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Breathing's Role in Aerobic Respiration
It's my understanding that aerobic cellular respiration is summarized in the formula $C_6H_{12}O_6+O_2→CO_2+H_2O+ATP$ (unbalanced). The glucose is thrown through a series of chemical reactions, ultimately resulting in the binding of a phosphate group to ADP to form ATP to store energy, and the carbon dioxide is a byproduct of this process. At the very end of this chain, though, there's a few electrons left hanging, and the oxygen is used to bind these to loose protons to form water.
It is also my understanding that the primary purposes of the lungs are to intake $O_2$ and exhale $CO_2$ for this process and their role in speech.
Assuming this is all correct, are the secondary, minor functions of the lungs important enough that if there was a way to siphon the $e^-$ and $CO_2$ to some other function and find something else to allow the larynx to work we wouldn't need to breathe?

There's a fairly large misconception here. The huge amount of energy that's available from respiration, and which drives the synthesis of ATP, in fact comes from that reaction that you consider secondary, and that's the transfer of electrons to oxygen.
If you want to think of it as two separate reactions, then the first one
$$Glucose + 12\ {NAD}^+ + 6 H2O ⇌ 6 CO_2 + 12 NADH$$ releases about 10 times less energy than the second one: $$6 O_2 + 12 NADH ⇌ 12 NAD^+ + 12 H_2O$$
The reason you get something resembling 30 ATP from a glucose molecule is because oxygen is such a great electron acceptor.
Many microbes can in fact use molecules other than oxygen as the electron acceptor, but in general it is much less energetically efficient than using oxygen.
You could try equilibrator for estimating the free energy available from various chemical reactions. First reaction and second reaction from above as examples.

That was not at all what I had in mind with secondary purposes. I was referring to the various substances it filters out of the blood, which I assumed could easily have been delegated to the kidneys. I had completely forgotten about that part of cellular respiration. Thanks!


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Is there a certain environment where all cellular functions (or at least some) increase their rate?
Is there a certain environment in which all the functions (or some) inside a cell increase in their rate? Would the increased rate cause any damage to the cell?

Increased temperature would be one "environment"

When you reach optimal temperature for certain enzymes, their activity will boost and this can e.g. cause extreme "usage" of nutrient and such (or whatever the function of those enzymes are) and cause rapped growth. Certain stimuli e.g. lactose (and no glucose present) can turn on different cell pathways and thus cause high activity for proteins in that pathway. What do you mean by "burn out" (cell dies?)?

@CuriousTree Yes, cell dies, or functions improperly.

@CuriousTree The lactose part is interesting, care to elaborate on more similar stimuli ? (preferably as an answer )

I changed speed to rate, which is what you mean I believe - also... What do you mean by "burn out"? That's not a scientific term.

@VanceLAlbaugh I mean any malfunction in the cell's internal functionality, any damages that are caused by the increase of rate.

I edited to try to circumscribe the "burn out".

There are optimal temperature, pressure and substrate concentration for each biochemical process. The optimal temperature and pressure for two or more (but not all) processes may overlap. So there is no SINGLE temperature or pressur where ALL of them will be at their maximum. Please note, by mentioning "cellular processes"  I meant all the biochemical(e.g glycolysis), physiological (cellular micro-transport) as well as physiochemical(transcription) processes. But we can try to provide substrates at reasonably high concentration ( keeping in mind negative feedback phenomena); we may reach the maximum achievable rate. All the above conditions follow bell-shaped curve; so I put the word 'resonably', as after the optimum condition is reached further increasing that condition will lead to decline in "speed" of reaction. We have to create an artificial enviornment using that substrate combination at proper concentration; as there is no such natural condition where that happens(cell always decrease one process while increasing another).
But it may seem to be a paradox - does anabolic and catabolic reactions both will increase simultaneously! E.g glycogenesis and glycogenolysis at the same time......well, as I already said this is not a natural condition; we are forcing substrates of one reaction at "reasonable" concentration keeping in mind the 'opposite' (is it??) reaction. E.g glucose produces glycogen by glycogenesis and that new glycogen is used in glycogenolysis; so we have to consider the concentration of glucose only. Isn't that easy! well, not so soon. Doing this requires lot of ATP, of course we'll get some from the glucose breakdown, but the need is even higher. So we have to provide additional ATP. Then there are second messengers (cAMP, DAG, IP3 to name a few of them). We have to nutralize them all( they favours unidirectional process).....this is a very complicated thing(just for example, we are supplying ATP, so cAMP will be automatically produced; so we should select all the enzyme blockers of cAMP production). But then electrolyte concentration will be disturbed and we need to monitor & regulate that also.
Thus it is clear that such condition requires sofisticated laborarory instruments.
N. B.
1. I considered only a single cell while discussing this.
2. The word "exhausted" was taken as progressive deterioration of cellular architecture, that leads to death.

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Where should I go for online information on animals endemic specifically in Mozambique?
I've been involved with the citizen science project "Wildcam Gorongosa" for over half a year now (website, forum). As there are lots of unexperienced volunteers, many questions are being asked. Often I'd like to answer, but also not having a biology background I usually have to do some research first to give an accurate answer. For this reason, I'm looking for informative, up-to-date online resources, like e.g. search engines, animal guides etc.
I have come across a few websites that give some information on animals in the whole of Africa (e.g. ultimateungulate.com) - but I wonder if there are more suitable places to go if I'm specifically looking for animals in Mozambique (or even Gorongosa National Park). I'm still relatively new to the topic - where would a scientist involved with research on Mozambican ecology go and look for this kind of "specific" information? As the project deals with pictures taken by wildlife cameras, I am only interested in animals of a certain size (I guess rat-sized and larger). I'd be happy to find e.g. more information on the appearance of each species, its geographic distribution, their respective habitats and their general behavior.
I realize that this question is somewhat broad - please do ask ahead, I'll try to add details if necessary!

Here is a large list of animals (sorted by guilds) that can be found throughout Mozambique.

Each animal in the list is linked to a page with picture and information!

Wikipedia maintains a few lists of animals found in Mozambique.

See here for  a list of mammals (sorted by order).
See here for a list of birds (sorted by order).
They also have 2 lists for mollusks (fresh-water, marine) and 1 for plants.

Gorongosa's own website provides a list of common animals found in Gorongosa:
http://www.gorongosa.org/explore-park/wildlife
As user Sudachi mentioned in a comment below,  iNaturalist and GBIF also have lots of well-managed species lists and observation data.

I'd also like to add a few resources. iNaturalist and GBIF also have lots of well-managed species lists and observation data.

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Confusion over equations for population's heterozygosity vs. heterozygous individuals
On page 24 of Gillespie's Population Genetics, 2nd ed, an equation for $H$, the probability that two randomly drawn alleles are different by state, is given.
$H$ is stated to be similar to the heterozygosity of the population, which I guess is expected to be $2pq$, where $p$ and $q$ are frequencies for different alleles. $ H′=(1−1/2N)×H$
On page 23, $H_t$, the probability that an individual chosen at random from the population after $t$ generations of random mating is heterozygous, is given :
$$H_t = H_0 \times (1-\frac{1}{2N})^t$$
For a current time $t$, are $H$ and $H_t$ measurements of the same thing, or are they different ?
I interpreted them as being the same, because drawing two alleles at random is similar to drawing a diploid individual at random.

One is a recurrence equation and the other is a general solution. These are basic concepts of mathematical modelling.
Reccurence equation
A recurrent equation describes the state of a system (here, heterozygosity $H$) at the next time step given the state in the previous time step. The recurrence relation is $H' = (1-1/2N)\times H$. Given the state $H$, at a given generation, one can know the state $H'$ at the following generation (given the population size $N$).
General solution
A general solution describes the state of a system at any time step given an initial state. Not all recurrence relation have a general solution. Here there is a general solution and it is $H_t = H_0 \times (1-\frac{1}{2N})^t$. Given the initial state $H_0$, one can know the state $H_t$ after $t$ generations (given the population size $N$).
Two equations for the same model
The two equations both refer to the same model and therefore the same statistic of expected heterozygosity which, as you said, is $H = 2 p (1-p)$ (for a bi-allelic locus) by definition.
Understanding the basics of mathematical modeling in ecology and evolution
Have a look at A Biologist's Guide to Mathematical Modeling in Ecology and Evolution by S. Otto for an introduction into mathematical modeling in the field of interest.

@ghgh Please let me know if my answer helped you or if something is still unclear.


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Can plants grow without photosynthesis?
Animals can survive without eating if nutrition is injected directly into their blood.
Can the equivalent be done with plants? By injecting carbohydrate rich nutrient solution, either without photosynthesis or in addition to photosynthesis.

To answer if the equivalent could be done with plants, we have to understand the histological and anatomical differences between plants and animals.
Just as spraying a nutritive solution over an animal (like you and me) doesn't work, spraying a nutritive solution over the leaves doesn't work as well: the nutritive molecules (let's use glucose in our hypothetical example) don't penetrate the leaf's epidermis. The same happens if you put the nutritive solution in the soil: there are several membrane layers between the external medium and the phloem, and glucose will never reach its destination.
Now, let's try to compare with a IV injection of nutrients, which we can do in an animal. The plant's structure that (kind of) can be compared to blood vessels is the phloem (actually, xylem and phloem, but in our case, dealing with nutrients, we're gonna talk only about the phloem). To inject the nutrients we have to reach the phloem, because the periderm in plants with secondary growth ("cork" in the image) is very impermeable:

Now, even if we reach the phloem, using methods like this...

...we still have a problem: in an animal like you and me, a substance injected in a given vein will quickly spread to all the systemic blood vessels. But the same doesn't happen with the phloem. The injected substance can go up or down (depending on the pressure flow), but it doesn't spread to all of the plant's tissues, unless we perforate the phloem in a lot of places.
Thus, so far, this method is used to deliver chemicals (like pesticides) into the tree. Notice that, just like a person in a hospital, the bag with the solution has to he higher than the perforation:

For a chemical treatment like this, the amounts of the substance are small. But for "feeding" a plant using this technique, the amounts of necessary nutrients are way higher...
Finally, answering your question: is it hypothetically possible to feed a plant in the dark with a nutritive solution? yes. Is it practical, or doable? very hardly.
Source: Utah State University

Thank you, I did suspect it was not very easy or practical. The reason I asked is because I am trying it imagine some kind of high-tech agriculture, beyond aeroponic vertical farming, that uses carbohydrates as its energy source rather than light. Imagine for example if a pollinated tomato flower could be 'plumbed' into some kind of artificial machine that appears to the developing tomato like the tomato plant. I know it sounds overly complicated, but maybe one day such a system could be automated.

If that's what you are imagining, there is something way more practical, efficient and actually doable: search "plant tissue culture" or "tissue culture growth".

@Nick Collier: Where would you get the carbohydrates from in the long run?

Good question @AlexDeLarge, it would be pointless to get them from other plants. Maybe some kind artificial photosynthesis if it were much more efficient than natural photosynthesis. Or maybe there is a way to turn electrical energy in to carbohydrates. I am speculating about the future here, I know none of this is practical now.

@Nick Collier: Yes, it's interesting yet speculative. You could also ask people in Worldbuilding.SE and see if they have further ideas as that question may also be addressable from a more science-creative perspective.

I was just about to link Worldbuilding!

Survive without eating: no
Survive without photosynthesis: 1. Yes, and 2. Yes-if considering only "nutritional" aspect of photosynthesis

Some parasitic plants lack photosynthesis (see the beautiful ghost plant)
Plants also grow during the night, and plants are able of respiration, which can exceed photosynthesis - and trees do so excessively when they are young and growing (learnt some time ago during an undergraduate lecture on botany)

Survive by adding carbohydrate rich nutrient solution: not sure
Survive without photosynthesis at a philosophical scale: probably not as most molecules of sugars, which we have on earth, had required photosynthesis for their generation

Very good answer! But as far as I know cellular respiration always exceeds photosynthesis. Photosynthesis, even though it does make some energy available for the plant directly, is only the process that provides glucose for respiration. The major ATP synthesis in plants also comes from cellular respiration. The difference is the carbon source. In that way, photosynthesis is analogous to animal eating as it provides the carbon source. However, the energy conversion of the carbon source then is very similar.

tsttst Yes, I am trying to imagine a way to produce food without photosynthesis on a philosophical scale. You have highlighted the other side to the problem, namely production of sugars without using plants in the first place. The reason I ask is because I am wondering if humans can survive on this planet in future without destroying most of its natural habitat for agriculture.

Hi Nick. Photosynthesis will have been required for carbon fixation and thus indirectly most present carbohydrates. Note that already now, most of the energy in ordinary plant-derived food comes indirectly from fertilizer, and not photosynthesis. (with some components of fertilizer coming indirectly from fossil oil....) . You might infer an unacceptable answer by reading the first chapter of Harari's "A Brief History of Mankind", which discusses the time before agriculture.

No, not in the long run at least. (Except for parasitic plants as I have just learned!)
Plants rely on photosynthesis to make up glucose but that is just the tip of the iceberg, there are tons of cascade reactions (also genes regulation) going on linked to the photosynthesis. Read this just to get an idea.
So, photosynthesis is so deeply linked to the metabolism of plants that replacing it with some nutrient-rich buffer will not be enough.
There are organisms that are facultative phototroph they do photosynthesis but they can live also without, they are not classified as plants, though. One example of such an organism is Chlamydomonas reinhardtii.

This is not true for all plants, as mentioned in another answer. There are parasitic plants that are incapable of photosynthesis.

True, I did not know about it.

@alec_dijinn: Thanks for editing (withdrawed the -1). As the exception of parasitic plants is there, I would not be so sure about the generality of your answer for all non-parasitc plants, though. Still a god thing to point out!


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What is the name of the bird which feeds on penguin blood and meat in Tristan island?
I just watched a National Geographic documentary "Unseen Islands: Atlantic Arks" and there was some thing strange in Tristan island. Some small bird which changed its diet to feed on the blood and meat of the penguins on this island.
I want to know more about this bird - or its name so I can search it - and if there are other examples of this behavior of changing diets.

You almost certainly mean the Tristan Thrush, Turdus eremita, which is endemic to Tristan da Cunha. The species is considered to be an opportunistic omnivorous scavenger, but their diet includes the eggs and chicks of many seabird species, as well as the adults of some smaller seabird species.
The Wikipedia page for the species mentions that Tristan Thrush has been recorded drinking penguin blood, citing a BBC documentary which I don't have access to. Five species of penguin have been recorded on Tristan da Cunha, but only the Northern Rockhopper Penguin breeds there (the others are rare visitors to the island). Given the nature of penguin colonies (i.e., densely-packed, and with abundant chicks as well as occasional sick adults), there would be many opportunities for an opportunistic omnivorous scavenger to eat penguin blood, chicks, eggs, or carrion.

The BBC documentary is “Southern Ocean”, the second of three episodes in the BBC Four series Britain’s Treasure Islands. A YouTube upload is available here; the Tristan thrush is introduced at 13:22, and at 13:54 you can see one pecking at a live(!) penguin and drinking blood from the open wound.


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How to prevent a old promoter region from attaching onto a plasmid instead of a new one during ligation?
What I am trying to do is take out a existing promoter region in a plasmid, and replace it with a new one. So first I use the appropriate restriction enzymes to get rid of the existing promoter region. Next, I add in the new promotor fragment which has the appropriate sticky ends, and then through ligation, I want to place the new promotor in the plasmid.
Since the old promotor region and new promotor region will have the same 'sticky ends', how do I prevent the old promotor region from getting placed into the plasmid instead of the new one during ligation?

Performing the ligation and sequencing 5 - 10 clones is an option. You only need one clone with the 'new' promoter which will be added to the ligation in excess right?

Run it out on a gel after digestion  and extract the vector only.
Treat with a phosphatase after digestion. This will prevent religation since you need at least one of your fragments to be phosphorylated for the ligation to work.
(A must regardless) sequence several colonies at the end.

I recommend doing all three.
Edit: option 4: digest with a third enzyme that cuts in your old promoter but not the vector or the new promoter.

If your new promoter is short and you are using a pair of oligos with sticky ends that don't need to be cut, you should either phosphorylate the oligos with polynucleotide kinase, or don't dephosphorylate the vector. You need one or the other to be phosphorylated to get the ligation to work. Also, picking many colonies is mandatory. I typically do 24 minipreps at a time because that's what fits in the centrifuge. Do as many as you can. There have been many times where only 1 miniprep was successful. Speaking of which, have a good way to screen, you need nice clear results.

So to confirm, once I get rid of the old promotor region, run it on a gel to isolate the 'opened plasmid with no promotor region'. Once I have this then I preform ligation with the new promotor region....

On the plasmid I will have amp. resistant gene as a way of tracking the succesful transformed bacteria.

@RadekMartinez Yes, you are describing the standard cloning procedure, cut, paste, check for good plasmids. What is your new promoter? How large is it?

I am not sure yet. However it is not like 20 - 30bp, much larger.


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What constitutes as the death of a bacteria?
I've read that some bacteria can survive a long time without food.
What constitutes the death of a bacteria ?
What process needs to take place for it to be considered dead?

When you talk about organisms like fungi and bacteria which can have a dormant form, and viruses, "dead" becomes somewhat harder to define. In fact, it has not been definitively defined for bacteria.
I would have guessed "when they are permanently unable to reproduce", but I may be wrong.
From one source[1]:

The observed coordinated gene expression continued even after cell death, in other words after all bacteria permanently lost their ability to reproduce. Transcription of a very limited number of genes correlated with cell viability under the applied killing regime. The transcripts of the expressed genes in living bacteria – but silent in dead bacteria-include those of essential genes encoding chaperones of the protein folding machinery and can serve as molecular biomarkers for bacterial cell viability.

From another[2]:

it is a challenge to determine if bacterial cells are dead, or viable but non-culturable (VBNC), and what is an agreed upon correct definition of dead bacteria.

Some viable but nonculturable cells (VBNC) can be "resuscitated" into dividing cells. [3]
Also4,

However, the simple binary definition live/dead probably does not accurately describe the complex physiological states possible with microbial cells.

Unfortunately the actual conclusion is behind a paywall.
Finally, another country heard from5 :

Programmed cell death is a gene-directed process involved in the development and homeostasis of multicellular organisms. The most common mode of programmed cell death is apoptosis, which is characterized by a stereotypical set of biochemical and morphological hallmarks. Here we report that Escherichia coli also exhibit characteristic markers of apoptosis—including phosphatidylserine exposure, chromosome condensation, and DNA fragmentation—when faced with cell death-triggering stress, namely bactericidal antibiotic treatment.

So, perhaps the answer is, a bacterium is dead when it is unable to reproduce, cannot be resuscitated, gene expression has ceased, and shows characteristic markers of apoptosis
[1] Transcriptional activity around bacterial cell death reveals molecular biomarkers for cell viability, Remco Kort, Bart J Keijser, Martien PM Caspers, Frank H Schuren and Roy Montijn, BMC Genomics 2008
[2] Can dead bacterial cells be defined and are genes expressed after cell death? Trevors JT1, J Microbiol Methods. 2012 Jul
[3] A matter of bacterial life and death Gregg Bogosian, Edward V Bourneuf
[4]Advances in microbial food safety: 23.
[5] Antibiotic-Induced Bacterial Cell Death Exhibits Physiological and Biochemical Hallmarks of Apoptosis, Daniel J. Dwyer, Diogo M. Camacho1, Michael A. Kohanski, Jarred M. Callura1, James J. Collins, Molecular Cell, Volume 46, Issue 5, 8 June 2012, Pages 561–572


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Good microscope?
Hi I am a teenager and I recently studied biology and found it very interesting. I want to get a microscope and study further into the microscopic world. What would be the best microscope for me? I would like to see the cells in living organisms. I am willing to spend about $200 as well.

Welcome to Biology.SE. What are you interested in observing? Do you want to be able to see individual cells? See bacteria?

So there are a couple of things you should ask yourself:
a) how 'small' do you want to see
b) what are you trying to study - (microspores can differ depending on that. Examples: Microbiology - (bacteriology), Plant biology...)
200 dollars for a 'proper prof. microscope'I do not think is enough. However I do not think that is what you are looking for (For example, the one I use in the lab is around 1,200$, and it is not even the best) However, I think this microspore will be good for a beginner home one:  http://www.microscopenet.com/40x2000x-amscope-binocular-biological-compound-microscope-p-10436.html?osCsid=l26ecpfe9nfvbvr306ddvbca14
I think this would be your best fit for the type of microscope you are looking for, however you can look around to see if you can find it for a better deal.
Hope this helps

If you are lucky and live in a university town with student shops, which are run by student organizations, I would recommend you to visit one of those shops.
Often they sell used microscopes, which are no longer needed. If you do not mind that these microscopes have been used before, you will get a much better quality for less money.
If you go to such a shop by yourself as a teenager, and tell them how eager you are about learning biology, I guess that they would not hesitate to sell you a good microscope for little money.


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What are the exceptions to Mendel's laws?
What are the exceptions to the $-$

Law of dominance
Law of independent assortment
Law of segregation

My knowledge:
Exception of law of dominance:

Incomplete dominance
In incomplete dominance when a red snapdragon flowered plant is crossed with a white flowered plant an intermediate phenotype appears in the F1 hybrid instead of a parental phenotype.
Codominance
Unlike dominance in codominance when a A ($I^AI^A$) blood group individual mates with B ($I^BI^B$) blood group individual the offsprings have blood group AB ($I^AI^B$) instead of A or B.

Exception of law of segregation:

Nondysjunction
During meiosis homologous chromosomes/sister chromatids and hence genes may move to a common gamete violating law of segregation.

Exception of law of independent assortment:

Linkage
When genes are present on the same chromosome they tend to remain together and enter into the same gamete. This is the reason behind deviation of dihybrid test cross ratio from 1:1:1:1 and occurrence of parental combination in high frequencies.

Am I correct? Are there any more exceptions to these laws?

One of the biggest exceptions is that these laws are not applicable to haploid organisms.

Recombination and linkage are different things or same ???

You are right but the list is certainly not exhaustive. Here are a few more concepts you may want to consider.
Exception of law of dominance:

epistasis
Allelic effect at a given locus depend on the variants at other loci
environment dependence and specific case of frequency dependence
The concept of dominance can be used for any quantitative trait. Typically, when the quantitative trait of interest is fitness, then the trait often depend on the environment. A typical and interesting case is when the fitness depends on the frequency of alleles in the population. Depending of the frequency of the allele at a given locus, the relationship might be a relationship of dominance, additivity or dominance for the other allele.

Exception of law of segregation:

meiotic drive
from wiki: "Meiotic drive is a type of intragenomic conflict, whereby one or more loci within a genome will affect a manipulation of the meiotic process in such a way as to favor the transmission of one or more alleles over another, regardless of its phenotypic expression. More simply, meiotic drive is when one copy of a gene is passed on to offspring more than the expected 50% of the time."

Exception of law of Independent assortment:

epistasis for fitness
Imagine a case where a given combination of allele is lethal at very young age, then you would never see these two alleles together in an individual. It is per se, not a case of exception to independent assortment but it gives the feeling of such exception. A case more extreme when a given combination of alleles prevents fecundation could however be considered as an exception to independent assortment.

Another e.g worth including Sex-linked genes, they do not follow mendelian law of Dominance.

Also Sex-limited traits [where a functional autosomal gene (allele) is completely slient in one sex] and sex-influenced traits [where a functional allele changes behaviour, dominant/recessive behaviour with sex of the bearer].


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What does "cell type composition" mean?
I am reading an article about detection of differential methylation. They use the term "cell type composition" in the following context:
"Researchers need to carefully design studies that associate phenotypes with DNA methylation. Some aspects, such as cell type composition, cannot be readily controlled by design; patients and therefore individual DNA samples simply differ in their cell type composition." (Robinson, MD., 2014)
I would like to know to what "cell type composition" refers?
Does it refer to the composition of a specific cell-type in terms of its methylation pattern (or can it refer to something more general outside this context)? It makes sense to me that different cell-types should have different methylation patterns, that's why there are different cell-types in the first place. But is it that even within one specific cell-type, the composition of methylation pattern is different across different individuals?

The problem is that for most sequencing operations you nowadays still need more than one cell - even though this will change soon.
Accordingly, you have to sample cells from a tissue which often, if not usually, contains more than one cell type, see e.g. this picture from a lung tissue from the Wikipedia article on tissues linked above:

It is not always easy to pick cells of one type only (think of trying it with blood, which is a tissue as well). So what you then get is a mixture of different cell types which probably differ in methylation patterns.

Does it refer to the composition of a specific cell-type in terms of its methylation pattern (or can it refer to something more general outside this context)?

No, it means that you have cells of different types within your sample.

It makes sense to me that different cell-types should have different methylation patterns, that's why there are different cell-types in the first place.

At least one of the reasons, there are more, e.g. other modifications and mutations.

But is it that even within one specific cell-type, the composition of methylation pattern is different across different individuals?

That is a different problem and may also be true. But this is not what your quotation, as I understand it, refers to. They refer to the problem that you might sample the same tissue across patients but still get a different composition of cells from different types due to sampling error.


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What is the acceleration profile of a cheetah?
I'm interested in the time it takes for a cheetah to reach maximum velocity as well as the acceleration over time that's typical of a cheetah prior to attaining this peak velocity.

According to a recent paper published on Nature, cheetahs can reach a top speed of 29ms-1 and very impressive accelerations, up to 100ms-2:

The mean top speed was 14.9 +- 3.4ms-1 and was usually only sustained for 1–2 s. The highest speed we recorded was a stride-averaged 25.9-1

Also impressive are the lateral accelerations:

Hunts involved considerable manoeuvring, with maximum lateral (centripetal) accelerations often exceeding 13ms-2

Here is the acceleration and speed chart:

The paper has several other charts: Locomotion dynamics of hunting in wildcheetahs

That's interesting. But, what about the cheetah's acceleration profile?

The paper has a chart, but without precise values for the accelerations (given in "g", 9.8ms^-2). Check figure 2-f and figure 3-d.

I have. The chart is too small for eyes to perceive and it's on the scale of days not seconds...They were interested in the cheetah's hunting patterns.

Days? the x-axis is time in seconds. I edited the answer with the chart, check it.


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How do I effectively visualize data showing change in a lot of samples over two time periods?
I've tallied the number of glands in a plant this year and last year. My full data set has about 20 plants in it (I've reproduced the data from 10 of the plants here). I want to show that the plants this year have had consistently lower gland counts than they did last year, but I don't want to bog readers down with too many data points in their faces. What kind of graph/chart should I use to best show this trend?
        Gland Count
PlantID  2015    2016
1        22.92   19.50
2        11.67   7.12
3        19.67   15.33
4        22.33   12.00
5        20.92   18.58
6        25.83   23.83
7        25.67   32.17
8        22.83   17.00
9        28.42   26.25
10       17.92   16.92

I'd highly recommend this PloS perspective article: "Beyond Bar and Line Graphs: Time for a New Data Presentation Paradigm". @Shawn is on the right lines with their answer.

IMO, this question is off-topic as it is about data visualization and not biology. I am voting to close.

@Remi.b I agree it is off-topic here,, but it might be on-topic for Cross Validated. Migrate?

@RHA This is not a statistics question either. Not suitable there as well. I am not sure which site would actually be suitable because usually questions like this are opinion-based.

@WYSIWYG "Cross Validated is a Q&A site for people interested in statistics, machine learning, data analysis, data mining and data visualization."

One solution is to plot exactly the data you are trying to describe - the delta in your values.
Consider a bar-plot (with confidence/error bars) showing the plant number along the x-axis and the y-axis showing the change in count with +ve and -ve values.
For example, using the data from your question, this visualisation shows clearly that all values bar one decreased from 2015 to 2016 (please forgive the crude diagram lacking titles etc):

Of course it would also be helpful to show a graph of the absolute values and it is obligatory to include a table of the exact values too.

Just had a few mins spare so have added a sample bar chart created trivially in Google sheets via mobile to more clearly show what I tried to describe using text. I'm willing to spend more time creating a less crudely drawn chart if this considered suitable for the OP's purposes.

Two styles of graph come to mind.

A simple 2 layer histogram showing the distribution of gland counts for each year. This is a kernel density as opposed to a histogram, but it gets the idea across.

Line graph with year on the x-axis and gland count on the y-axis, with a colored line for each plant. This would show a little more detail, and would be better if the mean gland count overall did not change much, but decreased significantly among individuals.

The line plots look great and are a very nice and direct way for showing trend for individual plants. However, care must be taken when expanding to n~20 that the graph does not become too crowded [especially when (print)size might be small].

Histograms are a poor choice here due the data not being neither continuous nor ordered (I presume the plant IDs are arbitrary and there is no "plant 1.5"). Overlaying bars could be a reasonable alternative if you can ensure the colours used clearly distinguish between the years.

I agree with the points that @tsttst raises and would add that this style of chart relies on the points/lines being visually distinct but does enable expansion to show data for a third/fourth etc year which is a definite bonus. One alteration to the example would be to also have different shapes (rather than only circles) as well as different colours to help with distinguishing which colour relates to a specific plant number.

Ensure that the visualization will not be misleading (if you intend to use visualization to argue in favor of a consistent reduction):

Count the number of plants, where the Gland Count would be lower in 2016 than in 2015 (to ensure that is lower for most plants).
Then perform a two-sided paired non-parametric test, such as the Wilcoxon signed-rank test, (to test that for most plants there was a change in the same direction), and provide the p-value.

Visualization:

Divide 2016 values of each plant by the 2015 value of the same plant, (perhaps log2-transform), and only plot the resulting values as individual dots along the y-axis, (perhaps add some background shading or line to indicate the boundary between reduction and increase of Gland Count, if it helps the visual understanding)
In case that you are preparing a publication: consider whether the limited gain of information (compared to representation by p-values or a supplemental table) is worth the space

@Jennser: With 20 individuals you could also think about a bootstrapping approach to calculate 95% confidence intervals for the means and/or medians for each year.

@tsttst. Hi. My background in statistics is not very strong, so forgive me if this question is very basic.
I performed a two-tailed paired t-test already on the data to ensure that there was a statistically significant change in gland counts between the two years. Does the Wilcoxon signed-rank test provide substantially different information from the t-test/ would it be more appropriate do use for some reason?

Hi Jennser, actually this is an excellent question (especially as Alex had hinted at your sample size, which might allow further statistical tests).  t-test assumes an underlying normal distribution of the gland counts. Unless there are safe reasons to assume such a distribution (or you can convincingly show its presence), it is better to be conservative, and use the Wilcoxon signed-rank test, which does not depend upon this assumption. -> Wilcoxon signed-rank means that there will be one thing less to worry about   (it yields p=0.06 on the 10 plants, and will likely get even better on 20)

Simple comparison of averages
The easiest and most common is to display the mean and standard error for each year.

If you have more years, you might then want to add indication on the graph corresponding to p.values of pairwise comparisons but I don't think you have more than two years.
Below is a short R code that does the job. Note that I estimated the standard error with bootstrap. You might want to switch to use Agresti-Coull method. Personally, I like bootstrap. Make sure to use the standard errors that make sense given the statistical test you performed on these data.
# Function to calculate the standard error
bootstrap_SE = function(x,reps=1e5, SEorCI="SE")
{
    means = vector("numeric",reps)
    for (rep in 1:reps)
    {
        means[rep] = mean(sample(x,replace=TRUE))
    }
    if (SEorCI == "SE") return ( sqrt(var(means)) )
    if (SEorCI == "CI") return ( quantile(means, c(0.025,0.975)) )
}

# Your data
d2015 = c(19.50, 7.12, 15.33, 12.00, 18.58, 23.83, 32.17, 17.00, 26.25, 16.92)
d2016 = c(22.92, 11.67, 19.67, 22.33, 20.92, 25.83, 25.67, 22.83, 28.42, 17.92)

# Calculate the averages
yAverages = c(mean(d2015),mean(d2016))

# Calculate standard errors
SE = c(bootstrap_SE(d2015),bootstrap_SE(d2016))

# x-axis
x = c(2015,2016)

# Make the plot
plot(y=yAverages,x=x, xlab="year", ylab="gland count", ylim=c(min(yAverages-SE),max(yAverages+SE)), xlim = c(2014.4,2016.5), xaxp=c(2015,2016,1))
arrows(
    x0=x,
    y0=yAverages,
    x1=x,
    y1=yAverages+SE,
    angle=90
)
arrows(
    x0=x,
    y0=yAverages,
    x1=x,
    y1=yAverages-SE,
    angle=90
)

Focus on systematic differences
If your goal is to insist on the existence of systematic differences for each plant, then I would recommend @kwah's solution (+1). I don't quite like @Shawn's solution (no offense), I found the graphs complicated, unintuitive for categorical variables and I found that they do a poor job to convey the concept of systematic differences in comparison to @kwah's solution.
If you're thinking at doing a paired-test, then going with @kwah's solution sounds like a clever idea.


text:
What is the acceleration profile of the greyhound?
I'm interested in the acceleration curve over time that's typical of an adult greyhound prior to attaining this peak velocity. My curiosity is motivated by a desire to understand the biomechanical reason why land mammals run so fast.

I'm a little unsure of what you want. I'm pretty sure I know a paper on acceleration of greyhounds specifically, but are you more interested in the physiology and morphology of fast terrestrial vertebrates in general? ( There are studies of cheetah acceleration, too, along with other critters.)

Both of those subjects interest me actually. In fact, in my mind they are inseparable. Would you mind sharing the paper?

I can do that. Give me a day or two.

I might recommend editing your question to make your end goal more specific -- if you're interested in locomotor adaptations for acceleration in mammals generally, as opposed to just greyhounds.

I'm going to try to break this up a bit to address your sub-questions. Most of it is summarized from Williams et al 2008--and almost all of the work I'm referencing comes from the Royal Veterinary College Structure and Motion Lab.
Acceleration Profiles:
So, I can't find an acceleration curve over time for these, but we do know about the potential acceleration range for greyhounds and cheetahs. Greyhounds can reach a max speed of about 17 m/s (Usherwood and Wilson 2005), cheetahs can reach up to 29 m/s (Hudson et al. 2010). Cheetah stride-averaged accelerations have been measured up to 120 W/kg --they can speed up by 3 m/s over a single stride, and slow down by up to 4 m/s (Wilson et al. 2013). Racing greyhounds have achieved 60 W/kg (Williams et al. 2009).  Maximum acceleration decreases with increasing speed
How Land Animals Can Be Fast

Augmentation or hypertrophy of proximal musculature. More than a fifth of a greyhound's limb muscle mass is associated with the proximal portion of the hindlimb (Williams et al. 2008). Muscle power (work/time, important for acceleration) is roughly proportional to muscle volume, so bigger muscles are better in this case.  In cheeetahs, a similarly large muscle mass is devoted to hip extensors (though different specific muscles; Hudson et al 2010). Big muscles = high power and high force production.  In addition, sprinting mammals tend to have longer muscle moment arms than non-sprinters--so they can produce greater torques for a given force.
Longer muscle fascicles. This may also be an adaptation for power output. Greyhounds have longer fascicle lengths in their hamstrings than your average domestic dog (Williams et al 2008), and human sprint athletes also have longer fascicle lengths than endurance runners (Abe et al. 2000).
Long limbs and flexible spines: Longer limbs w/ spinal flexion = greater stride length--and cheetahs have particular elongated hind limbs. A long hind limb also lets cheetahs maintain foot contact with the ground for longer, so lower peak forces are required.

These aren't nearly all of the things involved, but I suppose this is a start.
References:

Abe, T., K. Kumagai and W.F. Brechue. 2000. Fascicle length of leg muscles is greater in sprinters than distance runners. Med. Sci. Sports. Exerc. 32: 1125-1129.
Hudson, P. E. et al. 2010. Functional anatomy of the cheetah (Acinonyx jubatus) hindlimb. J. Anat. 218: 363–374.
Usherwood, J. R. and A. M. Wilson. 2005. No force limit on greyhound sprint speed. Nature. 438, 753-754.
Williams, S.B. et al., 2008. Functional anatomy and muscle moment arms of the pelvic limb of an elite sprinting athlete: the racing greyhound (Canis familiaris). J. Anat. 213:  361–372.
Williams, S. B. et al. 2009. Pitch then power: limitations to acceleration in quadrupeds. Biol. Lett. 5: 610-613.
Wilson, A. M. et al. 2013. Locomotion dynamics of hunting in wild cheetahs. Nature. 498: 185-189.


text:
What is the name of the groove down the middle of an anther?
I thought it had a name along the lines of interlocular groove, but I haven't been able to find that term anywhere.

You probably mean the filament.

There are two longitudinal ridges in a typical anther. An anther has two lobes each with two pollen sacs/thecae. So there is a groove both between the two lobes and also between the two thecae in one lobe. Having a look at the transverse section would help. Although I don't know what they are called, it would be better if you specify which of the two ridges you are refering to.

I think what you are looking for is the connective. Anthers are usually two-lobed and connected by a band of sterile tissue that also connects the anther with the filament - therefore the name, I guess (see Wikipedia article for stamen). It says

Most commonly anthers are two-lobed and are attached to the filament either at the base or in the middle area of the anther. The sterile tissue between the lobes is called the connective.

Each anther lobe usually consists of two pollen sacs (see Wikipedia article for microsporangia). It says:

Each anther lobe develops two pollen sacs. Thus, a two-lobed anther develops four pollen sacs situated at four corners of the anther.

And further (accentuation by me)

The cells of endothecium possess fibrous thickenings. They remain thin-walled and constitute stomium (line of dehiscence) in the shallow groove in between the two microsporangia of the anther lobe.

This groove frequently is called by its orientation, i.e. longitudinal groove, even though I do not think this really is a well-defined technical term (but do a quick Google search for "longitudinal groove" anther and you will find several biology books using the term, e.g. this).

I think that you're talking either about the connective that separates two lobes of the anther,  or the longitudinal groove that I think separates the two theca making it dithecous.

Welcome to Biology.SE! Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then either delete or [edit] your answer accordingly. It isn't clear that this adds anything to the existing answer. In addition, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. Finally, if you include a figure you must document where it came from. Thanks!


text:
How can I measure the curvature of bird's beak on the field?
I'm wondering if there is a standard tool to measure the bird's beak curvature.
It seems that a spherometer wouldn't work because the beaks that I'm measuring are not circular but more parabolic.
I guess something like this:

I feel that this can be a problem if your birds have different beak length.
What do you think?

There are possibly infinite superlinear curves that may denote beak morphology. I think what you can use is the maximum slope of the curve. That would generally tell you how curvy is the beak compared to a linear one.

I was thinking about a tool that I can bring with me on the field. Not something to calculate after with photos or something else. Is this what you propose?

Yes I was suggesting something like that. I am not aware of any tool like that. You can perhaps measure the actual beak length using a measuring tape and divide it by the direct point-to-point length (like displacement) to have an approximation of the curvature. The higher the ratio, the higher would be the curvature. For a semi-circle it would be π/2.

Bird beak morfology is often studied (try Google scholar). Aren't there any papers describing how they measure it?

They usually measure it afterwards on photos : https://www.researchgate.net/publication/40039501_Predatory_Functional_Morphology_in_Raptors_Interdigital_Variation_in_Talon_Size_Is_Related_to_Prey_Restraint_and_Immobilisation_Technique/figures?lo=1

Another good one is this: http://redpath-staff.mcgill.ca/hendry/Foster2007JEB21,263.pdf. But I'm thinking something more practical on the field.


text:
Codon tables and the wobble hypothesis
In E. coli, there are only 47 different tRNAs but 61 potential anticodons. This is because, from what I understand, the third base of the anticodon can pair by wobble rules.
However, it is known that there is some correlation between tRNA pools and expression levels.
So if, for example, GUA and GUG were covered by the same tRNA, why are their codon usages different in a codon table? If one were only concerned with expression level, shouldn't they theoretically affect translation rates similarly?

This is a good question as, although in higher eukaroyotes codon usage does not necessarily correlate with translational efficiency, it does to a large extent in Escherichia coli (see e.g. Boël et al., 2016). The answer is not simple, but the following may contribute.
To optimize the strength of base pairing
Although in particular circumstances ‘wobble’ allows one tRNA to decode more than one codon (see diagram in my answer to Redundancy and the Generic Code) the strength of base pairing will be less for the wobble base-pair:

It has been suggested this would generally disfavour (and hence reduce the incidence of) the degenerate codon that needs to be decoded by wobble. (In some cases a wobble interaction might be an advantage if the first two codon bases were G or C, so that the hydrogen bonding was not too strong.)
To utilize the spectrum of tRNAs able to decode degenerate codons
Although wobble enables a reduction in the total number of tRNAs necessary to decode the 61 amino-acid codons, additional tRNAs often exist that one might regard as unnecessary. Furthermore, where three codons are decoded by a tRNA with a 5'-I (inosine), the other tRNA sometimes has a 5'-G (rather than A) and can hence decode two codons. This is illustrated by the E.coli tRNAs for threonine:

Thus, the relative abundance of these three Thr-tRNAs could determine the codon usage, and Dong et al., 1996 reported that this is the case.
To reflect the overall GC-content of the genome
If the genome of a prokaryotic organism has a particular base composition, because there is so little non-coding genomic DNA the mRNA will necessarily reflect that base composition in its codon usage. Your might ask why doesn’t the base-composition of the genome just reflect that of the synonymous codons, but there are actually strong pressures on the GC-content of prokaryotic and viral genomes. In some bacteria this may reflect needs for thermal stability, but in others it seems to be random drift (see e.g. Biology SE questions on GC-content of genomes).

Codon usage is not necessarily associated with translation efficiency, as your example would illustrate. Though control of translational efficiency and accuracy is one of the well known reasons for the existence of codon usage there have been other hypotheses that link it with asymmetric mutagenesis rates and overall GC content (See "Why does codon usage bias exist?" Novoa & de Pouplana, 2012).
From the same article:

However, the search for a correlation between tRNA abundance and codon usage has been successful only in some organisms [5, 34]. In several species, including many bacteria and eukaryotes, this search has failed [35, 36], prompting the proposal that, in the latter organisms, translation efficiency might not be the primary factor influencing codon usage [36, 37]. However, it was recently reported that two distinct modifications at the wobble position of certain anticodons are at the core of this apparent lack of correlation [28].


text:
Robertsonian translocation on the same chromosome
is there any big difference between Robert-son-i-an translocation between two 13 chromosomes comparing to a translocation between 13 and 14 chromosomes


text:
Catalytic Triad of Serine Proteases
Is serine considered an acid in the catalytic triad involved in the mechanism of action of serine proteases? It is donating a proton to His but I am not sure if this really qualifies as an acid?

It depends how you define an acid. For what it‘s worth, the chemical definition Google presents when I search is “a molecule or other species which can donate a proton or accept an electron pair in reactions”. On that basis the serine residue in the catalytic triad is acting as a weakly ionizing acid.
Of course in aqueous solution a free serine hydroxyl group is not acidic, but one of the important features of enzyme catalysis is that amino acid residues are operating in a different environment that can enhance their activity. One factor is the proximity of other residues. Another is the effective dielectric constant can be different in the hydrophobic interior of a protein which can exclude water molecules.


text:
Strategy for tree and shrub identification
I often find it difficult to identify trees and shrubs even though I have many handbooks and manuals on trees and shrubs in my area (New England). The typical problem is that the species is not in the handbook, or that it is very similar to many other species. For example, hawthorns have many different species which are very similar to each other and most books do not exhaustively list the different hawthorns and their distinguishing characteristics, instead just listing one or two of them.
Web sites are even more fragmented than books and are usually a lot less detailed than the books so even if I search around, the results are often useless.
Am I going about this wrong? What improvements can I make to my strategy for identify trees and shrubs?

Species ID books with pictures, or photos, will generally never be comprehensive enough to include all species, although with some there will be additional information it the text that will give details about other related species, varieties, hybrids or cultivars.
Importantly look for ID books that include an ID key, generally at the start, and learn how to use it. They are usually accompanied with a good explanation of how it works.
The key takes the form of

Does it have this...?
If it does go to [3]
If it doesn't go to [7]

And so on, making successive distinctions until you end up with the species.
They can take some getting the hang of, and you need to know the botanical terms that they refer to.
Also importantly, if you don't already have and use one, you must have a decent hand lense, or magnifying loupe, that you take with you everywhere. Often the deciding features can only be properly be assessed when looking close up, and you need to get to know what the species you are familiar with look like under the lense.
An experienced ecologist friend, an expert in flora and fungi, has a couple of books that have no images in at all, it is just the species ID key, that he takes with him when he is surveying. Granted he already knows his species very well, but you can't remember everything all the time and so you need a book that can tell you the final distinguishing features, even if it is text.
But again a hand lense is a good place to start. My favourite is an Eschenbach 10/40 Pocket hand-held magnifier from Germany http://www.eschenbach.com/cdd40611-ceda-4188-a5c3-882565859296/products-hand-held-magnifiers-pocket-detail.htm
Someone gave this site http://dendro.cnre.vt.edu/dendrology/syllabus/key/key1.cfm?state=&zone= as a good resource for trees in the US


text:
Crossing over : Holliday model

In this figure out of the two heteroduplexes formed one is considered to be non-recombinant product(left) and the other recombinant product(right). My question is despite the exchange of middle DNA segment why is the right heteroduplex considered a non-recombinant product or patch. I've been reading two books:

Molecular Biology: Principles of Genome Function
By Nancy Lynn Craig, Rachel Green, Orna Cohen-Fix, Carol Greider, Gisela Storz, Cynthia
Molecular Biology
By Burton E. Tropp

both had the same illustration and descrpition.

Answer in brief

Heteroduplex called patch does not have double-stranded recombinant regions, there is a new fragment in a single strand only. It means that the two strands are not complementary at that regions and as soon as DNA repair systems detects it, the mistake will be corrected. In case of heteroduplex called splice, there are double-stranded changes, which do not go against the complementarity principle and thus, they will not be removed or corrected in any way.

Diagrammatic Explanation
After horizontal and vertical resolution patch and splice are formed respectively.

A better version of this diagram with complimentary base pairing is shown below $-$

In patch the heteroduplexes formed have only a single stranded middle recombinant region which is not complimentary to the other strand when this is detected by the DNA repair system and corrected the duplexes formed are same as the original duplexes (before crossing over) so the products of horizontal resolution is called non-recombinant products.
In splice the heteroduplexes formed have double stranded recombinant segments with middle non complementary region which when detected and fixed by the cell's DNA repair system two duplexes are formed having recombinant DNA segments, so they are together called recombinant products. The recombination in splice is well represented by the reversal of terminal genes.


text:
RNA processing in eukaryotes
Why does post-transcriptional  processing of eukaryotic mRNA involve addition of a 3' polyA tail, rather than one of polyU, -G, or -C?

Quite interesting question. It also evokes the question of abundance / availability, since ATP (which is also used for poly-adenylation - besides its role in providing energy for many biochemical reactions), also appears to be the most produced and consumed molecule in humans, link

This is likely an evolutionary selection result, with A having won out. Most likely dude to availability and stability. Once addition of As to ends of RNA increased fitness of RNA, it was selected for. Simalar question is why is ATP often a substrate when GTP and CTP and such carry near equiv energy.

@SciEnt Please answer questions as answers, not as comments. That's what it says when you click in the comment box.

@David everytime i amswer like you have without any citation i get downvoted or told to cite. Thus my comment feels more appropriate

@SciEnt — I'm sorry but the text in the comment box means what it says. It is basic to the model that the Stack Exchange network follows. If you answer you have to be prepared for criticism. I accept your implied criticism of my answer as valid, and I have now added a reference.

As others have mentioned poly-A seems to be favoured because of higher concentrations of ATP with respect to other NTPs, due to its ubiquitous role. There is no real proof for this like most "why" questions. However, the ubiquitous presence of ATP is itself an evidence for a random selection of ATP and a subsequent expansion of its role. There is no thermodynamic explanation for this. The selection is likely to have been random.
Polyuridylation is also known to happen in eukaryotic cells (reviewed by Munoz-Tello et al., 2015) and one of the well known cases is that of the let-7 pre-miRNA (Heo et al., 2008). Polyuridylation marks this pre-miRNA for degradation.

And then it's also interesting to ask why GTP has a similar but far less ubiquitous role than ATP and CTP and TTP (to my knowledge) have no such role at all. I like to think about these obviously contingent features evolution brought up ... and expand this idea to the notion of us humans assigning functions to observations that might simply be contingent.

Most probably because the concentration of ATP in cells is much higher than that of the other nucleoside triphosphates and there was no functional requirement for a particular base in the tail. Its main function seems to be to work with an appropriate nuclease system to regulate the mRNA lifetime (see, e.g. Wikipedia article).


text:
How is signalling disturbed in trophoblastic cancer cells?
Trophoblastic cancer seems to be a form of growth that no longer responds to the neural signals which try to inhibit them. Can someone please explain whether experiments have been performed as to how exactly cancer cells manage to "shut off," these neural signals?

Welcome to Biology.SE. I edited your question so that it now includes a reference to the Wikipedia article of the disease. I also tried to make it more clear and changed the title accordingly. However, I am not sure what you meant by "trophoblastic hypothesis of cancer". As the only trophoblastic cancers I am aware of are GTD (see link) and they are very rare, I would doubt that this is a general hypothesis for the various cancer forms. Then again, all cancers are a form of growth (this is one of the defining characteristics for tumours), so I am not really sure what you mean. Please clarify.

I just want to know why they dont respond to normal neural signals like other cells.

If that has already been discovered

@Lelouch have you done any research at all on the subject? Tumors don't respond to normal growth inhibition signals because they have been highly mutated. Please read up on cancer, what it is, and how it arises - it is very well known why tumors don't respond to inhibitory signaling. Also, the neural system doesn't carry growth or growth-inhibitory signals. A system of protein-based cytokines and growth factors does that, as well as hormones.

Thank you very much. Can you provide a link on the topic? I would be grateful.


text:
Product of reaction between HCl and bile
In the mammalian digestive system  HCl is the main acid and bile is the main alkali. What is the product of the reaction between these two chemicals?

HCl is neutralised by the bicarbonate in the pancreatic juice. I dont think it'd form any products of reaction with bile

@Polisetty On the Wikipedia page for bile it specifically says that bile is alkaline and that it neutralizes excess stomach acid.

General chemistry questions are off-topic here, but can be asked on [chemistry.se].

It's a simple acid-base-reaction. In order for bile to do its job, i.e work as an emulsifier, it needs to in a basic environment. Bile acids are therefore in their charged, negative state.
The reaction of HCl with bile acid would then be.
[BILE]-COO- + HCl --> BILE-COOH + Cl-
In the human body the reaction would be:
[BILE]-COO- + H3O+ --> BILE-COOH + H2O
There will be hardly any free HCl in the human body, it will immediately react with water to form H3O+ and Cl-. H3O+ will then react with ionized bile acid to give the neutral form of bile acid and water.
So, depending on how you look at it, the product is neutral bile acid and (water or chloride).

That is very interesting. What is "bilic acid"? When I do a web search on bilic acid it does not return any useful results.

What are bilic acids? A typo, I meant bile acids. The answer was updated accordingly.


text:
How did scientists establish the reactions that occur in metabolism?
How did scientists establish that macromolecules like proteins, carbohydrates and lipids are synthesized from other molecules with intermediate products by living cells. Did they observe this under microscope. I want to know this because I am studying bioenergetics and while studying photosynthesis and cellular respiration I have doubt that whether this all stuff is correct or not. I hope that you will help me to clear this doubt.

Welcome to Biology.SE. The way your question is currently written, it is hard to tell exactly what you're asking. See the How to Ask page for help clarifying this question. Please also take the [tour] and read through the [help] to learn more about the site, including what is on-topic and what is not, and how to ask a good question.

What exactly do you have a question about? The fields of metabolism and bioenergetics are huge, much too broad to be covered in a single question here. Is there something in specific you are unsure about?

In addition to biochemical methods, a lot of this was figured out using radioactive tracers. Cells would be fed a radioactive substrate and as they convert the substrate to other molecules through metabolic reactions, the radioactivity can be detected in the products and intermediates.
Calvin's 1940s-50s experiments to establish carbon flow during photosynthesis (i.e. the Calvin-Benson Cycle) using $^{14}CO_2$ remain some of the most elegant work along these lines. You can actually read some of his reports here, though maybe someone else has a good link to a less technical overview.
Similar methods are still used today, though stable isotopes instead of radioactive ones are more commonly used.

The short answer is no, you do not study metabolism under the microscope. (Modern high resolution microscopes can visualize macromolecular processes like transcription and translation, but that is not how they were studied originally.)
In brief, biochemical pathways were studied in broken cells by studying individual reactions or in whole tissues or animals studying chains of reactions. In broken cells chemical methods (often colorimetric, but historically by measuring the evolution of gases) were used to identify products of reactions when particular chemicals are added, and enzymes purified from tissues to find out what reactions they catalyse. Centrifugation methods were used to different organelles from cells (mitochondria, nuclei, ribosomes). In whole cells radioactive precursors are added and one separates and identifies the compounds in the cell to find out which compounds have acquired radioactivity, i.e. what the original compound has been converted to.
In bioenergetics the methods are/were more specialized using spectrometry to identify the oxygenation state of different cytochromes, and the oxygen electrode to measure the utilization of oxygen. In animal cells isolated mitochondria were often used.
This is a very wide area, although because it is not currently very active it is difficult to find an internet source to recommend you. Perhaps someone else knows of one.


text:
Martian Abiogenesis?
In the Miller-Urey experiment the probability of the chemical origin of life under (hypothetical) early Earth atmospheric conditions were assessed. For that water, methane, ammonia, and hydrogen were sealed in a bowl, heated and struck by artificial lightning (see this for the experimental setup). After cooling the mixture down several complex organic molecules (e.g. amino acids) were found by paper chromatography.
So my question is what would happen if instead of using early Earth gases, one puts a concoction similar to current or early atmospheric gases found on/expected to once be found on Mars.
Is it possible to foresee how well that experiment might do and what results it could bring?

Welcome to Biology.SE. I think your question is valid but please do not use references as parts of your questions. Rather (briefly) describe the experiment (the Miller-Urey experiment will probably known by almost everyone around here) and provide a reference for deeper reeding. I edited your question accordingly. Feel free to add anything to or change my edits.


text:
Symmetry in animals
Is symmetry in animals due to DNA or natural selection? By symmetry, I mean the left side is an almost (not perfect) reflection of the right half. Is this due to DNA trying to balance the two half or is it due to natural selection where unbalanced organisms die off more frequently and thus reproduces less. Or is it due to some other factor I had not considered?

Your question presents an artificial dichotomy - "Is symmetry in animals due to DNA or natural selection?" Everything about how an organism appears is ultimately programmed in its DNA, (sometimes heavily) influenced by environmental factors as well. Natural selection creates selective pressures that positively or negatively affect the propagation of different DNA sequences. To learn more about natural selection and evolution, I strongly recommend Understanding Evolution from the University of California, Berkeley - it's really great.

Welcome to Biology.SE. As MattDMo said, the question presents a very obvious dichotomy that is wrong and make the impossible to answer. DNA is a molecule while Natural Selection is a process. You should make sure to acquire some very basic understanding of evolutionary biology. I am voting to close as "unclear" as the question contains issues of semantic.

@Remi.b I have a basic understanding of the two concepts. You are saying it is a dichotomy but this is my question and it is not entirely unrelated. DNA is a molecule, but it is the one that holds the blue print to our bodies. To say it's just a molecule is ridiculous. I want to know if there is a trait in DNA that causes symmetry or if symmetry in complex organisms is do to the process of natural selection. Lastly, you say that I should learn about basic evolutionary biology, but how do I do this if people criticized me for making an effort to ask questions. Isn't that the point of this site?

@MattDMo it is not a duplicate of that post. His post is asking why some organs in the body is not symmetrical. I'm wondering what makes us symmetrical at all.

@MakPo you are not being criticized for making an effort to ask questions, and I was simply pointing out an external resource that could help clear up some of your misconceptions about evolution and natural selection. We are just pointing out that you're framing the question the wrong way - it's not DNA vs. natural selection, symmetry (and all other aspects of life) are a result of the processes of natural selection acting on DNA. While DNA is a very important molecule, it is "just a molecule". I would suggest you [edit] your question to focus on the basics - how did symmetry evolve?

@MakPo Sorry if my comments were discouraging. They were not meant to be. You need to get some knowledge (typically through the ressource that MattDMo suggested) in order to be able to understand why a sentence like I want to know if there is a trait in DNA that causes symmetry or if symmetry in complex organisms is do to the process of natural selection. makes no sense.

Before you consider the development of bilatteral symmetry (which is what you are talking about), you need to look at the overall changes relating to animal body plans.
To begin with, sponges (Porifera) completely lack symmetry and came very early in the evolution of animals. Basically, it's a large cluster of growing cells with some differentiation (ie: choanocytes, amoebocytes, etc.). So the lack of of symmetry is simply related to the lack of complexity.
Then, radial symmetry, which has a "top" and "bottom" but no "left/right" came into play with phyla like Cnidaria. An evolutionary jump from assymetry to bilateral, would be astronomical, so we can think of radial symmetry as an intermediate relating to the increasing complexity of body plan development.
On Bilatteral Symmetry, one key thing is the cephalization. Cephalization is where a majority of the nervous tissue and sensory tissue are clustered in one area (a head). In the evolution of animals, Cephalization came with the evolution of Flatworms (Ptalyhelminthes) where sensory tissue such as ocelli (eye spots) were placed in the head. With the head developed, a "sense of direction" can develop where the right/left/dorsal/ventral sides of the body naturally become distinguished.

Some of the information contained in this post requires additional references. Please [edit] to add citations to reliable sources that support the assertions made here. Unsourced material may be disputed or deleted.


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anabolism in plants
The question is as following:
Which substance has the greatest contribution to the anabolism of glucose in plants. A- Oxygen (O2). B- Water (H2O). C- carbon dioxide (CO2).
The official answer given in this question was C, however I believe H2O and CO2 are equally important in their contribution, because glucose consists of 6 carbon atoms and 12 hydrogen atoms which respectively come from the 6 water molecules and the 6 carbon dioxide molecules needed for the light reaction and calvin cycle. Which step am I missing to the answer? This was by the way a high school biology national olympiad question in my home country, nl.
Kind regards, I'm looking forward to your response!

Water is not rate limiting in these reactions and is not actively consumed in these reactions, whereas carbon dioxide is fixed by an enzyme called rubisco. Have a look at the Calvin-Benson cycle.

But sir how is water not actively consumed, don´t the 12 hydrogen atoms in glucose come from hydrolysis of water? I just came up with the idea that carbon has a far higher mass and thus contributes more to the amount of bio mass, could that be a correct explanation?

I meant that water is in such high concentrations that it is neither considered a reactant nor a product. Its production or consumption does not affect its total concentration or any other rate of reaction where it is involved.

I think what they mean is that since water is split during the light reaction and oxygen is released, most of the mass of the glucose comes from carbon dioxide, because it contributes to the oxygen and carbon part of glucose whereas water only contributes to the hydrogen part which is only a small fraction of the mass


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If the liver can regenerate why can alcohol abuse permanently damage it?
The liver is a fairly unique organ in that it has the ability to regenerate itself even if parts of it are removed/damaged. It is a well known fact that continual alcohol abuse damages the liver and can lead to many liver problems.
Why is this the case? If alcohol does damage the liver, why can it not simply regenerate it's damaged cells from healthy cells?

I'd suggest starting your research by reading about cirrhosis, and following the links as you are interested.

I know what cirrhosis is. I should have been more specific. I meant what exactly is the mechanism which causes cirrhosis in the first place? What is the reason the liver cannot recover from cirrhosis when it does happen?

A healthy hepatic tissue can regenerate: this is an epithelial tissue. That is, the epithelial tissue in the liver can regenerate. Cytotoxic drugs as alcohol lead to steatosis and cirrhosis. Cirrhosis is the substitution of epithelial tissue by connective tissue. This connective tissue not only can't regenerate as, the most important, doesn't perform hepatic functions.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4112892/


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Why does human chromosome 19 have the second highest number of protein-coding genes?
While chromosome 19 only is the 19th largest autosomal chromosome, it contains 1440 protein-coding genes, and thus has the second highest number of protein-coding genes of any human chromosome.
For comparison: If one would naively assume the same density of protein-coding genes as on chr1, which has the highest absolute number of protein coding genes (2109), the anticipation for chr19 would be ~540 protein-coding genes.
The x-axis of this graph highlights the increased density of protein-coding genes on chromosome 19;

I don't think there is any answer to "why".

Within any natural population there are going to be outliers. The distribution graph you show has a long tail, which is to be expected. Look for graphs on the distribution of height, for example, and you'll see that 90% of the values are within a fairly small range, but the 5% on either side stretch out quite far, as there are extreme outliers on both ends.

As extreme outliers in natural populations often are somehow special, and as a n of over 1000 genes would strongly argue against as many independent chance events, I was curious if there is something special about chr 19 or its genes, which could favor such a comparatively high gene density.

Well a very rough analogy type answer is that random mutation is not a very efficient way to make the genome, just like randomly tapping the keyboard is not a very efficient way to write computer code, you'll end up with variation in the efficiency of scripts

Paralogous genes normally lie on different chromosomes, which shows that the chromosomal location is not strictly given by the de-novo mutation / formation of a gene on a given chromosome.

I think that OP is correct that there is something to explain here (i.e., the standard null models for gene distribution across the genome would not predict such an outlier), but I think that nobody knows the answer.

@WYSIWYG I think "why" in this case translates to "what events led to".

This Nature paper from 2004, by Jane Grimwood et al. goes at least a long way towards giving an answer to the question of the OP. In short: there were inordinately many duplications, especially during an event 30-40 million years ago, as well as during a much more recent event. These duplications are, uncharacteristically, predominantly intra-chromosomal rather than inter-chromosomal. Also, chromosome 19 contains a lot of immunoglobin-like paralogues: a type of gene for which it is clearly evolutionarily adaptive to undergo rapid duplication followed by random mutation, as they play a role in adapting to potential antigens.

It's interesting that not only the leader 19, but also 16 and 17 follow a similar trend. Perhaps their size could be the best weight/length proportion to ensure a safe replication? Then what would have to be explained would be 18, so far to the left. That could be if 18 is newer, resulting from the split of a larger chromosome or the fusion of two smaller, having yet no time to accumulate a greater number of genes favoured by the advantages of the "genes positional co-evolution" (if such thing exists).