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"Higher plants" or "vascular plants"?
What is the difference — if any — between "higher plants" and "vascular plants"?
On Wikipedia, "higher plants" redirects to "vascular plants", which seems like an indication that both terms are essentially the same.
Is one of the terms preferred over the other?

Is one of the terms preferred over the other?

Absolutely: "vascular plants" is the preferred one. "Higher plants" should be avoided. Here is a long explanation:
The Great Chain of Being
This term "higher plants", together with the term "higher animals", is just a remnant of a completely wrong concept that has (or shouldn't have) no place in the world after 1859: the Great Chain of Being, or scala naturae  in Latin.
This is the typical medieval representation of the scala naturae:

The Latin text on the ladder says: stone, fire, plant, beast, man, heaven, angel, god.
And here a more "modern" version of it (but equally wrong):

Unfortunately, this absurdity survived until the late twentieth century, and can be seen even today in some books/sites/lectures.
Linnaean Taxonomy
To understand the use of "higher plants" (and "higher animals") in biology, we have to go back a little in time.
When Linnaeus published his Systema Naturae, he divided the nature (Imperium Naturae) in 3 Kingdoms:

Regnum Animale: the animals;
Regnum Vegetabile: the plants;
Regnum Lapideum: the minerals (you read it right).

Note that, in this classification, "animals" correspond to what nowadays we call animals and protozoans, and "plants" correspond to what nowadays we call plants, algae, fungi and bacteria.
You have to keep in mind that this book was first published in 1735, well before the evolutionary biology being proposed in the XIX century and established in the XX century. Therefore, it is a book published when fixism was the current paradigm, full of mentions to the scala naturae.
So, the plants (as well as the animals) showed a continuum of species, going to the lower plants (the bacteria) to the higher plants (the flowering ones). It's worth mentioning again that, by that time, bacteria were plants: Phylum Schyzophyta, to be more precise.
Thus, we have "lower plants" and "higher plants", "lower animals" and "higher animals", as well as "lower minerals" and "higher minerals"!
Unfortunately, this terminology is so embedded in the biological sciences that even today, as I mentioned, we struggle to get rid of it.
Just drop "higher plants", whatever it means
As your Wikipedia link says, "higher plants" is a synonym of vascular plants. However, there are a lot of problems here:
First, this is a remnant of the scala naturae and, just because of that, should be avoided. Think of it as a meaningless term, just like "more evolved organism".
Second, there is no clear and indisputable definition of what is a "higher" plant. Some authors used to define the "higher plants" as the Angiosperms only, or the seed plants (Angiosperms + Gymnosperms), or the vascular plants (Angiosperms, Gymnosperms and Pteridophyta).
For instance, in lusophone biology books, it was very common a division in three groups:

lower plants: bacteria and algae;
intermediate plants: bryophytes and pteridophytes;
higher plants: gymnosperms and angiosperms.

In those books, "higher plants" doesn't mean vascular plants, but seed plants instead. One could argument that those books use an incorrect definition, but my point here is exactly that the definition of "higher plants" is imprecise and wrong by its very nature: there is no correct use.
In conclusion: the definition of "higher plant" is not precise, and because it's related to a completely wrong concept, its use should be avoided.

Thank you for this great explanation. You should definitely think about adding this information to wikipedia, I think an article higher plant should be created.

@user1251007 Yes, that's a good idea.

The difference is specificity.
Higher plant is kind of a general term which refers to their complexity, but is not a very precise term.  As per Oxford Dictionary:

Plants of relatively complex or advanced characteristics, especially vascular plants (including flowering plants).

Vascular plants, on the other hand, are defined a bit more rigorously:

Any of various plants that have the vascular tissues xylem and phloem. The vascular plants include all seed-bearing plants (the gymnosperms and angiosperms) and the pteridophytes (including the ferns, lycophytes, and horsetails). Also called tracheophyte.

(From The American Heritage® Science Dictionary)

I consider them as synonymous, like Wikipedia:

Vascular plants (from Latin vasculum: duct), also known as Tracheophytes (from the equivalent Greek term trachea) and also higher plants, form a large group of plants

In general I would prefer Tracheophytes or vascular plants, because it make clear and implicit in the name what is the exact classification.
But I would prefer land plants instead of Embryophytes.
In any case I could use higher plants when speaking of phylogeny (or fossil plants), where I don't want to associate the character vascular to a  change, i.e. there is a "before" and a "after" but it is better to leave a blurred zone between the two.

I don't quite understand why the term "land plants" should be any better than "embryophytes". Embryophytes seem to be a lineage with a distinctive ability to form embryos at the early stage of their ontogenesis, while land plants include quite a few members which actually "returned" to water.

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What is an adjective that describes the property of conferring fitness?
I find it wordy to repeat

trait X is a trait that confers fitness.

I wonder if I can instead write

trait X is useful.

If not, is there an adjective that describes this property of conferring fitness?

Terms
A trait variant that is associated to a higher fitness than another variant is said to be beneficial or sometimes adaptive. On the other hand, a trait variant that is associated to a lower fitness is said to be deleterious or sometimes maladaptive.
"beneficial / deleterious" vs "adaptive / maladaptive"
The terms are very similar but I would tend to think that there are tendencies of using either "beneficial / deleterious" or "adaptive / maladaptive" depending upon the specific context.
These terms can also be used when talking about genetic variants and not only phenotypic trait variants. In evolutionary genetics, the terms "beneficial / deleterious" are used more often than "adaptive / maladaptive".
Also, in general, the terms "adaptive / maladaptive" are often used in absence of variation for the trait in question in the population while the terms "beneficial / deleterious" are most often used when there is variation in the population.
Note
Note that trait X is a trait that confers fitness does not make much sense as is explained here.

I'm not sure "conferring fitness" is the correct way of thinking about things, since fitness is typically a complex combination of traits, but I think the adjective you are looking for is "adaptive" - though this adjective implies that it has been selected as well as that it has contributed positively to fitness, for any inheritable trait that has been around through a reproductive cycle both would necessarily be true.
From https://www.merriam-webster.com/dictionary/adaptive one of the example sentences is:

Webbed feet is an adaptive trait in aquatic animals.

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How to calculate relative organ weight for a lab animal?
I am trying to calculate relative organ weight for a rat. Anyone knows of a proper formula. It needs to be expressed in g/kg BW.

Do you have access to the rat and the organs?

Basically the formula is:
$$w_r=\frac{w_{organ}}{w_{animal}}$$
Nominally this would be in g/g (since given the weight ranges for both rats and their organs, g is the most adequate unit, and the one you will likely be measuring in on your scales). If you want to force the g/kg unit, you would simply multiply by 1000:
$$w_r=1000\frac{w_{organ}}{w_{animal}}$$
If you have the weight of the organ, you would simply need to find out the weight of the rat:

Ideally this would be measured before the rat is killed.
If you have already extracted the organ, the weight of the rat would be determined from the sum of the weight of the organ and the weight of rest of the cadaver. This is, of course, assuming that the amount of blood and interstitial tissue lost during the operation is negligeable and that the animal was not perfused before organ extraction.
The latter asssumption may well be met, but the first one in all likelihood is not. So this estimate will be biased (towards a slightly higher value) but it may be the best you can do.
If the cadaver has already been discarded you can estimate the mean weight a rat of the same strain at the same age (measure a number of them and determine the mean), and use that value. This will be an even more unreliable estimate, and depending on your treatment (i.e. if you are manipulating the rat weight and not the organ weight) perhaps even worthless, but again, it may be the best you can do.

suppose mice weight is 35 gm and its liver weight is 1.5 gm then relative organ weight would be ;
per 35 gm body weight, liver weight is 1.5 gm
Then, 100 gm body weight, liver weight is?
Therefore= 100*1.5/35
         = 4.29 gm liver weight/100 gm body weight
means 4.29% of body weight is because of liver.
You can make formula in Excel and can carry out big data calculation at ease.

I suppose the OP knows about percentages. Moreover, the question explicitly asks that the relative organ weight has to be expressed in g/kg. Can you edit as to include it?

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Does evolution only give rise to traits that confer fitness?
Does evolution only give rise to traits that confer fitness? In other words, does the existence of a trait imply it's conferring of fitness? If not, what are some counter examples?

I think there's a very important sense in which your question is exactly backwards.  "Fitness" is not really something that is a priori measurable.  Instead, it's measured by an organism surviving to pass on its genes to future generations.  So everything which lives to reproduce is, by definition, "fit".

Rephrasing the question

Does evolution only give rise to traits that confer fitness?

The phrasing is actually a little nonsensical, but it is easy to understand what you mean. The reason is that "fitness" is not a characteristic of individuals but a measure (a variable if you wish) of a characteristic. Imagine you are talking about Shaquille O'Neal and you say "He is height!" instead of "He is tall!". Allow me to rephrase the question correctly. Note that because "high fitness" is a statement relative to the fitness of the others (just like being tall is relative to the average height), I highlighted in my rephrasing of the question this relativity.

Does evolution only give rise to trait variants that are associated with higher fitness than other variants?

Short answer
No!
Examples
Very simple examples include all the genetic diseases.
Reasons
In short, evolution is much more than natural selection. All of the following are reasons for why there are low fitness variants in nature.

genetic drift (incl. bottleneck or founder effect),
spatial variation in the environment and gene flow (hence migration load)
changing environment (incl. the biotic environment and the social environment) and non-equilibrium conditions in general
local peaks in fitness (and the concept of pseudo-species; fitness landscape)
trade-offs
genomic conflicts

and many others...
For more information on the "why" part of the question, you should start with an intro course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.

I saw you posted this as I was typing my own answer; since I already had the bit about beating @Remi.b in my answer I decided to submit it even though it's basically identical to yours.

Thanks, the counter example of genetic diseases is brilliant.

Just a follow up question: why was my phrasing incorrect, i.e. what is the difference between "trait variants that are associated with higher fitness than other variants" than "traits that confer fitness"? Thank you!

@HuiWang Good follow-up question. I edited my post to add more info. Let me know if this clear things up for you.

I'll try to beat @Remi.b to the suggestion that you review Understanding Evolution as a general overview of evolutionary topics.
For a quick answer: no.
Sometimes people confuse the great importance of natural selection in evolution with an equivalency between natural selection and evolution. However, there are many many contributors to evolution, many of which do not involve fitness.
I'll list just a couple examples:
Genetic drift is random change in allele frequency because of random sampling of reproductive organisms.
Founder effect is a somewhat related concept, referring to the change in allele frequency in a population that becomes isolated from the rest of the individuals of a species: that population has a selection of traits that might differ from the species as a whole, and lead to future speciation.
There are many more.


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Is working with (nitrile) gloves around a bunsen burner safe?
Recently I have started in a new microbiology lab, and with a new lab come new habits. When I was working with my bacterial (liquid) culture next to the flame (Bunsen burner) wearing nitrile gloves, my colleague warned me to not wear gloves close to the flame. Personally, I never experienced any problems with them and I think that wearing them provides better sterility.
Is it more dangerous to work with gloves close to the Bunsen burner than without?

new microbiology lab

What're the entry requirements for your lab? If you're working in BSL-2 or greater, the appropriate PPE ensemble is listed and required at all times while you're in there. Likewise, gloves are required whenever you're in contact with potentially infectious materials (OSHA 29CFR1910.1030). There shouldn't be leeway to decide when and when not to wear your PPE ensemble.
As bunsen burners do present a burn hazard, your work with a bunsen burner should be preceded by general lab safety training, and subject to work practice controls. It's safe to wear nitrile gloves working with an open flame, and your gloves are not readily combustible. Burns will typically result from a failure to exercise universal precaution and/or use the burner properly.
If you're working dangerously close to an open flame or with heated materials, consider controlling for injury with thermal gloves, tongs, or engineer out the burner with a biosafety cabinet.

Wearing gloves increases the risk of injury when working next to an open flame since they can melt onto your hand.
Not wearing gloves increases the risk of infection when working with pathogens.
As for sterility, standard examination gloves may be helpful but are not necessary. The gloves aren't packaged sterile, you don't use sterile technique when putting them on, and nothing you touch with them is sterile.
So, whether or not you wear gloves near a flame really depends on what you're doing and the safety requirements of your laboratory.


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Please identify this creature found on the beach
Found on beach in Atlantic Canada in November.
"Sack" is approx. 2" (approx. 5cm) in length.

any opening, or shell? looks like a n innkeeper worm.

Just a guess: https://en.wikipedia.org/wiki/Sipuncula

I've actually seen these before during an invertebrate zoology class in Maine! It's a rat-tailed sea cucumber, Caudina arenata. Though I don't have the taxonomic guide book anymore, I found this blog post that cites an old guide with more info about them.


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Are there special pairs present in the RC of both photosystem I and photosystem II?
I am confused regarding the existence of special pair (primarily regarding PS2). Do both, P680 and P700 have special pair?
I have checked various sources online and have come across conflicting information. For instance wikipedia article on Photosystem (https://en.m.wikipedia.org/wiki/Photosystem_II) says:

Unlike the reaction centers of all other photosystems which have a special pair of closely spaced chlorophyll molecules, the pigment that undergoes the initial photoinduced charge separation in PSII is a chlorophyll monomer.

This is hyperlinked to a study by AW Rutherford which says:

It is proposed that the key event in the evolution of PSII was a mutation that resulted in the separation of the two pigments that made up the special chlorophyll pair, making them into two chlorophylls that were neither special nor paired.

However, Voet and Voet 4ed says that there are two Chla molecules that are analogous to the special pair seen in Photosynthetic Bacteria Reaction Centre (PBRC).
Additionally, I found this (http://www.life.illinois.edu/crofts/ahab/psiistrc.html)

The nature of P680 (the primary donor Chl) is still controversial. The dimeric special pair expected from bacterial centers has not been unambiguously demonstrated, although H198 of D1, and the equivalent in D2, are conserved as putative ligands, and the near IR band of P680+ is diagnostic. Several suggestions have been made that P680 might be monomeric (8-10), and more equivalent to the ancillary Chls of the bacterial reaction center.

The article is not dated unfortunately but I checked that all the citations are prior to 2000.

"Electrons do not exist." --Kenneth Lee Wheeler
https://www.youtube.com/user/kathodosdotcom

@Martin Klvana - what is that? What do you want to say. I dont get it. Why'd you post that? Doesnt answer my question.

Your title and your body have different questions. Please, choose one. Also, if you have conflicting information, please share them. (by the way, both P680 and p700 have a special pair)

Hello Gerardo, please take look at the question again. I have made the required changes.

@Prateek Yadav: i did not intend to answer the question (for that i would use the "Your Anwser" section). i noticed the word "electron" in the title of  your question and commented on that using "Add Comment" section. Meanwhile, the word "electron" has somehow vanished from the title, which is quite appropriate for electron has no real existence.

Thanks so much for the edits, Gerardo. You made the question neat.


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Is it possible to artificially select for flight in pigs?
After reading this rant by Fodor, as a layperson, I was idly wondering whether it would be possible to artifically select for flight in  pigs. Of course by that time the porcine lineage will probably comprise an entirely new species, but what would be the first step in our breeding experiment? And how would it develop thence, hypothetically speaking?

If this is a classic breeding experiment the answer is: nobody can tell. Mutations are (more or less) random. You will have to wait what you get to decide what you can select for.

Nature/environment selects. Would you put selection pressure on pigs by throwing them off of buildings and selecting those who don't hit the ground?

@anongoodnurse : that would be one way but it might take longer than thinking about it a little first, deciding what changes you think you need to achieve flight in pigs & then working out the pre-adaptions & steps you think you'll need to get there then breeding for those stage by stage, which still takes a long time of course.

Intro course to evolutionary biology
I doubt you can get much from the below answer. At the end of the day, the only thing that would really allow you to increase your knowledge is probably an intro course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.
Question

Is it possible to artificially select for flight in pigs?

If by 'artificially select' you refer to selection on available genetic variance, then No, it is not! You'll need plenty of new mutations and it would take a very long time.
Selection
You cannot select for something that does not exist. Selection requires pre-existing phenotypic and genetic variation for the trait of interest. No pigs are flying today, so you cannot increase the frequency of individuals flying by selection.
You will need to wait for mutations that confer such flying ability. Of course, there won't be a single mutation that turns a pig into a flying pig. Simply because flight is really not a simple adaptation for a pig! There are few species you could have chosen for which flight would be harder to think of! You are going to go on a long step-by-step procedure, fixing mutations one at a time by selecting every one of them and that will probably take hundreds of thousands of years or maybe millions of years.
Step-by-step procedure
I suspect you would consider using their front limb for flying. Here is a potential and extremely simplified step-by-step procedure. Of course, if you were thinking of pigs flying using their ears, the procedure wold be drastically different!
You should probably start by attempting to modify their limbs then. You can maybe try to start by selecting for individuals that are better able to manipulate objects with the front limb. Also start selecting for lighter bodies. Also, remove any selection for the ability of fast displacement or moving in the mud as that would select for their current front limbs. Start with some very very simplistic manipulation and increase up to eventually ending up with individuals that have pretty flexible front limb. Make sure to select for front limb that can move perpendicular to the body axis.
Then I don't know if you should aim to make wings out of skin or out of hair-feather like structure. If you're aiming with feather-like structure, you can try play it out with sexual selection just like it evolved in birds. Let's say you're choosing skin wings. Then, maybe selecting for those having broad and thing front limbs might be a good way to go. In the meantime, you've reached anything like that, you probably managed to reduce the body size of your pigs to the size of a mouse with a very elongated body.
Select for jumping abilities and then slowly for flying abilities. You've got flying organisms who's ancestors were pigs! Be aware nobody is going to fund such a useless and incredibly long experiment.

"If by 'artificially select' you refer to selection on available genetic variance, then No, it is not! You'll need plenty of new mutations and it would take a very long time." hmm. "Yes, it is! But you'll need plenty of new mutations and it would take a very long time" there, fixed it for you :)

Evolution really is all about random rolls of the dice, with natural selection deciding the outcome. The question of pigs flying has a precedence. Birds evolved from therapod dinosaurs (one of which is T-rex). But birds have an awful lot of adaptations for flight, including many that must have functioned for some other purpose before they could fly, such as feathers for thermo-regulation. The first wings must have served some function other than flying.
Artificial selection is different from natural selection in that it is accelerated through selective breeding. But the principles are the same. You would first breed for small size and light weight. All three tetrapod species that evolved flight did so with their forelimbs. So you would need to look for long forelimbs, and skin in the armpits...Keep in mind these changes would be random. It would require a staggering number of generations. But perhaps, and entirely hypothetically (as you asked), one could try, and it could be done.

I think you have to consider constraints imposed by embryology in this case. Mutations are "random" in the sense that you can't look into the future and plan what would be good for the organism.  It doesn't mean that absolutely anything is possible. Wings could only evolve if the process of development allows them to.  So you could try with all your might to artificially select pigs that you think might have qualities that allow other flying animals to fly, but wings are never going to appear unless embryological processes are susceptible to this kind of modification.


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Muscle involved in carrying load on head
I have seen people carrying heavy load on their head especially in 3rd world countries, does carrying on head any benefit or harm, which muscle get strengthen in doing it?

Not really an answer, but an interesting related article: http://www.slate.com/articles/news_and_politics/explainer/2010/08/head_case.html


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What is the point in the Neuromuscular Junction?
Surely a direct connection (i.e. an electrical synapse) between motor neurone and the sarcolemma would allow for much faster neuromuscular transmission? It is my understanding that chemical synapses are only useful in facilitating spatial summation of action potentials from multiple presynaptic terminals... muscles have no need for this as they are innervated by a single motor neurone only?

The motor neurons develop from one germ layer, the muscles from another.  They are different cells. Are you asking why evolution didn't happen in another way?

@kmm An electrical synapse can be between any cells.

@kmm I am essentially asking whether there is any advantage in having a chemical synapse at a neuromuscular interface over having a electrical one (and from my understanding I can't see any). It seems strange to me that evolution would result in such a seemingly convoluted mechanism for neuromuscular transmission; I feel like there must be a good reason for having a chemical transmission

@BryanKrause Can be, but generally aren't: hence my question for the OP about why evolution didn't happen another way.

My point was just that them being different cell types doesn't exclude electrical synapses; maybe you weren't trying to imply that but your comment seemed to. Both chemical and electrical synapses are highly complex structures, chemical synapses arguable more so, so there's no a priori reason they couldn't form between dissimilar cells

After much searching on the internet I've found an answer to this question: the neuromuscular junction facilitates amplification of the motor neurone potential to generate a large enough current to depolarise a muscle fibre as muscle fibres have a much larger area of membrane (ie a larger capacitance) than neurons.
Source: Encyclopedia of Neuroscience: Volume One

The reason is the tremendous amplification of the neuromuscular junction. The amplification occurs since a small current is generated in a nerve can rekease large amounts of molecules of the transmitter acetyl-choline ($\require{mhchem} \ce{ACh}$), each of which can open channels in the much larger muscle membrane and can create much larger currents. In addition, a motor nerve fiber often branches profusely to innervate hundreds of muscle fibers, thus providing further amplification.
Finally, the capacitance of the muscular membrane has long been known to be much greater than the capacitance of the nerve membrane, because of the additional membranous systems, such as the transverse tubules in muscular fibers. Thus the capacity of the muscle to store charge is much greater than that of a nerve membrane and much more current must be supplied to depolarize muscle cells directly.


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Finding phylogenetic distance between sequences?
I'm working on a piece of software that does comparative genomic analysis; and I found out in homology methods for functional annotation, it's preferable to pick the high scoring homolog from a distant sequence (i.e. not closely related to the query sequence in the phylogenetic tree).  My question is: why? and also could NCBI taxid for each taxon be used for approximating this distance? if not, then is there a simple way of making this binary decision (close, not close) when given two sequences.

No, because it is really not a binary decision. There are attempts to associate percent pairwise difference with taxonomic ranks (particularly species), but this is problematic because every independent lineage can vary according to its own rate. You could use sequences from different families, or orders, or even phyla, but these two can depend on whether specialists in the field are lumpers, or splitters. For example, all ants are in the same family, and Formicidae is over 100 million years old, while birds that may have diverged from a common ancestor within the last 10 million years are in a different family. You can use pairwise distance OR higher-level taxonomy as a proxy. But it would be crude. Why not program your software to make hard decisions about homology, and then find the closest most distant homologue in terms of pairwise differences?

are you referring to these methods: https://en.wikipedia.org/wiki/Distance_matrices_in_phylogeny

and also what about the reason for picking a homolog that is not closely related to query sequence? is the sequence taxid useful at all?

Yes, distance can be calculated simply by counting the differences between pairs, and then sometimes correcting those distances with various models that assume some of these changes will be masked by multiple changes at the same sites. The taxid tells about classification. Picking a distant homolog far from the query gives you more information about how much a gene can change over time.


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Which life is supported in sterilized 100% pure water?
As sterilized 100% pure water does not contain any mineral and ion, so which type life can survive in sterilized 100% pure water?

Are you asking about what kinds of life can survive in 100% pure water, or what kinds of life can grow in 100% pure water?

If any living form is introduced to the system, that living should be able to survive without any external aid to support energy formation or supply.

If a lunged terrestrial animal is submerged in it, about a few minutes :-) this question needs more background and research to make sense.

Of course many life forms can survive for some time in 100% water. A human for example can survive about 4 minutes in 100% water but I doubt this is what you are interested in! Although there is no commonly accepted definition of life, I think we can say that we all agree that any life form needs to reproduce or somehow grow. So I take your question as

What life forms can reproduce or at least grow "potentially indefinitely" in 100% water?

Any life forms, to grow or reproduce needs matter to make its own constituents. As such, pure water won't provide with such nutrients and no life form can survive in the long run in 100% water.

by going in dormant stage or doing something magical to use the water for energy source. Or device some way to survive till their life expectancy?

Doing something magical :) Energy source is not so much the trouble as the could use solar energy. The main issue are the nutrients to create its own constituents. An organism cannot create a body part from water only. Sure, an organism can be dormant and survive in water for eventually a long time. However, I specifically explained why I would focus on life forms that can reproduce or at least grow in 100% water. Otherwise, pretty much all organisms, incl. humans, are able to survive some time (about 4 minutes for a human I think) in 100% water.

Theoretically, 100% steril
ized means devoid of any kind of microbe, i. e,  bacteria, fungi or virus. But it very difficult to  ensure this. And if we could were able to produce such a pure water then also it's not completely safe. Since other than viruses there are other non cellular pathogens like prions (malicious proteins) which can thrive in a microbe free system.  But it is not to be counted as living.


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How can cabbage worms (Pieris brassicae) smell/see cabbages from a distance?
Recently I did post a question on gardening stackexchange asking if cabbage worms could smell their way back into my cabbages after I moved them away outside my fence. Answers says yes they do, but it seemed to me opinion-based and I cant find anything to support this answers.
Can this type of worm smell/see or have any other type of sensorial navigation thing that can lead them towards cabbages?

Yes, caterpillars have antennae that provide an olfactory sense. I don't know how well this particular caterpillar can smell and if it can travel long distances, but it is able to identify its food source.

I don't understand why you are asking about the caterpillar? The most important way the caterpillar ends up at your plant is because the butterflies deposit their eggs.


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What is this insect from Brasil?

SE Brazil Atlantic rainforest Oct 2017. I'm assuming this is an early stage of an insect. It was crawling around a tree in the moss and was about 6-7mm.

SE atlantic rainforest brazil

I thought maybe a young stage cicada

You almost got it right: it's not a cicada, but it is close related.

This is, indeed, a nymph (what you called a young stage), but not from a cicada as you suspected: it's a nymph from a leafhopper, which are hemipterans from the Family Cicadellidae (cicadas are also hemipterans, but they belong to the Family Cicadidae). More specifically, this seems to be a sharpshooter, which are leafhoppers from the Tribe Proconiini.
Narrowing down to the Genus is more complicated, but I'd guess it is Oncometopia. Here is an image of Oncometopia orbona for comparison:

This other image (also Oncometopia orbona) is even more similar to yours:

Brillient GF   I have more questions on Brazilian insects to follow.


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Why are stem cell therapies more preferred (theoretically) over current measures?
i understand that when stem cells are used to treat injuries using induced pluripotent stem cells (IPS), they can prevent the risk of having any tissue rejection and thus, there isn't a need for use of immunosuppressant drugs.
However, based on the researches using animal models thus far, I note that surgeries are still the main mode of delivery of such stem cell-regenerated organs/organoids. Meaning, to transplant a part of a organ or a tissue into the animal model, a surgery still needs to be done - how is this different from current measures?
Specifically, how are stem cells going to aid or further research into areas such as curing heart or lung diseases and I wonder how are these methods going to be better than current ones.

Stem cell therapy was never going to replace surgery, and it isn't supposed to. We just don't have the tools to move stuff around inside the patient without breaking the skin.
Stem cells therapies offer replacement parts for organs that can't regenerate themselves. For example, after a heart attack the heart often forms a scar where heart tissue has been injured or died. The scar often doesn't conduct electrical signals properly or doesn't beat at all, both of which are a problem for a heart. The scar can't be surgically removed, because there's nothing to replace it with. Stem cell therapy would provide new heart muscle to replace the damaged tissue.
There are of course exceptions, some stem cell therapies are injected and left to 'settle' in the right tissues. That kind of therapy generally doesn't replace a surgery either, because that kind of problem can't be fixed with surgery at all.


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I would like to know what this insect is please

Noted on the side of a tree in the Brazilian Atlantic Rainforest in Oct 2017. About 3-4 cm long . Middle of a very hot day.

That is a planthopper, order Hemiptera, suborder Auchenorhycha, Superfamily Fulgoroidea. It looks to be in the Genus Phrictus. Very similar to a picture I saw on the web of Phrictus diadema.


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Regulation of Glycolysis and other pathways at ‘irreversible’ reaction steps
The hexokinase, phosphofructokinase and pyruvate kinase steps of glycolysis (1,3 and 10, below) are the only ones that are irreversible, and are also the steps where glycolysis is regulated.

Is it necessary for a regulatory step in glycolysis to be irreversible, and if so does this apply to metabolic pathways generally?

Is this a homework question? What is your basis for the generalization from one pathway — namely glycolysis? What have you done to try to answer this question yourself?

@David I rephrased it-please ignore that generalization. I've tried to find an explanation on Berg's 7th ed. Biochemistry. It (and Mathews' Biochemistry from which my course's lectures are taken) states that the reactions are essentially irreversible on physiological conditions, and go on explaining the control on these reactions' enzymes. We've been told at our course several times (with no explanation) that regulation of pathways usually occurs at irreversible steps.

This is not a homework question; I want to know if and why this is true, and if not are there any counter examples some of you may know.

Ok. I'll answer your question over the weekend if nobody else has stepped in first. Too busy with other things tonight.

As far as glycolyis is concerned, the answer is straightforward. In certain cells and tissues there is a pathway working in the opposite direction — gluconeogenesis — in which the ‘irreversible’ steps of glycolysis are, in fact (and of necessity), reversed by a different enzymic reaction in which the position of the equilibrium is in the opposite direction.

Obviously if it is metabolically appropriate for glycolysis to occur it is inappropriate for gluconeogenesis to occur. The only way of turning e.g. glycolysis off while at the same time turning gluconeogenesis on is by regulating the activity of the different enzymes at these three steps.
Glycolysis is, therefore a special case in sharing many reactions with another pathway working in the reverse direction. What about pathways in which the interconversions only proceed in one direction. Classic examples are biosynthetic pathways that are regulated by what is known as ‘feedback’ or ‘end-product’ inhibition. An example (for which I happen to have my own diagram) is the synthesis of isoleucine from threonine in bacteria:

When the concentration of isoleucine increases to a certain amount (sufficient for the cell’s needs) this inhibits the enzyme threonine deaminase, preventing the wasteful conversion of threonine to isoleucine.
The main point is not the position of equilibrium of the threonine deaminase reaction (I haven’t checked it yet) but that it is the first unique step in the synthesis pathway. Hence regulating this step prevents the unnecessary removal of threonine in a way that does not allow the wasteful accumulation of intermediates.
Moral
There is an old party game in which you pass a pair of scissor to your neighbour saying “I pass you these scissors crossed” or “I pass you these scissors uncrossed”. The initiates then tell you whether you have performed the operation correctly. The uninitiated player assumes that what is important is whether the scissors are crossed. In fact, it is whether or not your legs are crossed. Beware of false associations.

This is useful information, but there is also a different aspect on the question. Regardless of the pathway, I think the thermodynamics of an irreversible reaction make it a good candidate for regulation, in general. I believe this is related to the fact that a reaction with a large free energy difference can "drive" a pathway, while an equilibrium reaction cannot. This is explored in Metabolic Control Analysis, see https://en.wikipedia.org/wiki/Metabolic_control_analysis  I am not an expert in this stuff though ...

After consideration I deliberately avoided posing the question of whether all regulation steps in biosynthetic pathways  (e.g. theonine deaminase, above) are thermodynamically irreversible, partly because I did not know if this is so, and partly because I regard it as subsiary to the question of where to control a pathway. For example, if in all cases the first commited step in biosynthetic pathways were irreversible one would conclude that evolution pressures had selected from alternative chemistries. A good question but one I can't answer. The evidence interests me more than theory, though.

@Roland Thanks that's a nice way of looking at it.

@David This might be a digression but are there other criteria for which steps should be regulated other than the first unique ones?

@idnap — not that I can think of, although others may. I could envisage a situation where A ⇋ B → C ⇋D etc. in which B → C is regulated rather than A ⇋ B. If the A ⇋ B reaction didn't require energy or reducing power (e.g. an isomerization) and the equilibrium was midway between the two it wouldn't really matter if the next step were regulated. As A was drawn off in some other direction, B would be converted back to A. Can't think of any examples off the cuff.

@David I understand. Thanks a lot for all your help


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ID please SE Brazil

Noted higher in the hills of the Atlantic rainforest in SE Brazil during October 2016

Looks to me like a Lonomia obliqua, from South America, particularly southern Brazil.

(Coursety of inaturalist.org)

(Courtesy of televisionsworld.com)
The same hairy green projections, the same red bottomed legs, pointed at the front of the caterpillar.  You also notice on the second photo that it has those two black projections on the back.
The one thing that makes me just a hair uncertain is the colouration of the skin in your photo - it looks whiter.  But then again, your photo is much more saturated than any others I found, so it make be an illusion, or even just a genetic variance.

The similarity is definitly there - maybe a different moth of the same family ? The bright yellow head and orange dots on the flank were very obvious


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Why do classic psychedelics not cause withdrawal, despite high tolerance?
"Classical" psychedelics, such as LSD, DMT, and Mescaline, are serotonin agonists that cause hallucinogenic effects. They are notorious for having rapid tolerance, such that after consuming such substances, one would need to (at least) double the dose to feel the same effect if taken daily. No other substance, not even opiates, have such a high tolerance curve.  While this tolerance contributes to the less-addictiveness nature of psychedelics, there is no observed withdrawal. Furthermore, because of the high Therapeutic Index, some users may consume large doses.
Wouldn't such tolerance result from 5HT downregulation, and therefore cause withdrawal? Is it something with serotonin, or is the mechanism different?
There is evidence that 5HT downregulation is what actually causes the effects of anti-depressants. This explains why it takes a few weeks for SSRIs to kick in. Perhaps, this explains why psychedelics can have an antidepressant effect? Perhaps, unlike other neurotransmitters, activation and downregulation of 5HT is not harmful?
https://www.ncbi.nlm.nih.gov/pubmed/7972628

I would say it is very debatable if those drugs are non-addictive and do not cause withdrawal. (Also, withdrawal is not "just" a physical effect.)

It's not debatable: they are not addictive and there is no withdrawal.

@Remi.b the question core is all about tolerance, in turn boiling down to the [down]regulation of neurotransmitter-receptor systems. This is perfectly ontopic here imo.

Short answer
Withdrawal effects are generally associated with drugs that induce feelings of euphoria by stimulating the reward center of the brain, either directly (cocaine, morphine) or indirectly (alcohol, nicotine). The classic hallucinogens have little effect on the dopaminergic pathways and hence do not cause serious withdrawal effects as observed with other classes of psychoactive drugs.
Background
Withdrawal is defined by the WHO as:

a group of symptoms [that] occur on cessation or reduction of use of a
  psychoactive substance that has been taken repeatedly, usually for a
  prolonged period and/ or in high doses.

The typical drugs that are associated with withdrawal are alcohol and other sedatives, opioids, and stimulants.
Alcohol and sedative withdrawal can lead to anxiety, agitation, and depression. Opioid withdrawal results in drug-seeking behavior that may continue after the physical symptoms have abated. Stimulant withdrawal (the ''crash") is associated with depression, malaise, inertia, and instability (source: WHO).
All these characteristic symptoms are basically caused by the fact that the nervous system counteracts the drugs effects and downregulates the receptor systems activated by the drug. Therefore, more and more of the drug is needed. Indeed, downregulation is one of the physilogical mechanisms underlying tolerance (Stewart, 1993):

Tolerance refers to the decreased effectiveness of a given drug with repeated administration.

There are many factors underlying tolerance. For example, there is acute, short-term tolerance seen with cocaine use, but also a long-term tolerance form example seen in opioids. One factor in developing (long-term) tolerance is a downregulation of the receptor systems involved. Alcohol and other sedatives target the GABAA system. GABA being the primary inhibitory neurotransmitter in the central nervous system, it's not surprising that abstinence in a situation of tolerance results in over-stimulation of the nervous system (anxiety, agitation). Likewise, opioid tolerance results in mu-opioid receptor downregulation (Stafford et al., 2011). Given that mu receptors mediate positive reinforcement following direct (e.g.., morphine and other opioids), or indirect (e.g., alcohol, cannabinoids, nicotine) activation it is readily apparent why opioid abstinence results in the craving for the drug, as it is thought that after prolonged use, the user is unable to experience pleasure without the drug. At this point, the person is addicted (source: The Treatment Center). According to the NIH

Addiction is defined as a chronic, relapsing brain disease that is characterized by compulsive drug seeking and use, despite harmful consequences.

Now we come to the conclusion that dopamine is central to addiction, also for drugs not directly activating it, such as alcohol and nicotine. The latter group indirectly release dopamine in the brain's reward center (the limbic system).
The classic hallucinogens stimulate the serotinergic system, and specifically the 5HT2A receptors (López-Giménez, González-Maeso, 2017), but fail to activate the reward centers in the brain. Indeed, all addictive drugs activate the reward circuitry of the brain, thereby producing the subjective “high” that the drug abuser seeks (Gardner, 2011). Tolerance to these drugs has rarely been reported (Smith et al., 1999) and LSD  rarely produces serious withdrawal symptoms (source: LSD Abuse Help. But in rare cases, tolerance can develop and is associated with 5HT2A receptor downregulation (Gresch et al., 2005) and the development of hallucinogen persisting perception disorder (HPPD). An LSD tolerance can be developed quickly, although it usually dissipates within just a few days depending on the user, their dosages and frequency of use. Long term tolerances are uncommon because users do not frequently repeat doses of LSD without taking breaks in between (source: Hallucinogens).
The SSRIs you mention basically work by downregulation of presynaptic 5HT1A receptors (Celeda et al., 2004), which are unrelated to the effects of hallucinogens.
References
- Celeda et al., J Psychiatry Neurosci (2004); 29(4): 252–65
- Gardner, Adv Psychosom Med (2011); 30: 22–60
- Gresch et al., Neuropsychopharmacology (2005); 30: 1693–1702
- López-Giménez, González-Maeso, Curr Top Behav Neurosci (in press)
- Smith et al., Psychopharmacology (1999); 144(3): 248–54
- Stafford et al., Pharmacol Biochem Behav (2001); 69(1-2):233-7
- Stewart & Baidani, Behav Pharmacol (1993); 4(4): 289-312

You may add that tolerance to psychedelics disappear extremely fast, unlike tolerance to drugs like ethanol or morphine.

LSD is known to activate D2 receptors.

@GerardoFurtado - done

Great, good on you!

@GerardoFurtado being nicked AliceD I couldn't let this one pass, could I ;-)

@Remi.b I reckon this question is very on topic here, hence my +1 to both OP and answerer... this other one, from a couple of days ago, is a bit more off topic, but still an interesting one: https://biology.stackexchange.com/a/67793/24284 . Coincidentally, two interesting questions about psychotropics in the same week.

@Remi.b thanks for your comments! This question is better asked here than over at Health and in fact is spot on ontopic here imo. This post is all about pharmacodynamics and kinetics, receptor downregulation and neurotransmitter systems. More Bio you possibly can't get, right? But yes, withdrawal effects per se are also on topic at Health, but even more so on CogSci, but then, something being more ontopic elsewhere is no reason to close it here. But again, the question core is neurosci and therefore best asked here. And no, I'm not Alice, my surname starts with an S and I'm a bloke :-)

@AliceD What a deception on your name! I removed my comments and my close vote following you and Gerardo's comments. Thanks


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What is the meaning of pygo and pagus in the word pygopagus?
I know definition of the disease pygopagus but I want to know the meaning of separate parts of it, in fact what's the meaning of pygo- and -pagus in terminology?

I'm voting to close this question as off-topic because it is a question of ethymology and should be asked on english.SE. Note also, that biology is not medicine anyway. So,if you were looking for a definition of this disease, you should ask on Health.SE.

Firs of all, etymology not ethymology! as I mentioned I know the definition so I am not looking for the definition of disease! and as far as I know prefix and suffixes are studied in terminology, so I wanted to ask that is pagus a suffix or not?

First of all, First not Firs! Joking... thanks for correcting me on that. I'm sorry if you thought I said you were looking for a definition. I said if you were looking for a definition of this disease, you should ask on Health.SE. It was only indicative. Terminology (study of the terms of their use) questions (about terms used in biology) are on-topic. I don't think etymology questions (the study of the origin of words) are on-topic. I am voting to close. I think your question would be on-topic on english.SE or maybe linguistics.SE

Gr: Pygo/pyge (tail, rump) + pagus (fixed). Any decent dictionary will give you the etymology of the word.

FWIW Pygé is not "tail" (that's oura). Pygé means ass (or arse in British English), and it's a vulgar term in Ancient Greek.

According to Wiktionary.com:

pygo- means "rump" or "posterior" from Ancient Greek πυγή (pugḗ, “tail, rump”).

According to dictionary.com:

-pagus means "fixation" or "something fixed or solid" from Greek  págos.

So literally, pygopagus (or conjoined twins attached at the butt) means "fixed rumps".


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How long does it take to extract a tree core for dendrochronological analysis
I'm going to do research in the tropics and am considering using tree cores for part of my analysis. However, for my planning:
How long does it take on average to extract a tree core of a tree with dbh ~50 cm? Trees will vary in wood density between 0.2 and 0.8.
The time includes labelling and storing in a bag, etc.
Tools: increment haglof borer. So I won't take a whole cross section, rather a small core of ~5 mm diameter that goes until the core.
And no picture because I need a more high quality image to be able to do my analysis.

Extract the core?  What do you mean?  Do you mean cut a cross-section?  In any case, it will very much depend what tools you have, how fast you work, etc.

You want to store cross section of 50cm tree cross-section in a bag? Can't you just take pictures?

Oh I guess you're planning to drill a sample through the trunk, are you?

Exactly, that is the plan.

Given the assumption that you know how to properly core (i.e., you've done this before): taking into account fatigue, bark abnormalities, post-processing and storage, and walking between nearby trees, I'd guess you'd average 5-10 every hour across the course of a full day.


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Validity of Acoustic Weapon Effects on Biological Organisms?
There is alot of rather contradictory information present on the biological effects of acoustic weapons with a bevy of scientific articles claiming that they cause harm to biological organisms with effects such as nausia, gagging, and disorientation. These articles are mostly from older scientific articles and modern government scientific reports on the issue, and statements by military leaders overseeing the development of the weapons (including defence contractors). Contradictory claims are also being made by a multitude of scientific sources from a variety of different countries and backgrounds.
I am not sure which one is correct after reading about a dozen articles from both sides. Does anyone have any insight on this issue?
Of note, there are a multitude of crackpots and conspiracy theorists that believe that the acoustic weapons are real and can do outworldly things- the media seems to have bought into these speculations thouroughly and should probably not be trusted.
Here are two articles (one claiming they work and the other denying it especially pertaining to infrasound):
Bioeffects of Selected Nonlethal Weapons
Acoustic Weapons - A Prospective Assessment

technically a concussion grenade or even the bang part of a "flashbang" is an acoustic weapon.

There are a few things which can lead to miscommunication regarding the potency of acoustic weapons, but there are two main things to consider: source levels and duration.
Most organisms can tolerate loud sounds, within reason, for a short period of time. However, no matter how short, at certain levels acoustic weapons can cause temporary or permanent hearing loss, nausia, gagging, and disorientation.  Weapons with a lower source level played over a longer duration will be easier for organisms to initially ignore, but exposure to weaponized source levels over time will lead to internal issues with health, including a decrease in fecundity and nutrient digestion.
Often military and sometimes scientific reports will focus on one particular type of weapon used for a specific purpose, and deem its use acceptable or not. Many scientific studies take more factors or variations into consideration.
Ultimately, its risky because we don't have enough data about the long-term effects acoustic weapons can have on a population, and they also don't appear to be particularly effective when it comes to humans. The Acoustic Weapons (chapter 7) in 'Non-Lethal' Weapons1 by Neil Davison sums it up nicely.
Reference:
1: Davison, N. (2009). 'Non-Lethal' Weapons. Springer.

Welcome to Biology.SE! This looks like a good answer and it's great that you've provided a supporting reference. However, please include the complete reference information since links can (and do) break — for example journals may periodically reorganize their websites. One easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information. This is a good example of how to format references. Thanks!

Got it! Please see edit.  I hope that clear things up.

Yes that was better. (+1) I took the liberty of including the complete reference information since having the publisher can be helpful, but mostly to satisfy my OCD tendencies.

Thanks!  I see the difference now.


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Nerve excitability and K+ concentration
My book says that the excitability of the nerve is increased when increasing the the potassium ion (K+) concentration in the extracellular fluid and vice versa.
I don't understand this mechanism could someone explain it for me!
Thanks in advance!

Just for reference, what book are you speaking of?

my physiology book which my college provide.


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Does donating blood lower testosterone levels?
I'm a guy and I decided to donate blood because of persuasion. My testicles feel weak afterwards specifically. I mean they feel like they're compensating -- assuming that makes sense.
Is this because significant blood volume loss would affect testosterone? Are the testes working harder to produce testosterone after a loss of so much blood from the body?
I also feel a little weaker overall as well, but the question focuses on testosterone. Clarification?

No, on the contrary donating blood increases testosterone levels in blood.
Testosterone actually decreases the level of the iron-regulatory hormone; hepcidin, allowing for more iron to be absorbed from foods. This is one of the reasons why men tend to have higher hemoglobin levels and larger blood volume than women do but over the time excessive amounts of iron in body can suppress the function of the hypothalamus, pituitary gland, and testicular leydig- and sertoli-cells, resulting in lowered testosterone levels. Donating blood reduces excess iron build in men and boost testosterone level in blood.
Sometimes people who donate blood notice a few minor side effects like weakness, nausea, light-headedness, dizziness, or fainting, but these symptoms usually go away quickly. These symptoms occur because the donor's body usually replaces the liquid part of blood (plasma) within 72 hours after giving blood. It generally takes about 4–8 weeks to regenerate the red blood cells lost during a blood donation.
References
http://knowledgeofhealth.com/to-boost-testosterone-maybe-donate-blood/
https://www.anabolicmen.com/iron-and-testosterone/


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Which function do nicotinic receptors have in the periphery?
I came across this question today, it says:

Nicotinic receptors stimulation is directly responsible for …....

I should fill the spaces by one of the following choices:

Increasing the excitability of sympathetic postganglionic neurons.
increasing the the force of stomach contraction.
delaying the emptying of liquids from the stomach.
decreasing the excitability of sympathetic postganglionic neurons.

The only article speaking about the nicotinic receptors in my physiology book says that they are cholinergic receptors found in the autonomic ganglia, i.e., they are found on the postganglionic neurons.
So when I tried to solve the question, I thought the upper three answers are correct. Specifically, because stimulating the receptors on the postganglionic neurons will increase their excitability, option 1 seems to make sense.
But if that postganglionic cell happen to be sympathetic it may provoke the emptying of the liquids from stomach to be delayed (choice 3)?
And, if it was parasympathetic the force of stomach contraction would also increase (choice 2)?
I am confused as all three answers 1) 2) and 3) seem to be correct and the question asks specifically for one correct answer. Could someone help me find the correct answer, but put simply please, as I'm just a first-year dental student.

Short answer
1
Background
Nicotinic recepeptors (nAchRs) are widely distributed in the central and peripheral nervous system. Your question seems to focus on the peripheral nervous system. Taken from (Taylor, 2012):
In the periphery, nAchRs are found in:

Innervated skeletal muscle, especially postsynaptically in the motor end plate;
The presynaptic nerve ending in some motor neurons to control Ach release;
Ganglia at the postsynaptic dendrite and nerve cell bodies, and presynaptically to control Ach release.

Now in your answer the options 2 and 3 are incorrect, as muscarinic Ach receptors regulate gastric fluid secretion (Aihara, 2005) and contraction (Kitazawa et al., 2006). Given that nAchRs are excitatory receptors. In muscle cells, the binding of Ach leads to an opening of the associated ion channel, in turn producing a rapid increase in the cellular permeability of sodium and calcium ions, resulting in the depolarization and excitation of the muscle cell, thereby producing a muscular contraction (source: EMBL-EBI). This leaves only one opion left, namely 1). Since this was basically answering the question by exclusion, below Fig. 1 shows that answer 1) is indeed the correct one through a more positive approach - the top panel clrearly confirms that the sympathetic pathway deploys Acetylcholinergic neurons to stimulate its postganglionic adrenergic neurons.

Fig. 1. Ach in the peripehral nervous system. source: Austin Community College
References
- Ayhara, Gastroint, Liver Physiol (2005); 2886): G1199-207
- Kitazawa et al., Eur J Pharmacol (2007); 554(2-3): 212-22
- Taylor, Primer on the Autonomic Nervous System (3rd Ed. ( 2012}


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Correct migration rate expression in infinite island model
In Sewall Wright's infinite island model, where all demes exchange migrants each generation, I have seen the migration rate stated variously as $m$ or $\frac{m}{d - 1}$ (as in Matthew B. Hamilton's Population Genetics textbook, chapter 4, p. 132, figure 4.12), where d is the number of demes.
My question is, which expression for the migration rate is the correct one?
If it's the latter, then where does the "-1" come from?

Definition of $m$
There is no correct or wrong expression. It all depends what exactly you are interested in and what is the definition of m in a specific paper.
Def. 1
Some models assume that $m$ is the migration rate from a given population to another given population.
Def. 2
Some models assume that $m$ is the probability of migrating to any other population. In a two population case, this definition and the above are the same. In other case, the probability of migration to a given population is $\frac{m}{d-1}$
Def. 3
Some models assume a migration pool. With probability $m$ an individual is a migrant, goes to the migrant-pool and is then redistributed among all other populations (only works for island models). In such model, a migrant could be an individual that actually come back to the same population. So, the probability of really migrating is $\frac{m (d-1)}{d}$ and assuming equal migration rate among all populations, the probability to migrate to a given population is $\frac{m}{d-1}$.
Fst
If you're dealing with $F_{ST}$ in a finite island model, then you will have some $\frac{m d}{d-1}$ terms. I talk about it in this post but it is not complete, so you might want to read Slatkin (1991) and Charlesworth (1998)

Thanks! Though this is a bit more challenging. I am building an R simulation where I have $K$ subpopulations and a migration rate of individuals. Initially, I just set the migration rate equal to $m$ (or $\frac{m}{2}$ for Kimura's linear stepping-stone model), but now I see that it should also depend on $K$.

Well, it depends upon what definition you want to give to $m$. If you want to match your simulations with results of some other paper, then make sure to copy their definition of $m$. Otherwise, most people call $m$ as being the migration rate between any two populations (without migrant pool complication or anything). Note however, that if you have populations of different sizes (or if migration depends upon local population mean fitness aka. hard selection), then the forward and backward mutation rates may differ and you'll have to make your definition clear regarding this issue again.

R is extremely slow. You'll find plenty of simulation platforms written in C++ that will be infinitely faster that what you'll code in R. So, if you need speed,
you will find advice here. SimBit is a simulation platform I wrote myself if you are interested.

Thanks! I will take a look at SimBit. It sounds very interesting.

Do you know where the -1 in the equation for the migration probability comes from? My guess is that it is used as a correction factor to make the estimator unbiased, but I am uncertain.


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ID this insect please. SE Brazil Oct 2017

A number of these large flies were praying on smaller stuff / mid day / in the low altitude rainforest sections of SE Brazilian Rainforest

Welcome to Bio SE, @BBM56. Here is a tip: if an answer is useful, like my answer for your previous question, please accept it. If you don't accept - or upvote - the answers you get people stop answering (I mean I do).

This is, for sure, a robber fly (Diptera, Asilidae). My guess is that this one belongs to the Genus Promachus.
Here is a photo of Promachus rufipes (from North America) for comparison:

Coincidentally, even the prey (a wasp) is in the same position of the one in your photo!
This Genus has 9 species. If this is in fact Promachus, you'll have to find out which are found in South America.


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What is the function of the Hyoepiglottic ligament?
The hyoepiglottic ligament (ligamentum hyoepiglotticum) is an elastic band that connects the epiglottis to the hyoid bone.
Although I can find information about the clinical significance of this ligament (mentioned here), I have not been able to find a definitive or reputable description of its actual physiology/function.
Can anyone provide a reputably-supported description of the function (physiology) of the hyoepiglottic ligament?

My thought was that the hyoepiglottic ligament might act as a see-saw during swallowing. Specifically, my assumption was that as the hyoid is raised during swallowing (thus raising the hyo- end of the ligament), the opposite end of the hyoepiglottic ligament (attached to the epiglottis) is pushed down, forcing the epiglottis to cover the glottis to prevent food stuffs from getting into the trachea. Is this possibly right?

Note: I would be (almost) equally happy if someone can find a reputable source that claims we don't actually know its function (if that is indeed the case).

Have you read this paper? It has a brief review in the introduction of the proposed function of the hyoepiglottic ligament during swallowing, and the Discussion suggests a few mechanisms of function during phonation, respiration and swallowing. This paper which is older is also worth reading for a discussion of a model of its role in deglutition. Were you looking for something more evidence-based?

I'm not sure about the validity of your proposal - a ligament is quite 'stretchy' and I'm not aware of any central attachment point of the hyoepiglottic ligament, so I can''t visualise it being able to act as a 'seesaw'.

@anon yes, my proposal seemed not entirely likely to me, but I had not come up with anything better :p. Your linked abstracts are both interesting and much more on the topic of physiology than anything I had found. I'd say if you draw up an answer detailing/summarizing the main points of the actual full papers, I wouldn't mind accepting this as an answer worth awarding. Of course, I still welcome others to respond :)

It's an interesting question. This 2010 paper contains some discussion of the function of the hyoepiglottic ligament. The following is a quote from the introduction:

The epiglottis is connected to the
  hyoid bone by the hyoepiglottic ligament (ligamentum
  hyoepiglotticum), which is a connective tissue structure that
  serves as the roof of the paraglottic space and the
  preepiglottic space. Anatomically, the hyoepiglottic ligament
  separates the supraglottic larynx from the base of the
  tongue. Some clinical studies have shown that this
  ligament inhibits the spread and invasion of carcinoma... The hyoepiglottic ligament is elongated by
  approximation of the thyroid to the hyoid during swallowing.
  Tension on the ligament results in a “snap” retroversion
  of the epiglottis. Thus, the folded epiglottis represents a
  state of higher energy than that represented by the unfolded
  epiglottis; relaxation of the tension on the hyoepiglottic
  ligament releases the cartilage to automatically return to its
  normal resting position [emphasis mine].

In the study, the authors demonstrate histologically that the hyoepiglottic ligament is bipartite, with a part they call the pars hyoideus connecting the anterior epiglottis to the hyoid, and a part they call the pars lingualis connecting the epiglottis to the root of the tongue (they claim that this attachment to the tongue was previously unreported). Another quote from the paper follows:

It is suggested that the pars lingualis plays an
  important role in active mechanisms such as upward
  movement of the epiglottis during phonation associated
  with tension of the lingual muscle and supraglottic airway
  patency during respiration.

To get some idea of how tension in a ligament anterior to the epiglottis can cause posterior movement (i.e. closure of the epiglottic 'flap'), I found this 1979 paper useful. They used cinefluorography to investigate the biomechanics of the epiglottis. The following lengthy quote should help to clarify the proposed model:

The radiographic observations indicate that
  at the peak of the deglutitional excursion of the
  hyoid bone and the larynx the following circumstances
  prevail:
(1) Forward translation of the hyoid bone in
  conjunction with extreme thyroid-hyoid approximation
  causes extreme elongation and
  tension on the hyo-epiglottic ligament at its attachment
  to the margins of the epiglottic
  tubercle.
(2) The compression of the median thyrohyoid
  fold, secondary to extreme thyroidhyoid
  approximation, tends to make the epiglottic
  tubercle bulge backward transversely
  as well as vertically.
The principle of the mechanism of folding
  deduced from these observations is demonstrated
  in a working model that can be set up
  in a few seconds. All that is needed is a rectangular
  piece of fairly stiff paper. The piece
  of paper represents the complete epiglottic
  cartilage (epiglottis and tubercle). A $\Lambda$-shaped
  crease is applied at the center (Fig. 4) to simulate
  the groove on the back of the cartilage,
  between the epiglottic tubercle below and the
  epiglottis proper above. One next applies stress to the model from the opposite side, at
  the site of attachment of the hyo-epiglottic
  ligament. This is done by grasping the paper
  lightly at the edges, below the level of the
  crease, whereupon the part above the crease,
  representing the epiglottis, immediately begins
  to fold down.
  Each limb of the crease functions as the
  directrix of a cone; the apex of the crease is
  the vertex of the cone. When the paper is
  gripped the directrices rotate towards each
  other and pull the attached paper after them,
  giving it a conical shape.

I've attached the figure 4 from the paper to illustrate better (I'm not sure if that's allowed on SE; please delete it if that's appropriate):
$\hskip 2 in$
The authors of this paper and this paper argue that the model just given does not fully explain the motion of the epiglottis during swallowing. The latter paper describes the existence of distinct lateral hyoepiglottic ligaments attaching to the ends of the greater horns of the hyoid bone. These, they argue, transmit the biomechanical forces generated by the movements of the hyoid and thyroid cartilage to the epiglottis to cause downfolding, although their full argument is too long to reproduce here.
Hopefully all of that has shed a little light on the possible function of this ligament. It seems to be quite complex, but there appears to be a relative consensus that the transmission of tension via this ligament is important in causing the folding down of the epiglottis during swallowing.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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

Salt water macro algae ( calurpa ) discharge CO2 at night , but I don't know if it is from stomata.  I had a 75 salt tank with a lot of calurpa and few fish ; the pH would drop impressively each night considering the high buffering capacity. as I remember 8.7 to 8.3.

Land plants might do better to keep their CO2 to use in the morning, unless they produce way too much of it.
CO2 is present in air at concentration around 0.03%. (In recent years it's gone up to 0.04%.) That's a low concentration to work against.
Remember, in the daytime those plants are sending water vapor and O2 OUT the stomata. It's a pressure gradient. Why let CO2 out at night and then  depend on it coming IN against the flow the next day?
Plants have ways to grab onto CO2 so it won't just drift away. They convert it to things that aren't gases -- oxaloacetic acid or malate, or 3-phosphoglycerate, or possibly others that haven't been noticed yet.
These compounds can be stored. Then restore the CO2 precisely when and where it is needed.
Some CO2 gets this treatment at the roots (where CO2 concentration can sometimes be as high as 8%) and the storage compounds then get sent toward the leaves along with water and minerals.
CO2 from roots

Leaves have no need to 'exhale' carbon dioxide - it gets consumed by photosynthesis.
Elsewhere in the plant, metabolic processes produce carbon dioxide. This escapes via inter-cellular gas channels that, in woody plants, terminate as lenticels (little pores) on the stem surface. Oxygen for metabolism diffuses into the plant in the same inter-cellular spaces as carbon dioxide diffuses out.
With roots, the oxygen necessary for metabolic processes is dissolved in water.
If you've meant to ask about leaf adsorption of carbon dioxide and when stomata close, it depends on what carbon fixation scheme the plant exhibits, CAM, C4, or C3.
You might want to also consult an  answer I gave to a similar question previously posed here.

+1 just for mentioning carbon fixation schemes which will each asnwer this very differently..

OP is asking about the fate of CO2 at night, when the stomata are closed and there is no CO2 fixation.

I think your answer is quite good, but could use some expansion - what happens during the night with CAM, C4 or C3? And how do these affect carbon dioxide diffusion, and respiration? Further, how much respiration is occurring at night?

Okay, @GrumpyMammoth, I added a link to a prior similar question that I answered. My original answer to this question included links to' lenticels' and 'carbons fixation'. The Wikipedia articles explain those two aspects of plant function in good enough detail, IMO.

Carbon dioxide is gas and can easily diffuse out through epidermal cell following concentration gradient. As during night respiration is going on, lot of Carbon dioxide accumulates inside leaf to form a concentration gradient which is sufficient to cause diffusion.


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Why are the results of local BLAST and miRbase BLAST different?
I am trying to reproduce locally on my computer what I get running mirbase on their website using BLAST. The search sequences is: mature miRNAs which I had downloaded on my computer and make it as a BLAST database with command:
./makeblastdb -in /home/marianoavino/Downloads/mature.fa -dbtype 'nucl' -out /home/marianoavino/Downloads/mature

then on mirbase I see they use an e-value of 10, which I leave locally.
On mirbase at the end of the analysis they give you these parameter setting:
Search parameters
Search algorithm:
    BLASTN
Sequence database:
    mature
Evalue cutoff:
    10
Max alignments:
    100
Word size:
    4
Match score:
    +5
Mismatch penalty:
    -4

and this is the command line I use on my computer for BLAST
./blastn -db /home/marianoavino/Downloads/mature -evalue 10 -word_size 4 -query /home/marianoavino/Downloads/testinputblast.fasta -task "blastn" -out /home/marianoavino/Downloads/testBLast.out

The results of the two analysis are different, with mirbase finding much more stuff than local BLAST.
Do you have any idea on which parameters I should use on local blast command line to match those listed mirbase parameters in order to get the same answer?

The main problem I could identify is that your scoring matrix is not the same; as you said miRbase uses match score of +5 and mismatch penalty of -4.
The BLASTN defaults can be found here. However, I ran the local BLAST using the exact command that you mentioned and the default values that it used were:
reward = +1
penalty = -2
Matrix: blastn matrix 1 -2
Gap Penalties: Existence: 0, Extension: 2.5

The other reasons could be the difference in the database itself (the sequences used) or the version of BLAST used in the two cases.


text:
Facial uniqueness of some animals of the same species
Do birds of the same species ,such as each pigeon that we see in cities, have unique facial geometries (facial phenotypes) regardless of their feather ,colors, spots etc? Sometimes it is almost impossible to distinguish two pigeons between each other just looking at their facial structure and curvature of their heads.
Human face has evolved with countless of varieties such as shape of nose, distance between the eyes, proportion of mouth and the nose etc.
Billions of humans have existed so far and billions of humans will ever exist each have unique facial features.
However some animals of the same species (birds like pigeons, baby chicks, fish species like sardines and sea bream etc) look like sharing a limited amount of variations in their facial geometries therefore they become distinguishable only because of their colors, patterns etc. I know that mammals such as apes or dogs have unique faces almost  as distinctive as humans. I also know that human brain is already attuned to distinguish differences in human faces more than any other animal.
What I would like to understand whether all pigeons have existed so far and will exist furthermore have unique facial geometries like humans? Or do they all differ in millimetric level which cannot be captured by naked human eyes? Can two pigeons(or sardines) of the same species share exact same facial geometries unlike humans?  I couldn't have satisfactory answers in this subject so far. Can you please explain?

Looking forward to a good answer to this. I’ve pondered it many times myself.

Possibly a duplicate of Why do different humans look different? or Why are humans so variable in appearance.

unless you can provide a study showing greater variation in humans it is a duplicate question. humans are specialized in detected human features so we are naturally biased.


text:
Does pepsin digest plant protein?
This may sound trivial, but...
Protein is sourced from plants and animals. Pepsin and HCl digest meat (animal protein). Does pepsin also digest plant-based proteins?
I took a look at few articles online and this. None seems to explain what I am after.

What you probably are missing here is that plant proteins are fundamentally indifferent from animal proteins; both are polymers of amino acids, and pepsin just breaks these polymers into oligomers (or monomers).

@another'Homosapien' in this case, can we say that amount of the pepsin is required for plant protein cleaving is less than of meat and may I know why?

well, you can't really answer this question without including a lot more variables. To say at the simplest level, enzymes are catalysts, so digesting both plant proteins and animal proteins requires quite similar amount of pepsin. Again, this is the simplest one you can get, the more details you add, the more complicated it gets.

Yes, pepsin does digest plant proteins also. Pepsin is a protein and its job is to cut other proteins (also known as polypeptides) into smaller pieces. Proteins are made of amino acids and there are 20 amino acids found in proteins. Pepsin cuts the bond between two amino acids to break the protein into smaller pieces. When pepsin encounters a tryptophan (Trp), tyrosine (Tyr), and/or phenylalanine (Phe), it cuts the bond between that amino acid and the one next one, as shown below.

image source
Proteins from plants contain these amino acids so pepsin can cleave plant proteins.


text:
Is it possible to determine what tissue a DNA sample came from based solely on its sequence?
All cells have the same genome and differ only by the expression pattern. Is it possible to determine the tissue origin of a cell based on its DNA sequence using short tandem repeat (STR) analysis or copy number variation (CNV) analysis?

You say yourself that all cells have the same sequence, so how could you tell them apart based solely on sequence?

I don't know; that's why I am asking. Wikipedia page for STR analysis says that STR analysis can be used to track cancer cell progression, and I found a paper that claims CNV can occur in different tissues. I was wondering whether it would be possible to determine the origin of the cell using these or other similar molecular marker techniques.
http://www.pnas.org/content/109/44/18018.full.pdf

Let me rephrase my question as a statement: if all cells have the same sequence, you cannot differentiate them based on sequence. Cancer cells do not have the same sequence and thus could show STR expansion or CNV. I suppose you could also see mosaicism if such a mutation occurred early in development but I don't know the extent to which this occurs nor how strongly it would correlate with adult tissue types (other than in a broad classification such ecto-, meso-, endoderm). Too which paper are you referring?

Oh I see the paper in your edited comment. Yes they seem to be referring to mosaicism and the variations they discovered appear to be between tissues that developed from the same progenitor. Interesting stuff. If you were trying to determine the tissue from which a cell originates, you may consider profiling gene expression, such as by RNA-Seq

It's like looking at a binary code (101010101011110001110101) and asking "what would this do?" Actually binary is still far better than deciphering a genetic code...

The answer is in the question but I suppose you wanted to ensure you were not missing some info.
Answer
The DNA sequence is the same in all cells of a multicellular organism. Only the expression pattern varies among tissues. It is therefore impossible to tell from the DNA sequence alone what tissue a cell come from.
It would be feasible by looking at the transcriptome or the proteome or eventually by looking at epigenetic modifications.
Potential exception
Of course, as you talk about CNV, if you consider that the number of chromosome is part of the info present in a DNA sequence, then haploid cells (spermatozoids and ovules) are an exception and you could tell them apart. Similarly anucleated cells would be an exception as they contain no nuclear DNA.
Further potential exceptions are explained by @tsttst in his comment.

This answer may be wrong as transcription can affect mutagenesis as shown recently by Sankar et al., Nature 2016, https://www.nature.com/articles/nature18316; while their great study was on bacteria, it could be thinkable that also in animals there is a coupling between transcription and mutagenesis (--> thus tissue-specific transcription profiles may lead to tissue-specific somatic mutation patterns --> which would allow identification of tissue by DNA); P.S.:  A further exception would be https://en.wikipedia.org/wiki/V(D)J_recombination

There was a paper in Science, August of this year (apologies to the author for not remembering their name). They worked up a protocol for single cell bisulfite sequencing and through the use of known marker genes managed to identify multiple neuronal sub-types based on non-CpG methylation across gene bodies.
Non-CpG methylation across gene bodies is seen often to be inversely correlated to gene expression, through this you can infer an expression profile of known marker genes giving you have a solid poke at a cell type with only a DNA sequence.
(Edit: Assuming this holds true in tissues outside of the cortex)

i would rather start with an assumption that no two cells in the human body have the same genome. Mutations occur frequently; most of them are repaired, but some remain unrepaired. Human body is a genetic mosaic.
Abyzov et al. (Genome Research, 2017):

We estimate that on average a fibroblast cell in children has 1035
  mostly benign mosaic SNVs. (...) These findings reveal a large degree
  of somatic mosaicism in healthy human tissues, link de novo and cancer
  mutations to somatic mosaicism, and couple somatic mosaicism with cell
  proliferation.

https://www.ncbi.nlm.nih.gov/pubmed/28235832

Such mutations, being randomly driven, wouldn't help to identify which tissue the sample came from however.


text:
What is this 2-3cm insect found in South-Eastern Brazil?

Noted in South-Eastern Brazil rainforest at low level - about 2-3 cm from head to tail.
Maybe a Cassadine Beetle?

Maybe a cassadine beetle ?

You are correct! This insect does belong to the subfamily Cassidinae (common referred to as "tortoise beetles"), and is of the species Stolas aenea.


text:
And another insect from SE Brazil Oct 2017

Photographed in the low areas of the Brazilian Atlantic Rainforest - Oct 2017 and about 2cm in length.

I'm having a difficult time pin-pointing the species, however, I'm fairly certain this true bug belongs to the genus Zelurus.
Zelurus sp.

Zelurus sp.

Z. variegatus

Distribution

Interactive version can be found here.

source

Great answer from @Charles: I was still humming and hawing between a zelurus species and another of the zelus species such as the longpipe that has the distinct red colour. (I had to leave for a couple hours...)  Like him, I was having trouble finding one that looked really similar.  But I found one, labeled as the Zelurus Circumcintus:

However, further research revealed that this is a fairly undocumented species.  The only source I could find with pictures of a distinctly red one was Flickr, such as this one:

I'm guessing it actually is the zelurus circumcintus, but I have yet to find any official sources that back me up.

Zelurus species will be fine guys - brillient


text:
How are the axons in the white matter bundled?
I wonder if the following question concerning the axons in the white matter does make sense.
It is common knowledge that white matter is "composed mainly of bundles of myelinated axons" resp. is "mainly made up of myelinated axons, also called tracts" (= "bundle of nerve fibers (axons)".
For the following to make sense the following assumptions are made:

All axons making up a bundle are of approximately same length $L$. (Of course not all axons have the same length!)
Axons run in parallel as long as possible.
Axons normally don't branch inside the white matter. (Or is this a totally unrealistic assumption?)

Assume that it is a sensible definition of a bundle to be the set of axons running densely packed inside a virtual tube of length $l = \alpha L$, $\alpha < 1$. By this definition sub-bundles of a bundle would also be bundles, so we are interested only in maximal bundles.
It's important to notice that the definition of bundles depends on the parameter $\alpha$: smaller $\alpha$ means the axons must run in parallel only for a shorter distance (compared to their common length $L$), larger $\alpha$ means the axons must run in parallel for a longer distance. Smaller $\alpha$ means less but larger bundles, larger $\alpha$ means more, but smaller bundles.
Note that each bundle (independent of $\alpha$) defines two specific cortical regions (the two regions of the source and target neurons of the axons). For the smallest bundles (largest $\alpha$) their diameters correspond well to the size of the source and target regions (see picture below).
See here different partitions into bundles with $\alpha \approx 0.5$ (grey, 1 bundle), $\alpha \approx 0.75$ (blue, 2 bundles) and $\alpha \approx 1$ (red, 4 bundles):

For the sake of simplicity, assume that - for a given $\alpha$ - bundles don't overlap, i.e. each axon is contained in only one bundle. (This might be an oversimplification.)
My question is:

Can a rough estimate be given, how many bundles with a given number $N$ of neurons are there in the white matter (for a given $\alpha$)? (Choose the organism you like or know of.)

I suppose the largest bundle to be found in the brain is the corpus callosum which - as a tube - has a rather short length (small $\alpha$). It contains (in the macaca nemestrina brain) about $10^8$ axons.
For the sake of simplicity, let's consider only powers of ten. Then for a small $\alpha$ which would allow the corpus callosum to be a bundle, we will get as a "null hypothesis" (with purely hypothetical numbers of bundles!):

But maybe the distribution is somehow bimodal, e.g. like this:

Is a reliable answer to this question out of reach today? Don't we know enough about the long-range structure of the white matter? Or did just nobody take the effort to make this statistics? Or can I find it somewhere?


text:
Reference request - Neuroscience of Free Will
I am a computer science student taking a course on philosophy. My topic of research is on freedom of will and whether it is possible to create a machine capable (or closely) of doing so.
I felt that my first steps would be to find some articles related to the brain, to find out which part of the brain is fully / partially responsible free will, the activity that goes on in the brain when one is 'exercising his freedom of will'. I have been searching on google with keywords like 'free-will, neuroscience, brain' but have not found a good article.
I was hoping for the community to give me some nice references for a good start. Anything related would be kindly appreciated as well.

I'm sorry to say this question is likely outside our guidelines for a number of reasons. I recommend reading through the asking guidlines and the help center in general and then seeing if you can formulate a question that's more within the scope of this site.

You need to choose your definition of free will. Under the incompatibilist's view you are out of luck. Under the compatibilist's approach, the issue simply boils down to decision making, of which several computational models exist. Under a strict definition of free will, you must accept some source of causation other than physical determinism, something that is not compatible with the scientific approach. So, you'll either have to relax your definition or reject its existence.

You seem to be assuming that free will occurs at all in the universe.

You might want to search for publications by Felix Tretter (most are in German, unfortunately)

I'm voting to close this question as off-topic because ‘free will’ is a philosophic not a biological concept.

One potential argument has been introduced in an essay of the biologist Martin Heisenberg, and relates to the stochasticity of chemical reactions that occur within biology.
Note that, depending on the philosophic tradition, this may not be regarded as free will.
For a link to the original essay (paywall), and the follow-up comments (and objections) by other scientists - of which all appeared in the reputable journal of Nature - see: https://www.ncbi.nlm.nih.gov/pubmed/19444190


text:
Why are tumor suppressor genes recessive?
In my Intro. to Biochemistry course, we have been studying cancer. The professor has pointed out that tumor suppressor genes are "recessive" while proto-oncogenes are "dominant". Since only one mutation is necessary to turn a proto-oncogene into an oncogene; while two are needed for the malfunctioning of tumor suppressor genes, why is this not the other way around (i.e. tumor suppressor genes dominant; proto-oncogenes recessive)?
All help is greatly appreciated.

Just for the semantic, a gene is not dominance or recessive. An allele at a given gene (or locus to be more general) can be dominant or recessive in its relationship to another allele. So what you mean by dominant gene, you mean that the wild type allele is dominant over the mutant allele (and vice-versa for what you call recessive genes).

"proto-oncogenes"

why would they not be, why has a mechanism to sickle cell not evolved a regulator gene, in both cases it becasue the necessary mutations has not occurred. Dominance is a side effect of how the gene and its products function, it is not affect by the whether the allele is deleterious or not.

I was typing out an explanation, but then realized that this text book does a much better job:
Lodish et al. 2000. Section 24.2: Proto-Oncogenes and Tumor-Suppressor Genes in Molecular Cell Biology 4ed. WH Freeman
Proto-Oncogene:

Conversion, or activation, of a proto-oncogene into an oncogene generally involves a gain-of-function mutation. At least three mechanisms can produce oncogenes from the corresponding proto-oncogenes.

Point mutations in a proto-oncogene that result in a constitutively acting protein product
Localized reduplication (gene amplification) of a DNA segment that includes a proto-oncogene, leading to overexpression of the encoded protein
Chromosomal translocation that brings a growth-regulatory gene under the control of a different promoter and that causes inappropriate expression of the gene

An oncogene formed by the first mechanism encodes an oncoprotein that differs slightly from the normal protein encoded by the corresponding proto-oncogene. In contrast, the latter two mechanisms generate oncogenes whose protein products are identical with the normal proteins; their oncogenic effect is due to their being expressed at higher-than-normal levels or in cells where they normally are not expressed. However they arise, the gain-of-function mutations that convert proto-oncogenes to oncogenes act dominantly; that is, mutation in only one of the two alleles is sufficient for induction of cancer.

Tumour Supressor Gene:

Tumor-suppressor genes generally encode proteins that in one way or another inhibit cell proliferation.... Since generally one copy of a tumor-suppressor gene suffices to control cell proliferation, both alleles of a tumor-suppressor gene must be lost or inactivated in order to promote tumor development. Thus oncogenic loss-of-function mutations in tumor-suppressor genes act recessively.

A clarification that would improve this answer: As in Remi.b's comment, the alleles are recessive, not the genes. In the context of cancer, the key point is that cancer-causing alleles of tumor suppressor genes are recessive, not the genes themselves. Often loss-of-function alleles are recessive, because a single healthy copy is capable of performing most of the function.

Thank you! This clarifies things a lot. I am really sorry about the way I wrote my question -- I am aware that what we call recessive or dominant is an allele, not a gene as a whole. If I understand correctly then, in the context of cancer we say that the allele that for instance undergoes a loss-of-function mutation in a TSG is recessive (as canadianer quoted), but then... would the wild-type allele for a TSG be dominant with respect to the mutated allele? (TSG = tumor-suppressor gene). Thanks a lot to everyone!

@Bee You’re welcome! Yes, it would be dominant in relation to the the loss-of-function allele since its activity alone is sufficient for the wild-type phenotype.

Note that while this is generally true - there is also a phenomenon of haploinsufficiency with some tumour suppressors. That means losing one copy is enough to permit tumour development.
See http://www.sciencedirect.com/science/article/pii/S0304419X04000022?via%3Dihub


text:
Embolism risk in cancer
Why is there an increased risk of embolism in any malignancy? I studied that malignancy is a risk factor for pulmonary embolism. Can someone explain me the exact mechanism under which malignancy produces emboli?