by microcytic-hypochromic RBCs. I would like to ask how iron deficiency causes decrease in the volume of RBCs? If the volume is decreasing because of low hemoglobin, then why  does the concentration of hb too decreases causing hypochromic RBCs? Why don't they decrease in same pace?

@anongoodnurse please see the bold text in the question.

Still think it's a dupe (bolding didn't change anything.)

@anongoodnurse there question is just about size but I want to know if the size is decreasing since hb has less concentration then why do it's concentration too gets decreases in the new rbcs? Shouldn't the concentration be same since volume is decrased? So why don't they decrease with same pace?


text:
What is this spider I found in Idaho?

I live in Moscow, Idaho and saw this guy early in the morning last week. It was about quarter sized if I recall. I've never seen one before and was in a hurry so I couldn't get a better picture, sorry.

Looks like female mouse spider. But "Fangs" missing!

This looks like a black trapdoor spider (I'm guessing male by the size of the abdomen), check out the photos on the page I've linked below and see what you think - and this is a pretty good picture, usually the photos friends send me are far more blurry!
http://www.spiderzrule.com/trapdoor1.htm


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Could a man be proved positive for a pregnancy test?
From the question: Could a man be proved positive for a pregnancy test?. I don't mean if a man could be pregnant but if he runs a pregnancy test, it is possible for it to come out positive?

I agree the responses that beta-hCG is produced by both ovaries and testes. Males with testicular cancer can have elevated hCG levels, which could give a positive response with a pregnancy testing strip.

Pregnancy test, just like any test, has some non-zero false positive rate. So yes, of course a test could be positive when a man pees on it.
Pregnancy tests work by detecting the presence of a hormone called Beta-HCG. This hormone is produced by both genders but is produced in much higher dose during early pregnancy. Teenagers also produce a relatively high dose of Beta-HCG which can eventually inflate the false positive rate.
It just so happen that tumours from a particular type of testicular cancer also excrete Beta-HCG (see this blog post from the American Cancer Society). If your question arises from a personal experience, then I would strongly recommend that you talk about it with your doctor.

Yes it is possible. Pregnancy tests detect human chorionic gonadotropin (hCG), which in a healthy male can be produced by the pituitary gland. hCG consists of two subunits and the urine tests target a metabolite of the beta subunit. The levels of hCG in healthy adult males are below the sensitivity of pregnancy tests, they are similar to the hCG levels in non-pregnant adult females.
A postive test from a male may indicate a pathology that is elevating hCG. I know that hCG elevates during puberty but I am not sure whether the rise is sufficient to cause a positive pregnancy test.


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What are the main differences between tubers and taproots?
From reading accessible information about tubers and taproots I recognize that the main differences between tubers and taproots (as well as a fibrous root system) are:

Shape
Different nutrient synthesis: Tubers contain less complex sugars than taproots

A possible third difference
As one who prefer a vegan diet in general I read a lot about B12; in many places (for example) Wikipedia, something like this was written:

In the past, humans got Vitamin B12 from eating the roots of "short plants" that absorbed
  the vitamin from bacteria which produced it near to their roots.

This led me to assume that either tubers or taproots (as well as a fibrous root system) have Vitamin B12 absorption by dedicated receptors and if one has it and the other doesn't here is yet another difference.
An interesting side note: Tubers are always under soil while roots in general, aren't necessarily; as with aerial roots.
My question
What are the main differences between tubers and taproots?

Please edit your question to clarify what type of tuber you are interested in since the answer will vary significantly for stem tubers (e.g. potatoes) vs. root tubers (e.g. sweet potatoes). Also note that different sources will use "tuber" differently — in my experience it was used exclusive for underground shoots that served as storage organs. It would also make your questions more useful if you would add in references and links for your information sources.

@tyersome I didn't no about the difference; I thought there is only one general type of tubers. I don't have time now to deepen in the difference between the two kinds  --- if it instills closing the question; so be it.

I don't think you have to worry about it being closed, so take your time. Depending on what you decide your question is I may even be able to give you an answer.

When you do get around to editing your question, remember that even structurally related (e.g. stem) tubers can be found in multiple different plant families. This suggests that even structurally related tubers won't necessarily have much in common other than their homology (e.g. being derived from stems). That means that if you want a biochemical answer your question may need to be narrowed down to a comparison within in a specific plant family to be answerable ...

@tyersome please review the "a possible third difference chapter"; I think what I wrote is enough to understand what is my problem in understanding the difference.

They are actually completely different plant parts: a taproot is the central root of a taproot-system plant while a tuber is an engorged modified underground stem called a rhizome.

A morphological and functional difference between rhizomes and roots are that rhizomes (being modified stems) have nodes, while roots never do.

Note: a node = the location on a plant stem where buds (leaves, flowers, stem branches) initiate

According to "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001)1:

Taproot. The main root axis from which smaller root branches arise; a root system with a main root axis and smaller branches...Figure 1273

Root. The portion of the plant axis lacking nodes and leaves and usually found below ground.

Compared to...

Tuber. The thickened portion of a rhizome bearing nodes and buds; underground stem modified for food storage. Figure 1366

Rhizome. A horizontal underground stem. Figure 1052

See here for a photo of a potato plant showing a young tuber and an older tuber growing on the end of a rhizome.
According to here:

Tubers-are swollen regions of stems that store food for subsequent growth. The potato is an example. It is a stem because it has many nodes called eyes with spaces between eyes known as internodes. Potato tubers develop at the end of swollen underground stem structures, rhizomes.

Eyes of potatoes are really axillary buds which contain several small buds at each site. These buds can expand to form shoots which grow on to make whole plants.

You can explore histologic, anatomic, and physiologic differences of stems vs roots more generally to understand broader differences between the two plant parts.

Examples:

Proença & Sajo (2008)2 discuss root and rhizome anatomy in select bromeliads.

Figure 1 from Hernán et al. (2014) shows how the vascular and various tissue layers can differ quite a bit between roots and rhizomes on the same plant.

Notes:

Some structures characteristics of roots (e.g., casparian strips) can also occur in rhizomes. (E.g., see Lersten 19974.

Unlike potatoes (which are tubers), sweet potatoes (Ipomoea batatas) are actually a modified root called tuberous roots

Works Cited:
1 Harris, J.G. and Harris, M.W., 1994. Plant identification terminology: an illustrated glossary (No. QK9 H37 2001). Utah: Spring Lake Publishing.
2 Proença, S.L. and Sajo, M.D.G., 2008. Rhizome and root anatomy of 14 species of Bromeliaceae. Rodriguésia, 59(1), pp.113-128.
3 Hernán, G., Varela, B.G., Fortunato, R.H. and Wagner, M.L., 2014. Pharmacobotany of two Valeriana species (Valerianaceae) of Argentinian Patagonia known as “Ñancolahuen”. Lat Am J Pharm, 33(6), pp.891-6.
4 Lersten, N.R., 1997. Occurrence of endodermis with a casparian strip in stem and leaf. The Botanical Review, 63(3), pp.265-272.

Hello, I admit that I tried to read the answer twice but in both cases felt a bit confused; I suggest, and of course, you are welcome to reject the suggestion (no pun will be taken) to review the answer and contemplate how to maybe simplify it or ordering it a bit more so it will be more accessible for non biologists like myself.


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Mechanistically, how does calcium chloride aid in bacterial transformation?
I am looking to get more information about the mechanism of the $CaCl_2$ in the bacterial transformation. I read online about the topic but I didn't found any reverent information on the topic, I don't have access to most of the scientific publications. However, I found this website. According to this website, there is a lot of theory about the mechanism of calcium chloride in the bacterial transformation. Would it be possible to get a short scientific referenced explanation about the topic and I can or cannot be related to heat shocks?

Frankly, the mechanism is not known even now.

Duplicate of http://biology.stackexchange.com/q/50591/3340 but the other question is also unanswered.


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What is meant by `individuals do not evolve, populations do`?
My university professor stated that "individuals do not evolve, populations do". But aren't populations made up of individuals? That's like saying when a compound changes in stability, none of the elements' properties change. If someone could clear this up, that would be great.

If you pick pebbles of different colours, and then throw away all the light ones, is it the pebbles or your collection that have changed colour?

Populations are made up of individuals, but you have to remember that the individuals in the population now ("after the evolution happened") are different from the individuals in the population then ("before the evolution happened").

Or in simple terms evolution is an emergent characteristic, A single individual can no more evolve than a single number by itself can undergo addition or a single car can be called gridlock traffic.

The statement individuals do not evolve, populations do is rooted in the (classical population genetic) definition of evolution. Here is this definition:

Evolution is a change of allele frequency through time in a population

Evolution is defined for a population, it is not defined for an individual. And it makes intuitive sense once you get more used to how evolution works. For example, the so-called fundamental principle of natural selection states that at any given time, the rate of increase in the population mean fitness is exactly equal to the variance in fitness.
Indeed, evolution is all about phenotypic and genetic variance (for fitness or other phenotypic traits) and without a population to observe, there is no variance. It is within this framework that people say individuals do not evolve, populations do but you are correct that as populations evolve its constituents (the individuals) changes. The sentence has the advantage to reinforce the concept that evolution happens at the level of the population.

As an ecologist I would say that evolution is a bit more than the genetic definition of changes in allele frequency. It is the natural selection that occurs on these differences, were less adapted individuals produce less offspring on average. And in that sense, evolution does happen to individuals: they die or fail to reproduce. But the effect of the adaption occurs in the next generations, at the population level.

The sentence individuals do not evolve, populations do is more of a catchy phrase that force an intuition that a fact. By definition, NS is a fitness differential in the population. While the fitness are properties of individuals, fitness variation among individuals is a property of a population. Similar notion apply to any other evolutionary forces. If you do a tiny bit of modelling in evolutionary biology, you'll realize that you will always use population-level variables (variables that vary among individuals). It is with this in mind that the quote makes sense.

Evolution itself is a term that describes populations changing over time.
As Remi.b pointed out, if you take evolution to be genetic changes in a population over time, then it doesn't make sense for an individual to evolve. Evolution can only occur as genetic changes are inherited from parents to their offspring.
A given individual in a population can be subject to natural selection, but the individual itself cannot 'evolve' in the biological sense of the word. They can only contribute to the evolution of a population by affecting the allele frequencies in that population.
As an analogy,
The evolution of a population can be thought of as a motion picture of that population.
At any given moment, the genetic structure of a population can be thought of as a screenshot, and one person (or organism) can be thought of as a pixel.
Evolution is like watching a video of a population change through time.
So you might say:
"pixels do not play, videos do".

Actually, this does answer the question. If you think it's a bad answer, you can downvote it.

Evolution is about children differing from their parents. You are not identical to your parents.

Your cells' DNA does change (a little, through new random mutations from time to time, most of it being repaired but not always correctly), but incoherently through cells, and these mutations are not transmissible if they are not happening in your gametes (sex cells).
Non-lethal changes in your gametes are transmitted. Besides, errors in chromosome duplication is a way more efficient and fast way of evolving (mixing sentences makes sense more easily than mixing letters).

Downvoters, please justify.

I don't really see how your answer specifically answers the question. You talk a little bit about the mechanical origin of mutations but it does not quite relate to the core of the question. (I was not the one down voting btw but I kinda agree with the down vote).

because all the point is about :

many cells inheriting mutation of one single parent cell vs many cells mutating incoherently
mutation transmitted vs not transmitted
change by raw mutations vs change by replication error


text:
Are there any examples of viruses that have powered motion or do they all rely on passive diffusion?
Swimming, or any locomotion will presumably require energy which will in turn require metabolism which viruses lack supposedly.
Are they general able to direct their movement in any manner (e.g like sailing) or are they strictly limited to Brownian-like motion? If not, are there any exceptional examples that indeed can control their motion?

Click bait title ("can viruses swim") won't attract the people that know an answer IMO (feel free to roll back). I came here to close the question, but it's actually a reasonable and interesting question! Unfortunately, there is already a well answered duplicate.


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What is an appropriate measure of determination in genetic studies?
Main Question
What is an appropriate measure of determination in genetic studies?
I used to think that $R^2$ was such a measure, but I'm no longer so sure. Specifically, it seems that $R^2$ undermeasures low determination and overmeasures high determination.
The reason for my doubt in $R^2$ comes from the following simulation.
Simple model
For simplicity, let us assume that a characteristic such as height (weight, Intelligence Quotient, Autism Quotient, etc.) of an individual is inherited from a mother and a father in the following fashion:
(fathersHeight * fathersInfluence + mothersHeight * (1 - fathersInfluence))/2,
where fathersInfluence is a constant between 0 and 1.
To give a specific example, if mother is 170 cm and father is 190 cm, and fathersInfluence is 0.5 then we know that their child will be exactly 180 cm.
Let us further assume that we can only measure the characteristic of any father and any son. We can not measure the characteristic of any mother.
Let us say that we'll try to predict son's height from father's height using good old linear regression, and report how much of son's height is determined from father's height. This can be done easily enough in python
_, _, r_value, _, _ = scipy.stats.linregress(fathers, sons)
Entire simulation can be wrapped up into the following python function:
def sonsHeight(sampleSize, fathersInfluence=0.5):
    # loc = mean
    # scale = standard deviation
    fathers = scipy.stats.norm.rvs(loc=170, scale=10, size=sampleSize)
    mothers = scipy.stats.norm.rvs(loc=170, scale=10, size=sampleSize)

    def weightedAvg(fathersHeight, mothersHeight):
        return (fathersHeight * fathersInfluence + mothersHeight * (1 - fathersInfluence))/2

    sons = [weightedAvg(father, mother) for father, mother in zip(fathers, mothers)]

    _, _, r_value, _, _ = scipy.stats.linregress(fathers, sons)
    return r_value ** 2

If we take fathersInfluence = 0.5 I would expect that any successful measure of determination would report that father's height determines son's height in 50%. $R^2$ passes this check, running the simulation with 1 million sons and fathers gives:
>>> size = 1000000
>>> print(sonsHeight(size, fathersInfluence=0.5))
>>> 0.500071151111

which seems reassuring. However, the values of $R^2$ for fathersInfluence any different than 0.5, seems to converge in probability to unexpected values. In fact running the experiment 101 times, for values of fathersInfluence from 0 to 1 in steps of 0.01 we get the following nice curve, which reassuringly passes close to $(0, 0)$ and $(1, 1)$, but surprisingly is not a straight line!

It becomes more disturbing though when particular values of $R^2$ are looked at, especially for fathersInfluence close to 0 or close to 1 (all $R^2$ come from taking a sample of 1 million).
In particular, for small values of fathersInfluence, say
$0.01$, $0.02$, $0.03$
the values of $R^2$ look close to
$0.01^2$, $0.02^2$, $0.03^2$.
Even for fathersInfluence of $0.1$ the value of $R^2$ is scarcely above $1\%$!
fathersInfluence, R^2
0.01, 7.3243188318051775e-05
0.02, 0.00042435668897930067
0.03, 0.00097257546851807486
..., ...
0.1, 0.012287962714812851
..., ...
0.97, 0.99904501126494283
0.98, 0.9995837493389228
0.99, 0.99989808360606525

Questions

Is there a measure of determination, which plotted against fathersInfluence would give me a nice straight line passing through $(0, 0)$, $(1/2, 1/2)$ and $(1, 1)$?
Would such measure be desirable?
What other measures of determination can be used, especially when the determination is low?

Remarks
I realize that the presented model of how genetics works is probably too simplistic and perhaps not useful as stated. However, I believe it resembles a good model for genetics in several aspects:

We have a thing that we can measure (e.g. gene expression level) and are observing as random noise important things we can't measure (environmental factors).
The independent variable (gene expression level) may influence the dependent variable (height, IQ, etc) only slightly.

All the code used to run this simulation can be accessed on github.

fathersHeight * fathersInfluence + mothersHeight * (1 -
  fathersInfluence))/2

is a terrible model for genetics. It says that the genetic contributions of the two parents are exactly anti-correleated. In fact they are essentially independent. I think what you are looking for is the notion of heritability.

The model is not anti-correlated, becasue fathersInfluence is a real number in the interval $[0, 1]$ and each parent's trait is positively correlated with the offspring's trait.

Your model says that the larger the fathers's influence, the smaller the mother's influence. Genetics only rarely works that way. You may be thinking some sort of  dominance model for a single locus, but height is a complex trait involving many genes. If dad contributes a height enhancing version of gene A, and mom contributes a height enhancing version of gene B, the contributions of the two genes will typically be additive but independent of each other. I urge you to read the Wiki article I linked too to see the basics of a real genetic model.

Thanks, I certainly will study heredity in some good detail. I perhaps haven't put across my point very clearly. mothersHeight is meant to be pretty much anything we can't measure (environmental factors, and other factors outside of our study). fathersHeight is the thing we can measure (expression level of a particular gene). fathersHeight is obviously going to have very small influence on the total outcome of the characteristic (most genes do in the end!), in the range of 1-2%. The point I'm raising is that R^2 will undermeasure this influence by a factor of ~ 100 for the 1% influence

It is very possible (and expected!), and I will definitely check it, that heredity doesn't suffer from this problem.


text:
Does any organism use both photosynthesis and respiration?
Chlorophyll and hemoglobin are very similar molecules, as far as I understand. The important difference being one using an iron atom and the other a magnesium atom. Do any organisms use both to get energy from both oxygen and solar rays? If not, is there any good explanation of why?
And do organisms that use chemosynthesis also use macro molecules similar to chlorophyll and hemoglobin?

Plants actually DO respiration and have mitochondria to do it for them as well. It's more or less the same respiratory chain with oxygen as terminal electron acceptor. Hemoglobin is a transport molecule for oxygen that helps distributing the oxygen to all tissues in our bodies. Plants do not really need that as they produce the oxygen on the fly.

Related question on [worldbuilding.SE] (of all places!): Why aren't animals photosynthetic?

Salamander is photosynthetic vertebrate

Also see (on Worldbuilding) : Can a plant evolve to give off CO2?

@AlexDeLarge Well, they don't need hemoglobin because they use diffusion. Pretty much all the important stuff is close to the "body" surface. Don't forget that plants don't produce oxygen in the night - that's when they drain oxygen from air and release carbon dioxide.

Are you asking about "respiration" or "haemoglobin"? The answers will be very different.

I think you have the wrong idea about this site. You have asked a question. If you want a good answer then you need to engage and clarify ambiguities in that question. The question everyone has answered is "Does any organism use both photosynthesis and respiration?". But you might be trying to ask something like "Do any plants use haemoglobin?" or "Do any animals use chlorophyll?".

It seems that the answer by Brian is the one you were looking for.

Besides the unicellular organisms cited by other answers (and the fact that plants actually do respiration), there are some animals who are able to get, although indirectly, energy from photosynthesis through symbiosis with photosynthesizing organisms. You can try the spotted salamander Ambystoma maculatum:

The spotted salamander is similar to the sea-slug [another of these animals] in that in order to be partially photosynthetic, it maintains a symbiotic relationship with algae cells. While it has long been known that a relationship existed between the salamander and the algae, it was presumed to be a relationship in which both organisms worked separately. However, when researcher Ryan Kerney was studying a batch of spotted salamander embryos, he found a bright green color coming from inside their cells.
The chloroplasts were found near the mitochondria within the salamander’s cells, meaning that the mitochondria were likely directly consuming the oxygen and carbohydrates that are created through photosynthesis*. The most amazing part about this relationship is that all vertebrates have strong immune systems that tend to destroy any foreign material found within their cells. Although the reason for this is unknown, this makes the spotted salamander the first vertebrates to be discovered to have the ability to photosynthesize.

And according to its wikipedia page:

Eggs of A. maculatum can have a symbiotic relationship with a green alga, Oophila amblystomatis. Jelly coating prevents the eggs from drying out, but it inhibits oxygen diffusion (required for embryo development). The Oophila alga photosynthesizes and produces oxygen in the jelly. The developing salamander thus metabolizes the oxygen, producing carbon dioxide (which then the alga consumes). Photosynthetic algae are present within the somatic and possibly the germ cells of the salamander.

It should be noted that this animal is not able to directly perform photosynthesis, but it's still able to get energy from the sun and, being a vertebrate (and not a fish from the family Channichthyidae), it has hemoglobin.
Remember that the most plausible theory for the emergence of chloroplasts, the photosynthesizing organelle, in eukaryotes (aka organisms with cellular nucleus) lifeforms is through the addition of an external organism (probably a cyanobacteria) to the cell, since chloroplasts (and mitochondrias) have their own separated DNA:

Mitochondria and chloroplasts likely evolved from engulfed prokaryotes that once lived as independent organisms. At some point, a eukaryotic cell engulfed an aerobic prokaryote, which then formed an endosymbiotic relationship with the host eukaryote, gradually developing into a mitochondrion. Eukaryotic cells containing mitochondria then engulfed photosynthetic prokaryotes, which evolved to become specialized chloroplast organelles

tl;dr: Yes, all plants breathe.—
I'm not sure whether I understand the question correctly; because all plants use respiration! Some of the organic high-energy substances produced by photosynthesis are later "burnt" to produce energy in the same "respiration" process used by animals, producing CO2.
The difference to animals is that green plants synthesize their carbs (including the ones they burn for energy), fat and proteins from thin air, so to speak, while animals must eat them.
These antithetic processes, photosynthesis and respiration, are often tied to the day-night cycle. When light is available, the plants-only photosynthesis dominates so that the plant consumes CO2 and emits oxygen; at night, when photosynthesis becomes impossible, the usual common-place respiration causes the plant to consume oxygen and emit CO2, just like animals.
Only as long as the plant is growing, this cycle is tilted towards photosynthesis so that more oxygen is emitted than absorbed: the excess carbon and hydrogen is sequestered in the plant's growing biomass. But when the plant dies, all this high-energy biomass is burnt by animals and micro-organisms, making the overall balance carbon- and oxygen-neutral.2
So how do plants breathe — or rather, exchange gases with the atmosphere in general — if they don't have lungs or gills? The key is the large surface area of typical plants with leaves. Seen in this light, a tree looks well-designed for filtering stuff out of the atmosphere. Consider these two images. The first one is a lobe of a human lung3. The second one is a tree... or is it?

I found John W. Kimball's page about gas exchange in plants accessible and full of interesting information. Central to our discussion are three facts:

A plant's living cells, including the ones in the stem, are never far from the surface.
The rate (or "speed") of respiration, i.e. oxidizing carbohydrates, is lower than in animals. (Plants do not perform physical labor with muscles and do not have a brain, which are the two main energy consumers in the human body.)
Photosynthesis happens mostly in the thin leaves.

Because of these factors — smaller amounts of gases per time over shorter distances — plants do not need high-volume, long-distance gas transport in the fashion most large animals do, with blood circulation. The gas travels between and through the cells as needed, guided and regulated by mechanisms detailed in Kimball's text. The fluid traveling through the stem provides (lots of) water to the leaves in the upward direction and nutrients to the living cells downward, but apparently does not carry (much) gas.
The Arbor Day Foundation has a nice page detailing a tree trunk's structure with information about each layer's function. (I didn't know that the cells in the heartwood — the inner part of the trunk — are dead and do not participate in the transport of nutrients or water.1)

Your question seems to be triggered by a perceived similarity between the molecule giving blood its red color, hemoglobin, and the molecule which gives plants their green color, chlorophyll.
True, both are organic molecules with metal atoms embedded, but they are quite different, even apart from their color. Hemoglobin is a protein with a fairly complex spatial structure; look at the image on the Wikipedia page. It weighs as much as 64,000 hydrogen atoms, i.e. it has a molar mass of about 64,000 g/mole. Chlorophyll is also an organic molecule, i.e. it has carbon chains and rings, but it is not a protein. (In living cells Chlorophyll molecules are embedded in a protein complex, arranging them to work together; that is a different thing.) It does not fold in space, partly because it is not as big. Its molar mass is only close to 900 g/mole, almost 80 times lighter than hemoglobin. A model of one variety can be found on its Wikipedia page, too.
The jobs the two molecules do also are fairly different, even though both have to do with oxygen.

Hemoglobin has a transport job. It binds oxygen efficiently. The spongy, blood-heavy lung tissue absorbs oxygen, which dissolves in the blood and is bound to the hemoglobin swimming around in it. There is a lot of hemoglobin in our blood, increasing the blood's capacity for oxygen transport by a factor of 70 compared to just dissolving oxygen in water (and it dissolves actually quite well in water!). Thus, hemoglobin does not synthesize anything but simply transports gases, mainly oxygen, through the body to where they are needed. Some athletes dope by collecting their own hemoglobin and re-injecting it before a competition, thus increasing oxygen supply for their muscles.
Chlorophyll does not transport molecules but instead does some heavy chemical lifting. It absorbs light to harvest its energy through the mechanism called photosynthesis. The details are fairly complicated, but the big picture is not: It is a reversal of respiration, or chemically a reversal of oxidation, called reduction: Oxygen is separated from the hydrogen in H2O and carbon in CO2 and given off to the air. Doing this consumes the same amount of energy which is released during oxidation (be it by fire or by metabolization in the plant). The emerging oxygen-poor(er) compounds can be oxidized later elsewhere to release that energy, or can be used as building blocks for new cells.

1 My girlfriend thinks I'm stupid not to know that ;-).
2 Unless it is buried and taken out of the biosphere, fossilizing to peat and eventually coal, tar and mineral oil. Then the net CO2 balance of a plant's life is indeed negative, i.e. the plant has removed CO2 from the atmosphere; until somebody excavates the fossil fuels, re-injects them into the biosphere and and restores former CO2 levels and all the tropical climate which made the old jungles grow so well.
3 From wikipedia, https://upload.wikimedia.org/wikipedia/commons/a/a1/Lungs_diagram_detailed.svg. By Patrick J. Lynch, medical illustrator, via Wikimedia Commons. The "tree" is actually the same lobe, rotated and colored.

This seems more complicated than I imagined.

Well, or it's easier... the basic cellular chemistry is the same between plants and animals (oxidize combustibles to get energy for, well, living); just where the combustibles come from differs.

Tangentially related is the fact that a forest which is in balance (doesn't shrink or grow) does not produce any net oxygen over the course of a year... a common misconception ("hey, we need the forests for our oxygen" -- nope, bury them deep enough and you are fine, at least oxygen-wise). A growing tree does produce net oxygen, but when it eventually falls and gets eaten by the buggy bugs all the nice carbon gets burned back to CO2, using up all the nice oxygen...

@LocalFluff Why do you think plants produce sugars and fats? With the exception of fruit, it's not meant for animal consumption. They're doing it for themselves - for storage and (very slow) metabolism. Note how much we had to breed plants to make them truly useful for us - modern wheat is estimated to have at least ten times more yield (with some estimates going up to a hundred times more) than natural wheat. Only fruit is "designed" to be eaten, as a mechanism to spread seeds.

Chlorophyll and hemoglobin do have structure in common: the chlorin ring in chlorophyll is very similar to the heme ring in hemoglobin. But that's because they both need to ligate a metal atom.  What they do with the assistance of the metal atom is very different.  And there are probably hundreds of other enzymes that use similar rings for the same reason.

Indeed several organisms can do both.
Another good example following the answer from Prince of an organism that can do both photosynthesis and respiration would be cyanobacteria.
Source:
Photosynthesis and
Respiration in
Cyanobacteria

I know this question is a little bit awkward, but how did you provide the source, I've tried to figure that out, but all I could do was to post the website fully and not in words like you did to my answer, that is, how you changed the website I posted into three simple words.

@Prince  [Cool text](complete link)  :)

@Prince You can press edit on my answer and see how the text is written behind, that's how I learned some of that stuff ;)

@Prince If you ever need hovertext, you can add it like this: [Text](link "hovertext")

@trichoplax I don't understand your description on how to do a hovertext. Can you post a site where hovertext was used so that I can check it out there, that is, by trying to edit the question or answer.

@Prince Hover over the "Photosynthesis and Respiration in Cyanobacteria" link in my answer, I've added it :)

@Dart Feld sorry, don't have edit privileges yet. Why not you insert a hover text and I'll check it out. Sorry for the inconvenience.

@Prince you don't have to edit - just hold your mouse pointer over the link in the answer and the hover text will appear.


text:
State of voltage gated sodium channels in depolarised potentials
Case 1
We learn in Physiology that during the depolarization phase in the membrane, more sodium channels tend to open as the membrane potential increases i.e., less negative. This is a kind of positive feedback which leads to the action potential and explains the threshold of depolarization that is required for action potential.
So in short, as the membrane potential becomes less negative sodium channels tend to open.
Case 2
On the other hand there is famous graph from Bertram Katzung, Susan Masters, Anthony Trevor-Basic and Clinical Pharmacology, Edition 12. which shows the dependence of the sodium channel function based on the membrane potential preceding the stimulus.

To quote,

The fraction of sodium channels available for opening in response to a stimulus is determined by the membrane potential immediately preceding the stimulus. The decrease in the fraction available when the resting potential is depolarized in the absence of a drug (control curve) results from the voltage-dependent closure of h gates in the channels.

Both these cases look pretty contraindicating to me. But I attempted to explain this by the three stages of the Na+ channel.
Case 1 - may be addressing the transition from closed to open channels, i.e., opening of the m gate. (I'm just hypothesizing here so correct me if wrong)
Case 2 - as mentioned in the book, talks of closing of the h gate leading to inactivated gates at higher membrane potentials.
Do case 1 and case 2 happen one after another? Are the voltage ranges for each different? Is my explanation for case 1 correct?


text:
Fauna in deep great lakes
A significant amount of research has gone into the fauna of the deep oceans, but not so much that I can find on the deep great lakes (specifically the North American Great Lakes).  I'm interested in seeing pictures and learning more about the types of fauna in these lakes.  Can anyone provide a reference to get me going?

Contrary to oceans, deep lakes are always isolated from other deep lakes by land. Therefore, one might expect different fauna in every lake, with possibly a lot of endemic species. So it may be hard to study deep lakes in general.
The ancient and deep lake Ohrid, in the former yugoslav republic of Macedonia, has been researched relatively well. Here's a reference which will get you started. Or search "lake ohrid fauna".


text:
Have humans finished evolving?
I thought that massive changes among organisms are over long periods of time. This is caused by, to my knowledge:

Evolutionary pressure
Natural/artificial selection
Mutations
Genetic drift

Will mutations be the only factor in human change? Will humans change at all over a long time?

Issue in your introduction

I thought that massive changes among organisms are over long periods of time.

Actually, some evolutionary events can happen on a very short time scale. A single mutation can have a massive impact on the phenotype of an individual (see for example Doebley 2004). If this new phenotype has much higher fitness, then the mutation might spread over the whole population in a matter of weeks (typically if the population is not too large, without barriers to gene flow and more importantly if the generation time is short).

This is caused by, to my knowledge:

Evolutionary pressure

Natural/artificial selection

Non-detrimental mutations

The term evolutionary pressure typically encompass natural and artificial selection, mutations (regardless of their mutational effect, that is regardless of whether they are beneficial or detrimental) and other processes that you don't mention (such as genetic drift for example; you have now edited your post to include drift).
Answer to your questions

Will mutations be the only factor in human change?

By "human change", I will assume you mean "human evolution". The answer is: no, mutations are not the only process that leads to human evolution. All standard evolutionary processes are at play in humans as they are in other species. You might want to have a look at the posts Human Evolution in Modern Times and How is evolution possible in contemporary humans?.

Will humans change at all over a long time?

Yes, humans are currently (and will continue to do so in the future) evolving. Again, you might want to have a look at the linked posts.
Want to know more?
Your questions are quite introductory and show a number of misunderstanding you have about evolution. I would recommend having a quick look at Understanding Evolution by UC Berkeley which is a very introductory course to evolutionary biology that is fast and easy to follow.

Great references and thanks for the correction

@Adamawesome4 My pleasure! I added a small comment on the very first sentence too.

I disagree that humans will continue to change over time - evolve, yes, of course! But as the population grows and travel increases, there is no Galapagos-style isolation; the human genome is "averaging out" and similar traits may eventually dominate the species. Additionally "survival of the fittest" has been heavily reduced due to modern medicine - how can traits be filtered out?

@Zxyrra You can't say humans won't change over time but they will evolve as evolution is defined as being a change over time. Potential absence of complete reproductive barrier does not change anything to the fact that all standard evolutionary pressures exist. Medicine does reduce selection pressure for sure but selection pressures still exist. Plenty of examples exist, just have a look at the linked posts. You should have a look at an intro course to evolutionary biology and to the posts I link in my answer.

In sexed organisms, evolution is largely due to errors during chromosome duplication, cutting/copying/pasting/swapping/shortening/duplicating full genes sections. It is a way more efficient and fast way to evolve, since mixing sentences have more chances to make sense than mixing letters.
Many fast local evolutions can be seen: for instance, Sickle-cell_disease is favored a lot in some part of Africa because it happens to protect against malaria. At the scale of a few centuries, human height is growing, women pelvis is shrinking, etc.  At the scale of a few millenniums, some human can digest milk while the others can't. The population at altitude got different adaptation to multiply the amount of red blood cells. etc.

You first paragraph is very misleading (or even wrong). You should come up with a citation to support that rate of evolution (are you referring to phenotypic evolution I would assume but that was left unclear in your answer) is mainly caused by recombination. In any way, linkage disequilibrium gets away pretty quickly and therefore this first paragraph makes little sense. For your second paragraph, you could just link to other posts (see my answer) which offer much more thorough explanations of the examples you mention.

This answer is flat-out wrong. Chromosome duplication usually causes severe health problems. Random mutation edits to human cells usually either breaks the cells, causes malfunctions, or produces oncogenes that either cause cancer or predispose the cell's lineage to become cancerous in the future. There's a ton of research out there and many lists of indels, point mutations, genetic fusions, translocations, and duplications (copy number mutations) associated with cancer.

The genes associated with people who have more surviving and reproducing children will be more prevalent in the future. If you live in a multicultural society where different ethnic groups have different amounts of children you can get a perception of how the humans in your country will evolve over time. Also if you live in a country where there is a huge influx of people who are genetically different from the people who already live there, that will have a serious impact on the short-term change. But basically, if you want to get a hunch of where humans are evolving where you live, you can have a look at the people producing offspring and try to find out if they are different somehow in their genetic composition compared to the population at large. If stupid people are having more children, people will be dumber, if taller people are having more children, people will be taller etc.


text:
How to determine the probability that a mutation is lost / fixed?
I have a question about how to determine the probability that a mutation is lost or fixed after 1 or 2 generations in population genetics.
Let's say we have a randomly mixing population, with N diploid individuals (N=5), and there is one mutation that appears. I know it should follow a binomial distribution, but I also heard it may follow a Poisson distribution... and all I feel like saying is that the probability to get fixed is the same as the frequency at time 0, which is 1/2N, or here 1/10.
Furthermore, how do you calculate the probability that it exists in 2 copies?

your question assumes that a mutation is something that is "broken" - might want to reword a bit

Thanks a lot for your reply ! It helps a lot. However, shouldn't we use 10 among 2, instead of 5 among 2 in the binomial calculation, as we're looking at alleles in a diploid population ?

@VanceLAlbaugh 'fixed' is a technical term in population genetics. It has nothing to do with a mutation being 'broken'. Fixation is when a mutation reproduces through a population until  essentially 100% of the population has the mutation. Loss is the opposite process, where a mutation disappears from a population. Fixation and loss can be entirely chance processes, or they can be driven by a selective advantage or disadvantage of the mutation.

@CharlesE.Grant excellent - thanks for clarifying... might want to edit question to clarify that - as users unfamiliar with that (like myself) clearly interpreted that differently

How to determine the probability that a mutation is lost / fixed?

The probability that a neutral mutation gets fixed after an infinite amount of time is equal to its frequency $p$ as you said. Therefore the probability of being lost is $1-p$. This post offers an explanation but there many ways to make the demonstration. You might want to have a look at any good book in population genetics for this demo. Here are book recommendations.

how do you calculate the probability that it exists in 2 copies?

A probability always depends on a priori. What are your a priori? Let's assume that we know that the allele frequency was $\frac{4}{10}$ in the previous time step.
Under the Wright-Fisher model the probability of having 2 copies in the next generation is given by the binomial distribution. Let $N=5$ and therefore $2N=10$ and let the frequency of the allele of interest be $\frac{4}{10}$, the probability of having two alleles in the next generation is ${10 \choose 2} \left(\frac{4}{10}\right)^2 \left(\frac{6}{10}\right)^8 ≈ 0.12$.
Under the Moran model this probability is zero. Moran's model is a birth-death  model (Markov model) and therefore transition between time steps can only add or subtract (or make no change) a single allele. You will note that the time step does not mean the same thing for the two models. Loss of heterozygosity is twice as fast under the Wright-Fisher model but this discussion is definitely not what you were asking for!

@user27813 Thanks for your comment. You are right, you said diploid population with $N=5$ and I considered a haploid population in my answer. It is fixed now.

If you know the probability of an individual surviving, both without & with the change, you can calculate the probability of the gene surviving. This isn't actually knowable, so the details of the model used to estimate seem inescapably relevant to any answer to me. Am I missing something, here?

@TheNate I don't really understand your comment. Typically, what do you mean by "the change". These models are models of genetic drift, they assume all individuals have the same fitness. The probability of an individual to produce k offspring is given by a poisson distribution with rate \lambda=1.

"The change" I meant was the mutation of interest. I understand/understood what the models represent; you answered the question. That set of (apparently customary?) simplifying assumptions is exactly what I was missing.