text:
Does Mn always exist in Photosystem II?
I had the impression that PSII (photosystem II) always has four Manganese atoms
(4 Mn). Is there any reason that these atoms are needed?
Is Mn or Fe also present in bacteria LH1 or LH2?

I'm having some difficulty understanding your question... can you write everything out and not use abbreviations? This will help. Thanks!

I have wrote EVERYTHING out i.e. PSII is photosystem II, and Manganese is Mn.....what else? LH is light harvesting

Mn Fe are standard chemical symbols while PS2 is also standard abbreviation. Please stop these politics. Thanks.

I made some edits to your title because the previous isn't in the correct english syntax

I guess you are referring to Magnesium and not Manganese. Are you sure you are talking about manganese?

Thanks. I am not a native speaker. Therefore, my English surely have some problem. But manganese....I guess was copied from a paper....But what is really there?

Briefest answer; Yes, Manganese (Mn) atoms are part of Water splitting complex or OEC

Is Fe also part of Water splitting complex or OEC ?

Could this Mn be replaced by other atoms like Zn or Fe

Manganese is part of the oxygen-evolving complex and is essentiell for the oxidation of the water to generate electrons, protons and oxygen. This is done by changing the oxidation state of the mangane from +2 to +4, as shown in the figure (from here):

These manganese atoms are the center of the reaction - important here are the different oxidation states they can take, other examples are copper (in tyrosinase for example) or iron (hemoglobin) which are also present in the active center of enzymes.
For more information see references 1 and 2.
Anoxygenic bacterial photosynthesis also needs metal ions in the bacteriochlorophyll, this is magnesium (as in the chlorophyll of green plants), the light harvesting complexes contain iron-sulphur complexes.
For a general overview see reference 3, for more detail on the reaction centers and their evolution, see reference 4.
References:

Where water is oxidized to dioxygen: structure of the photosynthetic
Mn4Ca cluster.
Reduction-induced inhibition and Mn(II) release from the photosystem
II oxygen-evolving complex by hydroquinone or NH2OH are consistent
with a Mn(III)/Mn(III)/Mn(IV)/Mn(IV) oxidation state for the
dark-adapted enzyme.
Bacterial Photosynthesis
Reaction centres: the structure and evolution of biological solar
power.

There seems to have some LH1 or LH2 do not need such atoms. I am not sure whether PS I or PS II...

any physical reason why these atoms must be there? (for instance they need a spin or entropy...)

@latra Besides having the function as electron acceptors/donors? Not that I know of.

So, it is biochemistry instead of biophysics. The picture above came from a biophysics course note.

@latra If you want to see the real flow of the electrons on the molecular level, this is mixed biochemistry-biophysics.

Yes, I indeed want to see the real flow of ....photon...perhaps also electron...But is it possible?

what is wrong with the fourth paper ?  http://www.sciencedirect.com/science/article/pii/S0968000401020345   i got only junk codes

@latra I don't know, it worked. I have updated this to a different source, which should be ok.

no...the same...the title, the abstract, the figure caption and the section heading...are all in Greek letters........

You said in the above that Mn is the center of reaction. I think you are talking about type I RC. Only type I RC contains Mn.


text:
Why can't we half-close our eyes?
Can we half-close our eyes such that they don't vibrate?
If not, then why we are unable to half-close our eyes properly?
Alternatively, why isn't it possible to keep the upper eyelid close to the lower eyelid without it vibrating?

The motion of the eyelid is driven by the levator palpebrae superioris, i.e. elevating muscle of upper eyelid, and it can be positioned to the intermediate, half-closed positions. At least I can do it.
Yes, this muscle tends to shake or oscillate simply because it's a very weak muscle. It's similar with the muscles controlling the motion of the little finger (or ring finger). Vibration and "noise" is present in all muscles but the stronger muscle you have, the more accurately the random motion is averaged out.
If you connected $N$ eyelid muscles so that they move in unison, the noisy vibrations would be reduced by the factor of $\frac{1}{\sqrt{N}}$. This is the well-known scaling of the statistical errors in physics etc.
I would think that this question was totally appropriate at the Physics Stack Exchange.

What is the number N in this context? A muscle, even a small one as that of the eyelid, contains countless number of muscle fibers, and even more myofibrils ...

Roland, it isn't supposed to matter how much $N$ is. You may take $N$ to be the number of fibers. The point is that what matters is the ratio $N_1/N_2$ between two situations. The eyelid muscle is a lot thinner ($N_1/N_2$ is large) than the biceps so the relative oscillations are square root of lot times more pronounced in eyelids. The oscillations only appear in the middle because the eyelids are "supported" in both extreme positions. When a person with Parkinson's pushes his hand on the table, it cannot vibrate up and down...

That doesn't sound quite right to me. For very large N1, the statistical error (and therefore muscle tremor) should vanish, and then it's irrelevant if some other N2 is even larger than N1. So the 1/root(N) law should be important only when N is quite small. I would guess that the key factor is how many neurons innervate the muscle; very small muscles have few motor neurons, which makes for a small N. Can you elaborate and provide references?

Dear Roland, the number of neurons innervating an elementary muscle fiber was assumed to be the same while comparing the quivers of $N_1$ and $N_2$ nerves. It's plausible that the source of the oscillations is the small number of neurons around the muscles, not the thin mechanical part of the muscle. In that case, $N$ in my answer should be interpreted as the thickness of the nerves innervating the muscle. From a broader viewpoint, it's a detail. No, I don't have references, this was being answered as a physics problem which can be done even if no one else was solving it before.

I think this is not the cause, the muscle is already very much larger in terms of number of myosin bridges compared to the scale at which you'd expect oscillations of noticeable amplitude. And also, the motion is controlled by 2 muscles for the upper eyelid, and 1 for the lower but at a different angle than the levator.

Can you bring in some data on the expected amplitude of such oscillations?

The upper eyelid position is governed by two muscles (tarsus sup and  levator palpebrae sup) working against one another, but they are at a 90 degree angle:

See Wikipedia on tarsus.
When you are closing your eyelid, it is the tarsus that contracts and reduces its length. If you try to maintain the upper lid in a half-closed position, you need to counteract with the levator muscle. But because of the nearly 90 degree angle, a little force of the levator needs to be counterbalanced with a strong levator force, simply because of trigonometry:

You see above (upside down compared to eyelid muscles) that for a constant force of the levator (F, down), the force of the tarsus to the left and right need to be doubled when you go from 30 to 20 degree angle of the "eyelid". These variations grow even larger when the angle goes flatter, in fact, it is a $1/\tan \alpha$ singularity [EDIT]as $\alpha$ goes to zero[/EDIT]. Tough maths problem, and also tough control problem for your nerves!
And definitely, this question is very much physics!

Very interesting elaboration, thanks. But could you please be a little bit more specific which singularity appears near 30 or 20 degrees in tangent etc.? You surely don't dispute that tangent of 30 degrees is regular, finite, and of order one, do you?

@LubošMotl If $|F|=1$, then $|F_L|=|F_R|=1/(2 \tan \alpha)$. It is $1/\tan$ which is singular, as you well know.

Sorry, $\tan\alpha$ is singular for $\alpha=\pi/2$ or 90 degrees. None of your angles is 90 agrees, is it? Similarly, $1/\tan\alpha$ diverges for $\alpha=0$ but your $\alpha$ isn't zero. So there's nothing singular. Are you playing a shell game trying to sell an argument that obviously doesn't work or am I overlooking something?

OK, maybe this was unclear: we are looking for nearly closed eye, so nearly straight polyline joining $F_R$ and $F_L$, hence $\alpha$ small. I realise you have taken the angles in the diagrams as the only values considered, they are examples.

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text:
Is this formula describing the loss of unfixed genes from a population accurate?
In the 1954 science fiction novel Search the Sky by Frederick Pohl and Cyril M. Kornbluth, a formula is featured that "quantitatively describes the loss of unfixed genes from a population".
$$L_T=L_0 e^{-T/2N}$$

"A final word. There has been much loose talk among the troops about the slogan of the Joneses, which goes $L_T=L_0 e^{-T/2N}$. Some uninformed people actually believe it is an invocation which gives the Joneses supernatural power and invulnerability. It is not. It is merely an ancient and well-known formula in genetics which quantitatively describes the loss of unfixed genes from a population. By mouthing this formula, the Joneses are simply expressing in a compact way their ruthless determination that all genes except theirs shall disappear from the planet and the Joneses alone survive. In the formula $L_T$ means the number of genes after the lapse of $T$ years, $L_0$ means the original number of genes, $e$ means the base of the natural system of logarithms and $N$ means number of generations."

Is this formula indeed an accurate description?
Or was it made up by the authors? I find it suspicious that it contains two different measures of time, years and number of generations, while they seem related to me.

An earlier version of this question omitted the minus sign in the equation. I noticed it when finding it again on Google Books.

Honestly, you should really look at some scientific literature in this area. Do not judge it by speculation. If you can not find anything, then assume no.

@RadekMartinez - I assume that the point is to ask the experts, who might already know the right equation.

I also find this formula odd. Isn't the length of a generation generally fixed? And if so, shouldn't the number of generations in a given time be proportional to time, rendering T/N independent of time?

Number of generations would be proportional to number of years, but every species would have a different ratio. Since P & K were talking about only humans, that would be a constant. But it appears to be a more general formula with generation length independent of number of years. But you're right, It seems odd.

I have edited your title so readers have an idea what the formula relates to without having to read the question. Helps them and you. (Gentle hint for any future questions you ask.)

The expression is based on a real one, but missing a minus sign (EDIT: not anymore! See updated question), and the explanation is garbled. For the actual equation, see "eigenvalue effective population size" in, e.g., WJ Ewens, Mathematical Population Genetics. There should be a negative sign in the exponent: $L_T = L_0 e^{-T/2N}$. Note that you need this minus sign so that "genes" (actually heterozygosity) are lost with time rather than growing exponentially in number!
As for the errors in the explanation: $T$ should be measured in generations rather than years, and $N$ should be the number of individuals (or rather the "eigenvalue effective number") instead of the number of generations.

Oh yes, you are probably right! +1. So, the definition of the symbols were wrong (generation vs years), the meaning of the equation was wrong (loss of genes vs loss of heterozygosity) and the equation was wrong (minus sign missing). Wow, that's quite a distance from the original formulation!

I keep my answer for information purpose but the right answer is @DanielWeissman answer. It is made very clear once the OP noticed the missing minus sign.

I think this formula comes from nowhere. The supposed meaning of this formula is very unclear. As you said, it makes little sense to have two measures of time (in years and in generations) in the same equation.
Fixation of new alleles
I am not sure what is meant by gene loss. I would suppose, it refers to fixation of new alleles. Under the assumption that all mutations are neutral, then the probability of fixation of new alleles is $\frac{1}{2N}$, where $N$ is here the population size. If the neutral mutation rate is $\mu$, then the number of new mutations per generation is $2N\mu$ and therefore the rate of fixation of new alleles is $2N\mu\frac{1}{2N} = \mu$. Per consequence, after $t$ generations the number of new alleles $L_t$ is $L_t = L_0 + t \mu$ (assuming it makes sense to talk about the number of newly fixed allele at time $t=0$).
Loss of genes
Muller's ratchet (typically on the Y chromosome in mammals) does lead to systematic loss of genes. There are here a number of models and a final expression for the rate of loss of genes is not that easy.

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text:
The simplest organism that can learn?
What is the simplest organism that was observed to learn: change its behavior permanently in response to some event/stimuli in a way that this change persists even if the event does not happen again?

the real problem is defining  and testing learning.

Judging from the first source brought by Bryan Krause, the definition I had in mind was associative learning.

which may be possible for even a single celled organism. Bryan Krause provided a good link to possible associative learning in amoebae.

I don't know if it is definitively the simplest, but the simplest organism with a nervous system that has been studied extensively is probably C. elegans, which is definitely able to learn.
Some basic learning abilities have also been shown in amoebae.

References:

Ardiel, E. L., & Rankin, C. H. (2010). An elegant mind: learning and
memory in Caenorhabditis elegans. Learning & Memory, 17(4), 191-201.
Saigusa, T., Tero, A., Nakagaki, T., & Kuramoto, Y. (2008). Amoebae
anticipate periodic events. Physical review letters, 100(1), 018101.


text:
Is this a dust mite?
I dropped my phone onto the carpet and picked it up and saw this tiny mite crawling around on the screen.
It is too small to be a bed bug, but perhaps too big to be a dust mite (and doesn't look like the images I found).
Main image is an out of focus image with an iphone simtray for size comparison (the mite about 0.5mm).
The second picture from the left is the only one where I seemed to be able to get its head; all others it was moving away from my camera. I couldn't take any better photos so you'll need to click the image to see the mite in detail.
EDIT: I am in the UK

Dust mites are microscopic, and have 8 legs only.  You probably have a picture of a carpet beetle larva ('hairy').

Looks mite-like to me. Definitely doesn't look like any  carpet beetle larvae I've ever seen.  It doesn't  have  clear segments like the  larvae typical  of  beetle species...

@theforestecologist - I defer to your superior knowledge of insects. Carpet larvae was the only thing I could think of. But they certainly aren't the typical dust mite.


text:
In bacterial conjugation, how do F+/F- cells detect each other?
I've just learnt about bacterial conjugation and while it is interesting info about early sexual activity in microbes, one aspect confuses me and doesnt seem to be mentioned in the material I read:
How do the donor/recipient pairs find each other?
While cells in a culture all can have physical contact as they move about, either the F+ cell inserts pili into various cells looking for some chemical stimulus or physical contact with a F- cell provides some data that lets it know it has touched a cell with which it can now perform conjugation.

F+ cells have mechanisms in place that inhibit them from making contacting with other F+ cells, therefore, a F plasmid cannot be transferred from F+ to F+. Source: https://www.ncbi.nlm.nih.gov/books/NBK21351/


text:
High frequency tone/ringing in movies/music and its effects
I was watching a horror movie and I noticed during a scene that there was a high pitched noise playing in the background. It had been playing for a while before I noticed it and when I took notice it started to irritate my ears, however this isn't my concern. I noticed that while this noise played during the scene I was in a trance-like state almost felt like I was hypnotized, so my question is can these high pitched sounds be used put the viewer/listener into a trance-like state or hypnotize them and if so are there any scientific studies that prove or debunk my theory?

Firstly, my diagnosis: "nocebo effect". Secondly, this is probably entering the psychology/social sciences(/economics?) domain... See if this video hurts too: https://www.youtube.com/watch?v=O2hO4_UEe-4

Thank you for your input i didnt think id ever get any answers

Noo don't think like that! I am not saying you will not get any answers, I am saying, that if you modify the tags, it will very much likely boost your chances of getting those answers :). We need people like you, and the correct Stack Exchange site: http://cogsci.stackexchange.com/, or the correct tags will open your question up to different experts (see: @NormalHuman, believes in your question too).

I understand what you meant. I just didnt expect to get a reply since i posted this well over a month ago

Still I dont think it was a nocebo effect as I didnt feel I was in harms way at any point. It was more like i was being forced or tricked into focusing on what was on the screen the sound drew my in and before I knew it I was as i said earlier in a trance like state I was just kinda blank if that makes sense?

Hmm, I honestly do not know, as in I think I am not the expert here? Let's grab some popcorn and see who answers it fastest :)

I find that certain music puts me in a state where I fall out of consciousness and everthing around me just doesnt exist for a time so i wanted to know if this is something that can be intentionally induced through sound

Thanks for replying atleast this is something that is very intriguing to me as I would like to utilise this if a technique exists


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Why is traditional rank based taxomomy considered by some as logically inconsistent with phylogenetic knowledge?
Following is from wikpedia:

Under the traditional nomenclature codes, such as the International
  Code of Zoological Nomenclature and the International Code of
  Nomenclature for algae, fungi, and plants, taxa that are not
  explicitly associated with a rank cannot be formally named, because
  the application of a name to a taxon is based on both a type and a
  rank. The requirement for a rank is a major difference between
  traditional and phylogenetic nomenclature. It has several
  consequences: it limits the number of nested levels at which names can
  be applied; it causes the endings of names to change if a group has
  its rank changed, even if it has precisely the same members (i.e. the
  same circumscription); and it is logically inconsistent with all taxa
  being monophyletic.
Especially in recent decades (due to advances in phylogenetics),
  taxonomists have named many "nested" taxa (i.e. taxa which are
  contained inside other taxa). No system of nomenclature attempts to
  name every clade; this would be particularly difficult in traditional
  nomenclature since every named taxon must be given a lower rank than
  any named taxon in which it is nested, so the number of names that can
  be assigned in a nested set of taxa can be no greater than the number
  of generally recognized ranks. Gauthier et al. (1988)[6] suggested
  that, if Reptilia is assigned its traditional rank of class, then a
  phylogenetic classification has to assign the rank of genus to
  Aves.[7] In such a classification, all ~12,000 known species of extant
  and extinct birds would then have to be incorporated into this genus.

What is the precise meaning of "it is logically inconsistent with all taxa being monophyletic"?

I've changed your title, removing the "please explain". This could be included in almost every title, and though it may seem polite, it is an impediment to readers finding out what question you are asking.

Maybe your should also put your question in the discussion page corresponding to the wikipedia article you cite.

You can find discussions of problems with rank-based taxonomy in light of phylogenetics in Ereshefsky 1994, de Queiroz 1996 and Ereshefsky 2002. To summarize, the main problems they identify are:

It's hard to define what exactly an "order", "family" or "genus" is; in particular, taxa at the same rank aren't always comparable. For example, order Hymenoptera, which evolved 250 million years ago and consists of over 150,000 species, with order Carnivora, which evolved 42 million years ago and consists of "over 280 species".
Not enough ranks: NCBI recognizes 29 higher taxa for Homo sapiens. That would require dozens of sub-and-super ranks to render into Linnaean taxonomy.
Names based on ranks: current nomenclature allows certain ranks to be identified by their ending, for example names ending in "-ini" refer to tribes (e.g. Hominini, Canini). If one of these tribes turns out to be non-monophyletic, it may have to be moved to a higher or lower rank to keep its monophyly -- which would have to be renamed, increasing confusion.
Redundant taxa: take division Ginkgophyta. It contains a single class, the delightfully named Ginkgoopsida, which contains a single order, Ginkgoales. In the Linnaean hierarchy, each of these taxa contains the next one along, but in terms of monophyly, they are exactly identical to each other, as they share exactly the same most recent ancestor.


text:
How do the antibodies in colostrum survive the infant’s digestive system?
What happens when the antibodies in colostrum reach the infant's stomach? Why aren’t they destroyed by digestive enzymes?

I have edited your title to make it reflect your question, and (I hope) clarified your question, which seems quite valid to me, although I haven't checked the reason for the close votes.

I think the close votes for this question on the basis that it is too broad should be reassesed. It seems a fair question to me and I don't know the answer to it (although I haven't searched for an answer myself).

There are two main differences between adults and newborn babies which allow the passage of antibodies (while maintaining the activity) through the stomach and the resorption in the gut.

The digestive activity of the stomach in newborns is still immature and needs to develop. This results in almost no production of hydrochloric acid (which is responsible for the very low pH in the stomach). It can take up to two years to until the pH in the stomach of children reaches the level of adults (see chapter 5 in reference 1).  Because of this higher pH much more proteins (and other components of the milk like anti-microbial proteins, carbohydrates and lipids) can pass the stomach unaltered.
The other really important feature of newborns is their much greater permeability of their intestine. This allows an efficient transport from the antibodies into the blood stream and where they provide protection. See references 2 and 3 for more details.

References:

Breastfeeding and Human Lactation
Antibodies in  Milk
Intestinal permeability in the newborn

Thanks Chris for your answer. I hope this lets the poster and others realize that a clearly expressed question with a carefully constructed title will increase the changes of someone who knows seeing it and answering it.

Another important factor that the previous answer missed is that the antibody secreted in breastmilk is IgA dimer. IgA dimer is two IgA molecules linked by a protein called the secretory component, which protects the antibodies from being degraded in the digestive system.

Welcome to bio.  Can you add sources?


text:
How lymphocytes in lymphatic system get oxygen?
We know that the gas-transporting protein hemoglobin is absent from the lymphatic system. So, how does gas transportation takes place in lymphatic system? Is mere diffusion from surrounding blood vessels sufficient for lymphocytes and lymphatic endothelium to survive?

Besides carrier transport of oxygen and/or other gases that hemoglobin binds in the blood, there is also dissolved oxygen present in the plasma - this would also be present in the lymph fluid despite a lack of hemoglobin. With the complex network of arteries/arterioles/capillaries that deliver oxygen to tissues, do you think that lymph transport of gases is even important?

@Vance Yes , I think it's important because how does the cells forming lymph vessels(endothelium of vessels), lymphocytes in vessels and nodes get the required amount of oxygen?

@JM97 Dissolved gaseous oxygen moves fairly freely over short distances...lymph vessels will never be far from other vessels, including capillaries. So, essentially the lymphatic vessels are fed the same way as any other organ tissue.

@BryanKrause what about lymph nodes?

@JM97 Lymph nodes are highly vascularized.

So oxygen dissolved in lymph will support myriad of lymphocytes of lymph node? I don't think that's sufficient considering the very large density of lymphocytes in the node.

@JM97 Lymph nodes are highly vascularized, as Bryan Krause said. That means lots of RBCs delivering lots of oxygen to the node and all of the cells contained therein. It doesn't matter if you think it's sufficient, in reality it is.


text:
Evolution of Upside Down Catfish (Synodontis nigriventris)
My Biology teacher asked us to write 3 texts, explaining the evolution of the Upside Down Catfish Synodontis nigriventris, each one according to Lamarckism, Darwinism and Neodawrinism theories. She asked the same thing for other species but I'm having trouble with this one, since the other ones are simple to explain (like giraffes' necks or flamingo's legs).
She gave us a sheet in which there is some information:
They swim upside down, and their colors are inverted, because their backs are light and their bellies are dark (unlike the general fish). Their predators usually swim below them and it is harder for predators to find fish if their belly is light, because of the sun rays.
Well, all of this suggests that this fish swims upside down so that he can avoid predators, but how could he do this according to Lamarckism and Darwinism?
Also, how does he have inverted colors, and did he get them because of evolution?
I believe that the things which cause the evolution are the predators and the environment, but which characteristic is the first one and which is the one who appears because of the evolution? Also, both of them could be a product of evolution, right?
So how can I really explain this according to the theories of evolution?

Well, I haven't managed to find many studies that explores this but I suspect that their coloring was a result of their upside down swimming rather than the other way around.
They evolved from benthic (bottom-living) creatures that ate off the ground and would have had mouthparts evolved for that. So in order to feed at the surface they would have to turn themselves around. The areas that they lived in may have changed to have poorer benthic food quality making surface feeding more advantageous. They also do this for aquatic surface respiration in hypoxic (low oxygen) waters.
Check out "Chapman, L. J., Kaufman, L. and Chapman, C. A. (1994). Why swim upside down? A comparative study of two mochokid catfishes. Copeia" for more information.


text:
Photosystem I and the ETC
In the light reactions of photosynthesis, Photosystem I receives electrons from the ETC after Photosystem II sends them to the ETC. Then, when Photosystem I receives light, the electron becomes excited and passes the electron back to the ETC. This leads me to my question: In the following question, are both $B$ and $E$ correct?

Which of the following are directly associated with photosystem I?
$A)$ harvesting of light energy by ATP
$B)$ receiving electrons from the thylakoid membrane electron transport chain
$C)$ generation of molecular oxygen
$D)$ extraction of hydrogen electrons from the splitting of water
$E)$ passing electrons to the thylakoid membrane electron transport chain

What research have you done before asking it here?

@another'Homosapien' Looked online and in two biology textbooks

What answer is it, according to you, and why/why not?

@another'Homosapien' Please read my question first before commenting. Thanks.

You are correct as any college level Biology text should comfirm. Was this a "choose one answer only test"?

Yes; the answer was supposed be only $B$ but I thought that $E$ was also correct so I asked here

@suomynonA please read my full comment first before replying; I asked why too. This question is likely to be closed as homework unless you specifically ask why it should (not) be the answer you're saying.

@another'Homosapien' And that's why I wrote that little paragraph before writing the question.

It appears the author of the question is trying to use "thylakoid electron transport chain" in an overly specific way. The chain from which PS I receives electrons has far more components and is different from the shorter chain to which PS I passes its electrons. But according to my copy of Biology, Campbell & Reece 7th edition, both are called "electron transport chains" and both reside in, or on, the thylakoid membrane. Perhaps the "directly" in the question refers to the fact that PS I's electron is first captured by a "primary receptor" before being passed to ferredixon, the first member of the chain to which PS I passes electrons. But, again according to Campbell, this primary acceptor is considered part of the photosystem.
I used to teach this stuff. I'd toss out the question.


text:
p53 gene in benign tumors
In a benign tumor, p53 gene does not work. I know that our cells constantly are mutating and the p53 fixes this. Hence, why does it take so long(or in some cases never) for a benign tumor to become a malignant one? I would imagine a malignant cell would rise rather quickly.

There are a number of main reasons for this: The main reason here is that there is more than one needed to transform a cell. This is usually the silencing of tumor suppressor genes like p53 and the activation of proto-oncogenes. Only one of these is not sufficient to transform a cell. This is also seen in melanoma, where nevi which carry the activating BRAF V600E mutation (which is the most often occuring activating mutation in this cancer) can stay silent for a lifetime. This is called the Knudson Hypothesis (a short overview can be found in reference 1)).
So the turn-off of the control system is not enough, the cell needs to be further pushed to become a cancer cell. More details can be found in reference 2
Then, our immune system is very good in catching cells, which have gone malignant. Most cells, which turned into cancer cells, are eliminated by the immune system. This idea has been first formulated by Paul Ehrlich in the late 19th century, see the references 3 and 4 for details. The figure from paper 4 shows this schematically:

References:

Two-hit hypothesis
Tumor Suppressor (TS) Genes and the Two-Hit Hypothesis
Cancer immunoediting: from immunosurveillance to tumor escape.
The Immunobiology of Cancer Immunosurveillance and Immunoediting


text:
How do mesosomes respire?
So how can mesosomes (found in prokaryotes only) participate in cellular respiration, if a prokaryotic cell doesn't have mitochondria?


text:
In what ways have plants and animals evolved to support each other throughout history?
I'm curious about how plant and animal life have been able support each other throughout time and how each has evolved in a way that would help the other?
For example I have heard that plants have evolved to attract animals, such as bees in order to allow for pollination.  These plants produce smelly flowers that are usually white....  or colorful, non-smelling flowers.  By allowing bees to collect nectar for themselves and their hive, the plants are able to be pollinated in the process.
Earlier today I was noticing a bird hopping up branches of a tightly branched tree, which made me think of how plants and animals would support each other throughout time.  Trees are usually homes for a lot of animals, including birds, so I was curious about the evolution of trees to allow for tigher canopies to protect animals from the weather/elements.
My question is, how have plants and animals influenced each other's evolution, by helping each other throughout history?

This extremely vague and broad. You are basically asking about all sorts of coevolution and symbiosis, and this is a huge topic within evolutionary ecology.

There are probably a few cases of this and exactly how animals and plants co-evolve probably differs between different scenarios. One 'famous' example I like is between ants and acacia plants. The acacia plant has evolved to produce food for a particular species of ant and in return the ants protect it from the grazing of herbivores.
Explained better here: http://bioblog.biotunes.org/bioblog/2007/10/02/cool-bug-9-acacia-ants/

Thanks for the information.  This actually reminded me of something I heard regarding grass.  It was mentioning the smell that we get from cut grass is apparently a defense mechanism that will alert certain insects to help protect the grass from predators...  I believe there was mention of some sort of sound/vibration that aids this, but I could be wrong and it could just be the smell factor.


text:
Do young children grow in spurts
It is a commonplace of my friends and relatives to remark that a young child (younger than 3 years) has had a recent "growth spurt". The underlying assumption is that young children do not grow taller continuously and steadily,  but have periods of rapid growth between periods of slow growth. But is that assumption true? I'm sceptical; I'm inclined to believe that growth is steady, and the idea of growth spurts is a flaw of perception.
So, what research have I done so far on this question? I've seen the height-age charts for children, and they are smooth, so there are no growth spurts synchronised across all children. But that smooth averaged growth could result from the average of many non smooth growth rates. So the question is about when considering a single child. A web search about children's growth spurts shows numerous parenting web-sites that assume that growth-spurts happen, without asking whether growth spurts actually happen. I found an old press release from Emory University about some research supporting the idea, but no better information.

What research have you done to answer this yourself? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure.

@MattDMo The community might have so agreed, but the Help Center information about what is on topic does not say so. The Help Center does say that doing research is part of asking a good question.

@MattDMo I didn't find any Bilogy Meta posts that support your assertion that the the "community has agreed that questions that show little or not prior research effort are off topic". And in fact I did mention some research, of sorts: the content of height-charts for children. I have now amended my question with the, near useless, results of a Web search.

I have to agree with @MattDMo - there needs to be some sort of research on the question being asked or else you get (1) exceedingly vague questions that are unanswerable or (2) questions that are so basic that they are easily answered by looking at a Wikipedia page or some other basic website. If the person asking the question wants someone in the community to take time to write a thoughtful answer, I think we should expect the question asker to do the same.

@Raedwald you found right in the help center where it says you need to research your question beforehand and tell us what you know, so I don't understand why you're making such a big deal out of this. You've been part of the SO/SE system long enough that you should know that you need to try and help yourself before seeking the help of others.

Growth is neither even nor constant, It can vary quite a bit from month to month as hormone levels change, the growth curves you are seeing are a rough average.
You are having a hard time finding anything because it one of those pieces of knowledge that is so old people only rarely research it directly focusing more on deviations from it and you will likely only find good reference to it in textbooks. For a layman this means searches based on the terms you think you should use never find what you want, something as simple as adding the word "textbook" can make a huge difference. Google scholar will also help.
http://adc.bmj.com/content/51/3/170.short
https://books.google.com/books?id=YA-LdtyHJ9QC&pg=PA226&dq=evolution+of+the+growth+spurt&hl=en&sa=X&ved=0ahUKEwjkl4zCztjRAhVB74MKHRiuB7kQ6AEIHzAA#v=onepage&q&f=false


text:
Translation of Poly-U in the Nirenberg and Matthaei experiment
In the Nirenberg and Matthaei experiment the artificial mRNA, polyU, was translated into polyphenylalanine in a cell-free system, establishing that UUU was the codon for Phe. How did this work as the artificial mRNA lacked an AUG initiation codon, which we now know is required for translation of cellular mRNAs?

I have modified your question, eliminating the question of whether there was AUG present. Obviously not — as this was the experiment that established the first codon and nothing was known about AUG and initiation. PolyU was PolyU was PolyU. I think I have clarified your question (as well as answering it below). If not, let me know.

This is an intelligent question that highlights the ‘sleight of hand’ simplifications employed in many text books to make experimental science appear cleaner and more logical than is in fact the case. From what we now know about the requirement for an AUG initiation codon in protein biosynthesis these experiments should not have worked.
The reason they did was that they were performed at an unphysiologically high concentration of Mg2+ which overcomes the need for specific initiation (and, incidentally, allows other reactions of protein synthesis to proceed in an abnormal manner, particularly the codon-directed tRNA binding reaction used to finish the deciphering of the genetic code). You should also bear in mind that the efficiency of the reaction was probably much less than that within the cell, but this was of no concern as all that was required was that a product be synthesised.
Reference
I worked in this area in the late 60s/early 70s and the importance of magnesium concentration was just common knowledge in the field, so it is difficult to cite a reference to support my assertion. However a brief search brought up a contemporay paper on the effect of magnesium on initiation of protein synthesis in phage RNA, illustrating its importance. There are, no doubt, others.


text:
Why should you use an annealing temperature about 5°C below the Tm of your primers?
Why should you use an annealing temperature about 5°C below the Tm of your primers?
According to my current research, I think it has something to do with the other reactents in the PCR, but I am not sure.

What's your problem with the answer? Some criticism would help to make it better...

My understanding of this concept was recently corrected by a prof, and your explanation did not seem to get to the point. I will add the answer the prof gave me.

I haven't seen this yet - do you have a literature source for it?

The annealing temperature of a primer is defined as the temperature in which 50% of the nucleotides of the primer are bound to the DNA. 50% annealing proportion will not yield an optimal PCT product. Thus, by lowering the temperature by around 5oC, the proportion of bound primer changes to more then 50% (perhaps around 70 - 80%) thus getting a more precise yield.
This is why we subtract 5oC from the theoretical annealing temperature.

You want to have primers which bind under the conditions of the reaction only to your sequence of interest. If you go too far off the optimal annealing temperature (5°C below the Tm is indeed a relatively good choice in my experience), your will affect the PCR efficency and thus the yield of your reaction.
An annealing temperature, which is much too low allows annealing of your primers to other sites than your intended target with partial annealing or internal base mismatches. This leads to unspecific amplification and lower yields.
If the annealing temperature is too high no primer binding can happen and you will get not PCR product. Alternatively, partial binding can also lead to misprimed products, although this is much less likely than getting no product at all.


text:
Why doesn’t p53 cause the repair of cellular DNA that has been altered experimentally?
When scientists mutate bacteria or even embryos of lambs and other animals, why doesn't the p53 reverse whatever mutation the scientists cause? I know that the p53 stops the DNA from mutating and since the restriction enzymes essentially mutate the DNA, why doesn't the p53 stop it? Does the p53 gene have to be temporarily turned off?

You seem confused. Explain why you would expect p53 to do this from what you know about it. Then we can address your misconception.

@David Is this better?

Yes. Anyone who knows about p53 (not me) will be able to focus on your concern.

I have altered your title, which was misleading in its mention of restriction enzymes, and hope that this has made it clearer and more likely to attract answers other than my own.

I am no expert in this area, and this answer is only based on a reading of the Wikipedia article on p53, which you should perhaps have read carefully. I welcome edits or correction by persons more knowledgeable than me on this topic.
First, although the Wikipedia article neglects to mention it, you can forget about bacteria as the protein is only found in eukaryotes.
Second, one needs to consider what exactly p53 does in relation to protection of DNA from mutation, how it is activated to do this, and hence whether this would occur in the circumstances of the introduction of mutated DNA into a eukaryotic genome.
From the article it appears that “It (p53) can activate DNA repair proteins when DNA has sustained damage”, and that “p53 becomes activated in response to… stressors, including… DNA damage (induced by either UV, IR, or chemical agents such as hydrogen peroxide)…”
The manipulation of animal DNA will be performed outside of the target organism, and the modified DNA re-introduced into the genome by one of several mechanisms that are unlikely to evoke the stress signals that are evoked by agents that damage DNA ‘naturally’. Hence there is no reason to expect the activation and action of p53 in response to this type of experiment.


text:
Are humans capable of both anaerobic respiration, and lactic acid fermentation?
Are humans capable of both anaerobic respiration, and lactic acid fermentation?
And if so, when do they do each?
I understand that the difference between respiration and fermentation is that respiration takes place in the electron transport chain. I understand that aerobic respiration uses oxygen in the electron transport chain, and anaerobic respiration uses some other molecule in the electron transport chain instead of oxygen, like nitrate. Whereas fermentation doesn't use the electron transport chain at all.
I know humans have an anaerobic metabolic process that produces lactic acid, but I'm not clear whether it's respiration or fermentation, or whether it could be either, in which case when it is which?
added
some further discussion w roland at  the chat link / https://pastebin.com/raw/mkxckeqA / http://archive.is/CwCRL   and on this q at chat link here / https://pastebin.com/raw/9sV38LnQ / http://archive.is/HJVVe     and example of conflicting definitions available https://pastebin.com/raw/3EKGmEb6 / http://archive.is/9sAlY

lactic acid fermentation produces lactate not lactic acid(it's named after the bacteria that do it).see https://biology.stackexchange.com/questions/61315/does-glycolysis-produce-lactate-or-pyruvate where a post mentions the bacteria.Like dna is a misnomer,it does stand for ...acid, but the actual substance is really deoxyribonucleotide.   There r 2 types of lactic acid fermentation,humans do homolactic fermentation that produces lactate and no ethanol, as opposed to heterolactic fermentation that produces lactate and ethanol http://onlinebiologynotes.com/different-fermentation-pathway-bacteria

Humans have no anaerobic respiration, if we define this as oxidation of a substrate with an external electron acceptor other than oxygen. In humans, the terminal electron acceptor in respiration is always oxygen, which is reduced at complex IV in the respiratory chain. Alternative electron acceptors are mostly found in bacteria and archaea.
I would call the anaerobic metabolism of glucose to lactate in humans a fermentation process. It consists of glycolysis, which converts glucose to pyruvate, which in turn is converted to lactate by lactate dehydrogenase. There is no terminal electron acceptor in this case; instead, energy is extracted from glucose by rearranging the molecular structure of the sugar into a more favorable ("low energy") configuration, without any net donation of electrons.

Note: this is how I use the terms, and I believe this is the most common usage in biochemistry today. But I am sure you can find other sources that define them differently. This is rather common in biology and biochemistry, and these terms are very old and fraught with all sorts of historical connotations. But names are not crucial; understanding the biochemical processes is. The important distinction here is that conversion of glucose to lactate does not oxidize the substrate and therefore needs no external electron acceptor; in this way it is fundamentally different from oxidative metabolism.

Comments are not for extended discussion; this conversation has been moved to chat.

and just in case they try to delete the chat link, it's also here https://pastebin.com/raw/mkxckeqA

Muscle tissue is a good example of anaerobic fermentation. Lactic Acid is fermented and builds up in this tissue when we do large amounts of exercise. We use the Pyruvate molecule and LDH to produce Lactate when required but it is only for short bursts of energy in specific tissues.
Try a google image search for the glycolytic pathway. Usually Aerobic and Anaerobic paths are listed after the Pyruvate molecule is formed at the end of this pathway.

When you say muscle cells do fermentation, are you saying it's not respiration?

you write "Lactic Acid is fermented "     <-- From what I understand, the term lactic acid fermentation is named after the bacteria (lactic acid bacteria) that do the process. But lactic acid is not produced. And when you say "s fermented"  I suppose you mean is produced by (that) fermentation, So you mean Lactate is produced by the fermentation, not lactic acid. see https://biology.stackexchange.com/questions/61315/does-glycolysis-produce-lactate-or-pyruvate where a post there mentions that and lactic acid bacteria

specifically humans do homolactic fermentation that produces lactate and no ethanol, as opposed to heterolactic fermentation that produces lactate and ethanol  https://www.onlinebiologynotes.com/different-fermentation-pathway-bacteria/

I mentioned in comment quite early "apparently humans don't do anaerobic respiration at all. They only do a)aerobic respiration and b)fermentation. Humans can't use nitrate or sulfite as acceptors in the electron transport chain"
I'll expand on that a bit.. https://www.khanacademy.org/science/biology/cellular-respiration-and-fermentation/variations-on-cellular-respiration/a/fermentation-and-anaerobic-respiration
"Anaerobic cellular respiration is similar to aerobic cellular respiration in that electrons extracted from a fuel molecule are passed through an electron transport chain, driving ATP synthesis. Some organisms use sulfate as the final electron acceptor at the end of the transport chain, while others use nitrate, sulfur, or one of a variety of other molecules..
What kinds of organisms use anaerobic cellular respiration? Some prokaryotes—bacteria and archaea—that live in low-oxygen environments rely on anaerobic respiration to break down fuels."  (i.e. not humans)
and "Fermentation is a widespread pathway, but it is not the only way to get energy from fuels anaerobically (in the absence of oxygen). Some living systems instead use an inorganic molecule other than O2, such as sulfate, as a final electron acceptor for an electron transport chain. This process, called anaerobic cellular respiration, is performed by some bacteria and archaea."
Humans aren't able to use sulfate or nitrate(or any inorganic molecule other than o2) in the electron transport chain. So they can't do anaerobic respiration.
That is certainly the point made by khanacademy, and made by another microbiologist I spoke to, and echoed by Roland's answer.
Note- as of writing, Roland has undermined his answer somewhat.. Since the first sentence of his answer says "Humans have no anaerobic respiration" But a comment he made, says "I think these terms are defined somewhat differently depending on who you ask, and I agree with @David that it's not very interesting to argue over definitions. But my own preference would be to use the term "anaerobic respiration" only for oxidation of substrates that delivers electrons to a terminal electron acceptor other than O2, and "fermentation" to mean a process that does not result in any net oxidation. This is a major biochemical difference, so it motivates different terms, imho. With these definitions, muscle does not do anaerobic respiration"
i.e. he's saying the definition is only his preference. And that while it has good reason behind it, it's just still his preference. And so it's a question of some peoples' preferred definitions, over others.
I have spoken to a microbiologist who says all the advanced scientific texts use that definition (introductory texts aside, and human biology tests aside), i.e. it's not just some peoples' preference.  I have added further re that -  And what I have found strong evidence/proof that supports that there is a strict distinction made, in the non-introductory microbiology texts. He is probably correct that scientific journals such as PNAS, Nature and Science, make the distinction too.
Added
The microbiologist that I spoke to said that often biology 101 texts get it wrong so e.g. that boundless biology textbook, even the title gives away that it's a very intro level book.  So no surprise that it gets it wrong.  He said often introductory undergraduate books get it wrong.  And books on human biology, since they don't need to distinguish between types of anaerobic metabolising, can get it wrong sometimes, because they don't need as much clarity as they aren't needing to distinguish between anaerobic processes.  But the science journals such as PNAS, Science, Nature. And the advanced microbiology texts get it right.  Sure it's possible for a person to use a very general definition of respiration and then to ask whether the electron transport chain is used, but the microbiology texts have no need for that question to even be asked, since they define their terms to make that distinction.
If one goes to google books and searches microbiology,  I see he is correct.
For example, googling in google books for microbiology fermentation respiration
The first result is introductory so I won't look at it.
The second result is Microbiology & Plant Pathology by Dr. P.D. Sharma
"heterotrophs exhibit two basic strategies the fermentation and respiration"
"In contrast to fermentation, respiration requires an external electron acceptor"
agrees
The third result    distinguishes but is by the same author so i'll skip it.
agrees
The fourth result   - Principles of Microbiology - Page 530
"A comparison of aerobic respiration, anaerobic respiration, and fermentation"
And it distinguishes

agrees
The fifth result   "Microbiology: A Clinical Approach, Second Edition: - Page 39"   here
has a diagram that distinguishes

agrees
The sixth result  Alcamo's Fundamentals of Microbiology - Page 183
"a different inorganic molecule as a final electron acceptor"
note- can't be pyruvate as final one, as pyruvate contains carbon so is organic.
He then gives the examples of a species of bacteria that uses nitrate and a species that uses sulfate
agrees
It is indeed the case that fermentation doesn't involve an electron transport chain, but also, fermentation does involve a final electron acceptor, just it's pyruvate or a pyruvate derivative.
Microbiology By Cynthia Nau Cornelissen, Richard A. Harvey, Bruce D. Fisher here
"the terminal electron acceptor in fermentation, is pyruvate or a pyruvate derivative"
And as the microbiologist I spoke to said, it's more a question of whether the final electron acceptor is internal/endogenous (i.e. produced by the organism itself), or whether it's external. (rather than whether it's organic/inorganic)
One thing boundless biology says (using the strict definition of fermentation and respiration), and consistent with that.   https://www.boundless.com/microbiology/textbooks/boundless-microbiology-textbook/microbial-metabolism-5/anaerobic-respiration-49/electron-donors-and-acceptors-in-anaerobic-respiration-313-8023/
" Both inorganic and organic compounds may be used as electron acceptors in anaerobic respiration. Inorganic compounds include sulfate (SO42-), nitrate (NO3-), and ferric iron (Fe3+). Organic compounds include DMSO."
(DMSO for example is organic/carbon based, but it's an external electron acceptor, thus, still respiration when it's used)
related chat- https://web.archive.org/web/20210507000853/https://pastebin.com/raw/mkxckeqA
Conclusion-
That  and all those definitions clearly distinguish respiration and fermentation, with the same strict definition, that confirms that humans do not do anaerobic respiration, they do fermentation, which is not a form of respiration.
Nevertheless, despite that, it's clearly the case that outside of advanced microbiology texts.. (And I suppose outside of scientific journals), so in introductory biology texts, and in human biology texts, and high school texts.. and among many on this website who clearly have a deep interest in biology, that general definition of respiration is still around. And in such a situation, it makes sense to pay less attention to the term but to ask regarding specific features e.g. "Does it involve the electron transport chain" / Does it use an inorganic compound such as nitrate or sulfate as an alternative to O2?  if one wants to know if it's respiration, Or if one doesn't care what the term is and just wants to know what the features are so may ask that and further questions like "Does it use oxygen", or features that aren't even relevant to the term,  such as what interested in commenter in how they think of the terms - "Is it being done by an animal, or not(so directly from the environment to the cell)".
Further conclusion
further clarification on the distinction..
When I asked this question to the microbiologist-
I understand respiration is usually done with an inorganic substance (O2) as terminal electron acceptor, but that it can be done with an organic substance DMSO. So, is there still an enormous chemical difference between respiration and fermentation, when respiration is done with DMSO?  I don't see how the final electron acceptor being internal vs being external, would cause a major different in the chemistry.
I got a very good answer-
He said - Fermentation doesn't use a proton gradient and chemiosmotic force to generate ATP.  Oxidative phosphorylation vs substrate-level phosphorylation
Looking further..  I see Glycolysis produces ATP via substrate-level phosphorylation. Looking at the distinct parts of respiration and fermentation i.e. after glycolysis. (some define respiration and fermentation as excluding glycolysis anyway). Then, (after glycolysis),  Respiration uses oxidative phosphorylation.   Fermentation, if it produces ATP (which it usually does), then it is done via substrate-level phosphorylation.
(Physiology and Biochemstiry of Prokaryotes   https://i.stack.imgur.com/PkRw9.png    Taking pyruvate to acetate gets you oATP.  Taking pyruvate to propionate does not.  It's Fermentation either way. If it produces ATP it's substrate level phosphorylation, and if it doesn't then there's no phosphorylation)
Many sources online explain how a)those two types of phosphorylation are very different chemical processes  and b)oxidative phosphorylation uses the electron transport chain whereas substrate level phosphorylation doesn't.  So that explains the significance/relevance/reason of the distinction between fermentation and respiration.
Added important note
An exception to this is oxidative fermentation, which does use the electron transport chain. Apparently part of the metabolic pathway doesn't use the ETC and part of it does, in such a way that it's in some way a mixture of respiration and fermentation and they decided to call it fermentation. Also see Do acetic acid bacteria use the electron transport chain when converting ethanol to acetic acid?


text:
Is glycolysis the beginning part of fermentation, or does fermentation follow glycolysis?
Is glycolysis the beginning part of fermentation, or does fermentation follow glycolysis?
I see conflicting information from different sources
https://honchemistry.wikispaces.com/Lactic+Acid+and+Alcohol+Fermentation+in+Humans

"..Alcohol fermentation follows glycolysis, just like lactic acid
  fermentation..."  <-- So glycolysis is preceding fermentation, not part of fermentation

and

" The Actual Fermentation Part
Glycolysis and fermentation are two separate processes. Glycolysis was
  explained briefly to give the reader an idea of the events leading up
  to fermentation and the starting conditions in terms of molecules
  available for reaction.....Going into the fermentation, the molecules NADH and pyruvic acid are present. "  <---  so glycolysis is preceding fermentation, not part of fermentation.

Whereas these two links put glycolysis as part of fermentation, not a preceding stage before fermentation.
https://www.khanacademy.org/science/biology/cellular-respiration-and-fermentation/variations-on-cellular-respiration/a/fermentation-and-anaerobic-respiration

"Fermentation and cellular respiration begin the same way, with
  glycolysis" <-- glycolysis is part of fermentation, not preceding it.

and
http://study.com/academy/lesson/anaerobic-respiration-lactic-acid-alcoholic-fermentation.html

"fermentation, which is a process that anaerobically generates ATP by
  performing glycolysis..." <-- fermentation includes glycolysis,  so glycolysis is part of fermentation, not preceding it.

So, which is it?
Is it a)like khanacademy and study.com,  or b)like honchemistry.wikispaces.com
I have heard the idea that glycolysis is independent, in that it can produce some (not much, but some), energy on its own, and it can happen without fermentation or cellular respiration following. Though when would glycolysis occur without fermentation or respiration following? And even if glycolysis is that independent, it may still be at the beginning of respiration and fermentation and not preceding it.
Wikipedia speaks in a contrary way..
https://en.wikipedia.org/wiki/Fermentation

"Before fermentation takes place, one glucose molecule is broken down
  into two pyruvate molecules. This is known as glycolysis." <-- so glycolysis is preceding fermentation, not part of it.

so the above quote from wikipedia suggests that glycolysis is not the beginning part of fermentation, but a step preceding it
whereas still on the fermentation wikipedia page, it says

"Fermentation is a metabolic process that converts sugar to acids,
  gases, or alcohol....The first step, glycolysis" <-- so glycolysis is part of fermentation.

Links on respiration are more unambiguous that glycolysis is part of respiration.. the links on fermentation vary a bit on whether glycolysis precedes fermentation or is part of it.

This would not be a natural distinction, it is symantical. The only way to state for sure would be if some universally accepted governing board declared it so. Or, if you're a student, it's what the teacher says, at least until after the exam!

@bpedit But biologists have scientific journals.. Is there inconsistency even within a journal, with some papers defining it one way and some defining it the other way?

@barlop — There is no call to define it. Papers typically will have titles like "Delayed Lactose Fermentation by Enterobacteriaceae" (to quote a 1966 paper I found by Googling) and, for example,measure the amount of lactose converted to lactic acid or whatever in different strains (or more likely assay the activity of various enzymes). But this is not a question that concerns anyone in a field that has been moribund for the past 50 years.

The very popular college text from which I used to teach AP Biology, Biology, Campbell & Reece, uses fermentation to describe the entire process. I agree with @David below, that is probably the more standard approach.

As @bpedit indicates in his comment, this is a semantic question — i.e. one regarding the meaning and usage of words. I will explain how I and others use these words and why. If you are convinced by my logic you will wish to use them in the same way, if not you are free to use them differently. However there is no ‘universal truth’ here, and if you are student I have no idea what your instructor thinks.
The problem is that ‘fermentation’ and ‘ferment’ (both as a noun and a verb) are old words, predating any understanding of the processes involved. Thus the Oxford English Dictionary quotes a relevant early example of the use of ‘ferment’ as a verb as follows:

1663 Cowley Verses, to Royal Society iv, All their juyce did .. Ferment into a .. refreshing Wine.

From this, it is clear that the idea of the fermentation process is the conversion of some initial compound (the sugar in the ‘juyce’) to some final compound (the alcohol in the wine). This usage is still current in referring to the process of fermentation, for example a Google search brings up a BBC Science educational page which states:

Beer and wine are alcoholic drinks made by fermentation reactions that use yeast to convert sugars into ethanol.

You may or may not be aware that term ‘ferment’ was historically used to mean what we now term yeast, and ‘Zwischenferment’, the obsolete German term for certain enzymes in yeast, is derived from this. So the original concept was merely of some biological conversion effected by yeast, although this has later been extended to bacteria and the idea changed to indicate metabolic processes capable of generating ATP anaerobically.
Part of the discrepancy in definition may be the emphasis on the end-product of the fermentation — ethanol fermentation, lactic acid fermentation etc. However, it seems clear to me that the fermentation is the whole chain of metabolic events from sugar (or whatever) to alcohol (or whatever); and if glycolysis is part of that process (which it is in this example) then glycolysis is part of the fermentation. (Of course, glycolysis can occur in other circumstances where the product, pyruvate, is oxidised in the tricarboxylic acid cycle, which is not a fermentation process.)
Footnote
The extent to which one can tie oneself in knots with trying to define fermentation is illustrated in the best-selling and well-respected text book, originally written by Lubert Streyer and subsequently maintained by Berg et al. I mention this text both because an older edition is available on-line, and because a book of such value to the publishers is carefully vetted by referees. In the chapter on Glycolysis there is an attempt to define Fermentation:

Fermentation: An ATP-generating process in which organic compounds act as both donors and acceptors of electrons. Fermentation can take place in the absence of O2. Discovered by Louis Pasteur, who described fermentation as “la vie sans l’air” (“life without air”).

So the biochemical lawyers have produced a definition that very few readers will be able to take in at first sight. What is this business about electron donors and acceptors? Well what it means in relation to the fermentation process in which lactic acid is produced (note my legalistic choice of words) is that one organic compound is reduced (glyceraldehyde 3-phosphate) — by NAD+ — and one organic compound is oxidized (pyruvate) — by NADH. And as the production of ATP is included in the definition this means that Berg et al. include glycolysis in this definition of fermentation.
…except that on the same page there is the following statement:

pyruvate is converted, or fermented, into lactic acid in lactic acid fermentation or into ethanol in alcoholic fermentation

So here it seems that the word is being used for the conversion of pyruvate to lactate or ethanol, i.e. it excludes glycolysis.
Pasteur managed to talk about fermentation without being aware of glycolysis or ATP, and it is clear to me that you can write whatever carefully phrased definitions you like, but people are going to continue to use venerable terms like fermentation in whatever way seems natual to them.

I  concur, that's the way in which I generally use the term.

I see the definition apparently used by that statement from BBC science, is consistent with the old definition(that requires sugar be the start), and the new one(which mandates no electron transport chain).   I see what you mean that a current usage, from BBC science, is using the new definition but is consistent with the old one, by including sugar at the start.

However,  BBC science is a bit dodgy for example http://www.bbc.co.uk/schools/gcsebitesize/science/add_ocr_21c/life_processes/energyrev3.shtml    says "Anaerobic respiration in plant cells and some microorganisms (such as yeast) "  <-- And that's wrong.  Yeast mitochondia, are  (like most eurkaryotic organisms's mitochondria), only capable of using oxygen as the terminal electron acceptor in their electron transport chain. So, like humans, yeast,cannot do anaerobic respiration. They do aerobic respiration, and they do fermentation. So I guess their definition of respiration is wrong?

@barlop — My quote from the BBC was just to show that the 17thC usage persists to the present day. I do not intend to cite the BBC as a scientific authority. However, perhaps it was late at night when you wrote "So, like humans, yeast,cannot do anaerobic respiration". The word "respiration" is a semantic minefield as in common usage it is equivalent to 'breathing", so "anaerobic respiration" seems an oxymoron. However biochemically respiration is used to mean obtaining energy from metabolism of nutrients, and anaerobic respiration is what fermentation (in yeast and bacteria) is all about.

Glycolysis is the beginning portion of BOTH types of respiration; aerobic and anaerobic. It makes a couple of ATP. If aerobic respiration occurs, it recharges more ATP. If anaerobic respiration occurs, the organism can make other compounds (like Lactic Acid) but doesn't generate any more ATP. I actually made a diagram that you might find helpful. It's posted here on Twitter:
https://twitter.com/BOGObiology/status/829757759470067713
And have now included it in this post below

I also made a series of videos for my students that might be useful as well. They're on Youtube:  Below is a video on cellular respiration that goes into more detail.
https://www.youtube.com/watch?v=Vh7vg7zG3cQ

Can you please not advertize yourself but write an answer, which stands for itself? So adding pictures here instead of linking them, for example. References are for further reading...

Thanks.. And I think this is the case of fermentation too.   It'd be awesome if you can address this question too.  http://biology.stackexchange.com/questions/55505/are-humans-capable-of-both-anaerobic-respiration-and-lactic-acid-fermentation

@Chris i'm not sure if it's possible to add pics sometimes,  until rep is higher, but i've edited her post to add the picture from the link she gave, and i've put the references more in a context of sources and further information. It's great to have an educator contributing.

I think you're right it's part of the beginning of both. However, it's kind of wrong/questionable though to count fermentation under respiration, (which your diagram does) see my answer http://biology.stackexchange.com/questions/55505/are-humans-capable-of-both-anaerobic-respiration-and-lactic-acid-fermentation

I think you're right it's part of the beginning of both. However, it's kind of wrong/questionable though to count fermentation under respiration, (which your diagram does) see my answer  that i've just posted here

This was my first post here, so I didn't realize I could embed directly, I thought I had to think them. Sorry.

I will post an answer that uses an advanced microbiology book, as they are  careful to get their terms very accurate.
Glycolysis is part of both respiration and fermentation.
Microbiology: A Clinical Approach, Second Edition
By Anthony Strelkauskas, Angela Edwards, Beatrix Fahnert, Greg Pryor, Jennifer Strelkauskas

(Side note-  Non-introductory microbiology books don't count fermentation as part of respiration. As I discovered when looking into whether humans did anaerobic respiration, here Are humans capable of both anaerobic respiration, and lactic acid fermentation?   And as is shown in the diagram above, from that advanced microbiology text.  Biology 101 texts, and human biology texts, are more relaxed(arguably wrong), with their definition)


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Insect identification (Brazil, orthoptera?)
This insect appeared in my indoor yard, in southeastern Brazil. The body is roughly 2cm in length and it makes very distinct beeping sounds, in a pattern that sounds almost like morse code, unlike the crickets I've seen around here. Any ideas?

According to the author of this blog, this appears to be an Endecous Phalangopsinae/Luzarinae, but they don't rest with the wings like that. I'll try to capture it the next time. http://www.ib.usp.br/~silvionihei/2014%20Souza-Dias%20Endecous%20apterus.pdf https://www.researchgate.net/publication/230188107_New_Brazilian_species_of_Endecous_Saussure_1878_Phallic_sclerites_calling_song_and_tegmen_morphometry_Orthoptera_Grylloidea_Phalangopsinae

The species in the question's picture could very well be related, but the papers you reference describe different colored/sized species that, more importantly, live in different habitats (i.e., caves). Unless your yard is near a cave or major source of bat guano, I'd say you'll have to keep hoping someone finds a more accurate answer.

@theforestecologist The identification seems to be fair, see my answer appended. Disclaimer: I am no specialist myself but I really trust the web of contacts at the blog

By far the best online forum and resource for the identification of Brazilian arthropods is the website below (in Portuguese): http://www.insetologia.com.br It adds to the discussion offered by @theforestecologist in this thread, given the identification of similar specimens at: http://www.insetologia.com.br/2017/12/provavel-grilo-endecous-em-sao-paulo.html http://www.insetologia.com.br/2017/01/possivel-grilo-endecous-em-minas-gerais.html
[This one looks like the OP here?] This is one interesting occurrence.

Its a cricket with bad moulted wings. (Probably)


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Is cancer caused by vitamin B17 deficiency?
I have read in an article on the internet that cancer is caused due to deficiency of vitamin B17 which has been removed from our diets long ago in the western food. But some people say that vitamin B17 does not work. So, is it deficiency of vitamin B17 which causes cancer i.e. can this vitamin really be used to cure cancer?

It is mentioned as cancer quackery in this paper which you might find useful.

@user39315 Please open new questions, and do not ask in the comments.

@Kiritee I see we just found the same paper :-)

https://en.wikipedia.org/wiki/Amygdalin

I'm voting to close this question as off-topic because it's not about biology.

I have no idea why it was not closed or migrated before. I would suggest migrating it to skeptics but it is too late. I find this type of question comes in the category http://biology.stackexchange.com/help/dont-ask. Did you really post this expecting an answer Yes? The motley crew on this list have some special insider knowledge about cancer cures denied to the rest of mankind? That I am going to say, Yes there is a medical conspiracy, I met a man in the pub last week and he told me that his brother-in-law...? Allowing this kind of non-question really drags this site down.

@david I would disagree with your last point. Since this is a conspiracy, it is indeed better to have an answer regarding why those claims are false and why amygdalin is indeed harmful rather than useful. For the question title, I agree that it could be framed better.

@another'Homosapien' — that assumes these posters are open to rationale argument. It's like politics or religion — did you ever get anyone to change their mind on these topics by arguing with them? And this is a question and answer site. Allowing this sort of crap is like a SE site in geology or the like fielding questions from flat-earthers all the time. Remember what they say about not feeding the trolls.

Its not about the trolls. I meant it would be useful for the ones who don't know about this matter; if they read this post and get to know the truth behind the conspiracy, then how can't it be better?

If you wish medical information or advice I would suggest you do not come here. The British, NHS Choices site (http://www.nhs.uk/Conditions/Pages/hub.aspx) or the US NIH Health Information (https://www.nih.gov/health-information) are reputable sources. If there is a conspiracy, of course, these sites will be part of it. But then, perhaps Elvis has really become a Tibetan monk.

Short Answer: No.
Background: First of all, there is no such thing as vitamin B17. The compound, amygdalin or laetrile, which is referred to by this term, is not a vitamin1. Amygdalin is indeed a cyanogenic glycoside (like glucosinolates, see this answer) which is poisonous to organisms including humans, because it forms cyanide which is toxic2. See this image for its structure:

The notion that amygdalin is a vitamin started when Ernest Krebs Jr., inventor of 'laetrile' (a modified form of amygdalin), rebranded it as a vitamin to get around the new FDA drug regulations and get it approved as nutrient supplement instead of pharmaceutical3. Ernest Krebs Sr., in 1920s, formulated a theory that amygdalin could kill cancer cells4 and the notion was carried forward by his son, though Ernest Krebs Sr. himself considered amygdalin as too toxic for human consumption. This view received a huge uplift when, in 1973, a public relations officer at Sloan Kettering Hospital, which was given the task by the NIH of performing a series of laetrile trials, alleged a cover up of, and leaked, data that claimed potential for laetrile as an anti-cancer agent5, though nobody else was able to reproduce the same test results in a series of followups. Yet, perhaps the most prominent force which still keeps this myth alive is the book World Without Cancer: The Story of Vitamin B17 by G. E. Griffith (interestingly, reviewed by 'Dr.' Ernest Krebs Jr.). According to all these reports, laetrile might work in following ways6:

malignant cells have higher levels of $\beta$-glucuronidase and lesser levels of rhodanase, because of which they are more susceptible to effects of laetrile.
malignant cells have higher levels of $\beta$-glucosidase (different from $\beta$-glucuronidase) and lesser levels of rhodanase, because of which they are more susceptible to effects of laetrile.
cancer is due to deficiency of vitamin B17 (laetrile) and vitamin B17 is required by cells to restore health (though there is no evidence for this).
cyanide released by laetrile has a toxic effect beyond its interference with oxygen utilization by cells. According to this theory, cyanide increases the acid content of tumors and leads to the destruction of lysosomes. The injured lysosomes release their contents, thereby killing the cancer cells and arresting tumor growth.

Laetrile is even supposed to raise the red count in blood, be of value in treating sickle cell anemia, treat parasitic diseases, help regulate intestinal flora, cause lowering of blood pressure in cancer victims and provide relief from arthritis3.
However, all clinical tests have concluded that laetrile is poisonous to humans (and other organisms) due to cyanide poisoning and thus, its effect in cancer treatment is unambiguously negative6,7,8. In fact, use of laetrile has even led to a number of deaths9.
In reality, when amygdalin is ingested, the enzymes  $\beta$-glucosidase, emulsin and amygdalase hydrolyze it into gentiobiose and L-mandelonitrile. Gentiobiose is further hydrolyzed to glucose, whereas L-mandelonitrile is converted into benzaldehyde and hydrogen cyanide, which causes cyanide poisoning2. The concerned process looks like10:

If the quantity of cyanide generated is under the acceptable daily intake limit (0.05 mg/kg body weight)11, then it can be handled easily by enzymes, like rhodanase which converts toxic CN- to non-toxic SCN- ion12. But this quantity is often beyond the limit; a single apricot seed contains about 0.5 mg cyanide13. Hence, it results in cyanide poisoning.
Thus, the so-called vitamin B17 cannot cure cancer.
References:
 1. Lerner IJ (1981). "Laetrile: a lesson in cancer quackery". CA Cancer J Clin. 31 (2): 91–5
 2. Wikipedia contributors. "Amygdalin." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 10 Mar. 2017. Web. 11 Apr. 2017.
 3. United States, Food and Drug Administration. “Laetrile, the Commissioner’s decision” 1978
 4. (1991), Unproven methods of cancer management: Laetrile. CA: A Cancer Journal for Clinicians, 41: 187–192. doi:10.3322/canjclin.41.3.187
 5. WADE, NICHOLAS (1977). Laetrile at Sloan-Kettering: A Question of Ambiguity. Science, 198, 1231-1234.
 6. Ellison NM, et al. “Special report on Laetrile: the NCI Laetrile Review. Results of the National Cancer Institute’s retrospective Laetrile analysis.” N Engl J Med. 7 September 1978.
 7. Milazzo S, Horneber M. Laetrile treatment for cancer. Cochrane Database of Systematic Reviews 2015, Issue 4. Art. No.: CD005476. DOI: 10.1002/14651858.CD005476.pub4.
 8. Milazzo S, Ernst E, Lejeune S, Boehm K, Horneber M (2011). "Laetrile treatment for cancer". Cochrane Database Syst Rev (Systematic review) (11): CD005476. doi:10.1002/14651858.CD005476.pub3. PMID 22071824.
 9. Editors of Consumer Reports Books (1980). "Laetrile: the Political Success of a Scientific Failure". Health Quackery. Vernon, New York: Consumers Union. pp. 16–40. ISBN 0-89043-014-4
 10. Amygdalin - TradMPD
 11. FAO Meeting Report No. PL/1965/10/2;
    WHO/Food Add/28.65;
    Evaluation of the hazards to Consumers resulting from the use of
    Fumigants in the protection of foods
 12. Cipollone R, Ascenzi P, Tomao P, Imperi F, Visca P (2008). "Enzymatic detoxification of cyanide: clues from Pseudomonas aeruginosa Rhodanese". J. Mol. Microbiol. Biotechnol. 15 (2-3): 199–211.
 13. S Krashen. Are Apricot Kernels Toxic?. The Internet Journal of Health. 2008 Volume 9 Number 2.

+1 Great answer. It's cool how your answer and my answer here are actually saying the same thing in terms of how laetrile/amygdalin is useless as cancer medication, but with slightly different narratives and lines of evidence (and also references).

@AlexDeLarge thanks for appreciation! I first thought of answering that question, but then I saw this question and thought it would be better to answer this one ;)

Short version: This is nonsense, cancer does not arise from nutritional deficiencies.
Long version: The substance is called Amygdalin, a poisonous cyanogenic glycoside. It can be found in higher concentration in the kernels of several plants including apricots, plums, bitter almonds, peach, plum. The semisynthetic, modified form is called Laetrile. Taking up this substances with the oral route can lead to cyanide poisoning up to death due to the release of cyanide from the molecules.
There is nothing like a vitamin B17 (which suggests that the substance is an essential vitamin to the human body), this has been invented by cancer quacks. None of the two substances have shown any activity in clinical cancer trials. See references 1 and 2 for details. The second is a systematic review of the Cochrane Foundation which analyses all available articles on this topic.
References:

Laetrile: A lesson in cancer quackery
Laetrile treatment for cancer

As far as toxicity of laterite is concerned, all currently approved neoplastic agents have enough toxicity and patients succumb to the effects of such more than the disease itself.  Not to mention the extravagant cost. There definitely needs more in depth analysis on the disease process to find a simple cure. This disease appears to go beyond genetics alone.  A few viral and bacterial variants have been discovered hpv and h. Pylori when earlier it was denied that it is caused by any microorganism.

Welcome to Biology.SE! Please add some references to your answer.

Cancer is not a simple disease and there won't be a simple (meaning always working) cure. There has been quite a lot of success lately with targeted and immune therapies - cancer treatment is by far not only chemotherapy.


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Why do most fish move fins orthogonally with their axis of symmetry?
So recently I read the question why are most fishes vertical (in the sense of distribution of their body mass) and it got me thinking what is the reason behind the direction they move their fins. My explanation is that they need to catch the image they several times to truly percieve it, so the eyes have to be orthogonal on the direction they move their fins. Am I correct, therefore they swim like this  rather than this
 because there is more to see on the horizontal dimension in shallow waters?

Can't see a difference in the two pics?

@AliceD The waves illustrate the direction of gravity

The upper fish looks normal, the fish bellow swims breaststroke

I think it's much more a consequence of the way their muscles are arranged.  Dolphins & whales work perfectly well by moving their flukes vertically.

@jamesqf Dolphins...haven't thought about them :) Anyway - is there some kind of evolutionary pattern in the way their muscles are arranged?

@Probably: I really don't know enough about the evolution to do more than guess, but if I had to, I'd guess that somewhere along the line the ancestors of mammals somehow evolved in such a way that it was easier to bend up and down rather than side to side - think of walking movement, then swimming with fins.  Thus when dolphin ancestors started back to the sea, their natural movement was up & down, and that evolved in the direction of improved up & down...

@jamesqf Oh, you might have got it! Dolphins and whales have to breath and this might be the fastest way to get up / there could be predators

@Probably: Not quite what I meant.  Think of Tiktaalik http://tiktaalik.uchicago.edu/meetTik2.html crawling out of the water and scrabbling around on its fins.  Carry on through amphibians & reptiles, and you see legs awkwardly splayed out to the sides, with a lot of side-to-side movement (carried to the extreme in snakes).  But somewhere along the line to becoming mammals, creatures got their legs directly underneath them, which allowed more efficient locomotion - think of a horse or dog running.  Now mammals have this new body plan...

...and those which go back to the sea have to start evolving better swimming from what they now have, and wound up waving their tails up & down rather than back & forth.  But as I said, this is just me guessing...

@jamesqf Oh, that's even more cool than I thought, thanks


text:
Help in identifying an unknown arthropod
I'm not even sure it's an insect:  the best I can do is identify it as an arthropod.  I captured this slow-moving organism and after a period of observation under high magnification, I concluded that it appears to construct a "shell" from miscellaneous particles or debris.  With a scalpel, I carefully cut this outer casing open to observe the organism, and the pictures show what I found.  It seems to have six legs, like an insect, but is oddly worm-like and wingless.  Total length is approximately 1 cm.  I do not believe that this is a juvenile/larval/instar form.  I've seen several of these where I live, and they always look like this (with maybe a +/- 20% size variation).

Edit:  This specimen was found in San Diego County, California, United States.

Closely related question/answer: http://biology.stackexchange.com/questions/15845/what-insect-is-this/15856#15856

We have a lot of these in our house.

We have a ton of these in our garage! (Los Angeles) Thanks so much for asking, I've always been curious about them.

These case building moths have shown up a few times on this site. Hands down, though, these are the best pictures.

It is the larva of household casebearer moth (a Lepidoptera), named after the larval stage. It is scientifically called Phereoeca uterella.
It is found through out South and North America.

The larva constructs a protective case from silk and camouflages it with other materials such as soil, sand and insect droppings.

References:

Wikipedia
bugguide

Further reading: Household Casebearer, Phereoeca uterella by
Juan A. Villanueva-Jimenez and Thomas R. Fasulo

so does cutting off it's shell (like the OP did) harm it? Or can it just grow another shell?

@user17915 There is no scientific work on the impact of removal of the larva from its case but I think it does affect the larva if done so because there must be a real significance behind spending a lot of energy synthesising the threads of the case which begins even before the larva hatches out.


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Analysis over single chromosome data
I have no expertise in biology, I'm a data scientist, and I would like to know if it makes sense, from the biological point of view, to analyze data (SNP data) coming from a single chromosome, and not all 22 chromosomes, to predict the risk of a certain disease.
Should I obligatorily use data from all chromosomes? Why?
Thank you very much. And sorry if it is a very basic question, but I really would like to understand this.

You can analyse a single chromosome. All the bioinformatics tools I know, allow that. Consider only the reads that map to the desired chromosome (or any segment of the genome). However, most next-gen sequencing experiments sequence the whole genome and not just a single chromosome. You'll just end up losing information by not considering other chromosomes.

Ok, understood. So you are sying that it finally depends on the final objective of the analysis, right?
In my case, I want to analyse the data (dataset 1: lung cancer individuals, and dataset 2: type 2 diabetes individuals) to create a final prediction model. Also the idea is to perform feature selection and detect relevant/significant SNPs to later identify related genes and see if they are related with the disease or not.
So the ultimate question would be, for complex diseases like lung cancer and type 2 diabetes, should I analyse data from all chromosomes or only some?

Even though tools let the individual analysis of a single chromosome, is it biologically correct? Does it make sense from a biological point of view? Does it depend on the disease being analyzed?
I'm asking because biologists have told me that the conclusions of the analysis I'm doing, can olny come from the analysis of data from all chromosomes, but I would like to know the biological justification of this.
Hope I made my self clear. Thank you!

@mgvaldes it would not be a good idea to restrict yourself to one chromosome unless you have a good reason to do so (for example, X-linked genes). Biological justification for this is that complex traits are dependent on many genes that are scattered across different chromosomes.

Perfect. That's what I wanted to be sure of, since I'm not a biology expert. Thank you very much!

On top of @WYSIWYG's answer, suppose you want to analyze production of certain protein A produced by gene A on some chromosome A. Your data will be like say, luminosity/fluorescence values coming out of tagging this specific protein. But to predict this effect of production (on what period this values might be higher, like in a prediction model), the gene/factor that might be activating gene A might be on some other chromosome B. Until you know the activity of that, you will not be able to accurately predict the production of this.
In a Regression/Tree model, your $X's$ will be categorical/continuous showing the activity of effecting genes(B) while activity of gene A is dependent $Y$.
Hope this helps.

I'm concretly applying ML learning techniques to SNP data from all 22 chromosomes of two separate types of individuals (dataset 1: lung cancer, dataset 2: type 2 diabetes). The final idea is to create a predictive model for each use case and rely on feature selection techniques to identify relevant SNPs realted to the disease. Read the other comments I've given to @WYSIWYG's answer.


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Treatment of cancer
In treatment of cancer, radiation is given, but radiation can also be the cause of cancer. In the drugs of chemotherapy it is written that it is highly carcinogenic. Then why are such methods performed? Is there any recently discovered new method to cure cancer?

It is clearly a trade-off between benefit and harm. Often cancers which are irradiated are the ones, that cannot be removed surgically (or completely). Then the tumor is immediately dangerous for the patient. From the dose the patient gets, you can calculate how likely additional damage is. And then you need to make a decision.
The same is true for the "classic" chemotherapeutic drugs (like Paclitaxel or Carboplatin), which attack all dividing cells. They have a lot of side-effects, but again, there is a trade-off between the benefit this drug has and the harm it causes. See references 1 and 2 for some more details.
There are quite a few new therapy options besides the "classic" ones. These include oncolytic viruses aimed against the tumor (see reference 3), as well as targeted therapies (see reference 4) which only attack certain molecules or proteins important for the cancer. And last, but not least the probably most important new therapy option are immunotherapies to turn the immune system against the tumor. This gives (when the patient is susceptible), spectacular results and I think there will be a lot of development in this field in the future. See reference 5 for details.
An overview over the new therapy options can be found in reference 6.
References:

Long term side effects of brain tumour radiotherapy
Therapy-Related Secondary Cancers
Oncolytic viruses: a new class of immunotherapy drugs
Targeted Cancer Therapies
Immunotherapy: Using the Immune System to Treat Cancer
Overview of Targeted Therapies for Cancer


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Question about genetic recombination
I am having some difficulty understanding a few things about genetic recombination, in part because of confusion from different diagrams in books.

First of all, I wanted to verify whether I have understood correctly: It seems to me that when homologous chromosomes (which at this point are as sister chromatids joined at the centromere) join during the zygotene/pachytene stage, only one of the chromatids from each homologous chromosome form synaptonemal complexes with one of the chromatids in the other chromosome. Is this correct? Then only one of each of the chromatids is involved in the DNA recombination...

Leading on from my previous point, I think this would mean that in the final four zygotes that are formed, there are four different chromosome possibilities: the maternal chromosome (call it m) which has not had any recombination events; the maternal chromosome M whih has had recombination events with the paternal chromatid. Then the corresponding paternal chromatid p and chromatic which has undergone recombination event P. Is my understanding correct here?
Also, I have seen in some diagrams there is a single chiasmata forming between the homologous-chromosome chromatids and in other diagrams I have seen more than one chiasmata. I think the one chiasmata picture is a simplification and there can in fact be more than 1 crossing over point between the chromatids of homologous chromosomes.
Finally, if it is so that only one of each pf the sister chromatids is involved in recombination between homologous chromosomes, is there a a preference as to which chromatid this is, or is it random?

I realise that if both of the sister chromatids undergo these recombination events, then many of my questions would be redundant! However from the books I am looking at now, it seems that only one chromatid undergoes these crossings over...

I can't imagine point 1 being correct. I've taught out of many textbooks and have never encountered this. I can't think of a mechanism which would inform one chromatid that synapsis is occuring on the other and then prevent it from occuring on that chromatid.


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What is the purpose of ultrahydrophobicity in lotus flower leaves?
I read about the lotus effect on wikipedia, but I haven't found an explanation as to why droplets collecting dirt on the surface of a leaf is helpful to the flower's survival.

Lotus benefits from hydrophobicity for that it decreases the likeliness of being infected by pathogens (found in "dirt") and increase the ability to perform photosynthesis.
According to a study by Darmanin and Guittard, the plants (not only lotus) with ultraphobicity benefits from these structure for :

self cleaning

and

these structures are able to stabilize the presence of air underwater and be submerged for several weeks

Let's talk a little about the second part : having a good access to gas is vital for plants to do photosynthesis. In an environment which is very wet (like the one the lotus lives in), it is better to be dry to maximise air/plant surface area.
Now, about the self cleaning.
First, lotus lives in backwater or muddy environment
In this study by W. Barthlott and C. Neinhuis, it is said that big particles can occlude stomas, the small "holes" that allows the plant to breath.
Wet environment is ideal for bacterial/fungal growth and different kind of disease. Unclean water could also block light and make photosynthesis less efficient.

Again, wettability
  is important for the adhesion of microorganisms to
  leaf surfaces. In addition, on waterrepellent
  surfaces, spores and conidia are deprived of the water necessary for germination. Therefore, the epicuticular
  wax crystalloids and their physical properties
  may be regarded as the first line of defense against
  pathogens.