text:
How does Halosulfuron-methyl kill nutsedge, while leaving lawn grass and most weeds undamaged?
I use Halosulfuron-methyl to control yellow and purple nutsedge in lawns. This chemical acts by interfering with the acetolactate synthase enzyme, which quickly slows cell division, and growth at all points.

How does this work without also interfering with enzymes in the lawn grass?

http://hortsci.ashspublications.org/content/30/2/285.full.pdf

@DevashishDas The paper does not seem to be relevant in answering this question.

Halosulfuron-methyl is a member of the family of sulfonylurea herbicides. Brown (2006) mentions in his abstract the following, and I quote:

This class of herbicides acts through inhibition of acetolactate synthase [...], thereby blocking the biosynthesis of the branched-chain amino acids valine, leucine and isoleucine. This inhibition leads to the rapid cessation of plant cell division and growth. [...] Crop selectivity results from rapid metabolic inactivation of the herbicide in the tolerant crop. Under growth-room conditions, metabolic half-lives in tolerant crop plants range from 1–5 h, while sensitive plant species metabolize these herbicides much more slowly, with half-lives > 20 h. Pathways by which sulfonylurea herbicides are inactivated among these plants include aryl and aliphatic hydroxylation followed by glucose conjugation, sulfonylurea bridge hydrolysis and sulfonamide bond cleavage, oxidative O-demethylation and direct conjugation with (homo)glutathione.

Hence, metabolic inactivation activity differs between susceptible and insusceptible species. To get to your question: this means that the enzymes in lawn grass are also inhibited, but to a lesser extent, as the herbicide is metabolized and inactivated more rapidly in grasses.
Reference
Brown, Pesticide Science 2006;29:241–378


text:
Breakdown of energy expenditure at the level of a single cell
The metabolic rate measures how much energy an organism expends over a unit of time. Its breakdown for the human body in terms of its functions is well documented : so much for the heart, for the brain, etc.
In West et al, 2002 I have found an estimate for the metabolic rate of a single cell. But how does this breakdown in terms of elementary functions in the cell?
E.g., how much of the energy made available from nutrients is used in the process of replicating genome, of expressing proteins, of trafficking...?
Following Jeremy Kemball's link suggestions, I find in this paper the fraction of ATP consumption for the following processes:
Protein synthesis    0.34
Na+/K+ ATPase        0.16
Ca2+ ATPase          0.17
RNA/DNA synthesis    0.25
Unidentified         0.09

(which adds up to 1.01 rather than 1 for spurious reasons). Their measurement is indirect, based on $O_2$ consumption for an assumed steady-state regeneration of ATP. I wonder how GTP-based processes are accounted for? Or are they negligible compared to ATP ones?
This is for a specific cell type, rat thymocyte, is there a reason to expect that this will be hugely different for say a fibroblast? Also, they stimulate their thymocyte with concanavalin A. I understood they are not getting RNA/DNA consumption signal without Con-A, but didn't get why it would be so.
Finally, what would be in the remaining 9% ? One candidate for ATP consumption suggested by Jeremy Kemball is actin turnover, I guess it fits only in the "unidentified" line. Tubulin turnover is a GTP process, not sure about intermediate filaments (do they turnover?). All ATP-molecular motors (myosin, kinesin, dynein at least?) have to be there too.  What else?
I am particularly interested in the total amount of ATP energy that goes to myosin.

@DevashishDas: Maybe my question was not clear enough: I'm not looking for a description of ATP production from glucose (and other related processes making energy usable), but of its usage. Some of it actually has to go back to energy production, but some also goes to protein synthesis, etc. Besides, I am looking for numbers (e.g., DNA replication would consume so much over 1 cycle of 24 hrs, which makes so much % of cell metabolic rate)

My instinct is that these figures are going to be hard to find. PET scans and things using fluoridated glucose can pretty easily ballpark metabolic demand for individual organs, but tracking where and when ATP is consumed is going to be much more difficult. A fun complication: ATP consumption and production rates change wildly across an individual cell during normal cell replication, even if the environment is constant. I wish you luck.

@JeremyKemball: thanks for your message. Already knowing that these figures may be completely unavailable is helpful...! I would anyhow be interested in any estimate available: there may be some from a mixture of in-vitro and in-vivo approaches, e.g. a lower estimate for DNA replication might be around, as we know how many b.p. we need to replicate and probably how much energy it takes to replicate one.

@JeremyKemball: Do you have a reference for the fact that "ATP consumption and production rates change wildly across an individual cell during normal cell replication"? Cheers.

I need to get in the habit of finding sources for things I say, even in comments where they won't fit. Just because I say things that seem plausible but turn out to be wrong when you actually do the math, uh, fairly often. :/

Note that any GTP process gets its energy indirectly from ATP.

@forest: Thx for your comment, can you point to an explanation of these energy fluxes?  https://en.wikipedia.org/wiki/Guanosine_triphosphate#Biosynthesis e.g. is not that clear on this.

What do you mean by energy fluxes?

You were writing that GTP processes get their energy from ATP. In physics, you'd call this a flux of energy from one biochemical storage to another.

I was musing on this and did some strange googling, and have some ballpark figures  for a bunch of different organisms. It's far from a complete answer but it's at least a start, and all this won't fit in a comment.
DNA replication, I assumed, was a huge metabolic drain on the cell. Turns out that is far from the case. Many helicases are passive, requiring no ATP, and the amount of ATP-equivalent triphosphates to synthesize the entire genome is pretty small compared to the amount that gets used and recycled every day.
According to these guys humans go through their bodyweight in ATP every day, about 50% of which is actin turnover, and 30% is synthesis (60% or more in rapid bacteria). Proteins cost about 4-5 ATP per AA to break down and rebuild.
You're not going to get a really good general breakdown, I don't think, but in crop plants or E. coli there are numbers for this, sort of. A lot of them are based on indirect measurements of protein uptake/turnover and ATP cost per AA or BP. They're fascinating but insane and often contradictory.

The 50% going into actin turn-over is for brain tissue, probably over-estimated for other tissue. However your link about synthesis lead me to this paper where there are numbers for thymocytes: 1/3rd of ATP consumption for protein synthesis, 1/3rd for calcium+sodium cycling, 1/4th for DNA/RNA synthesis and 1/10th for "all the rest". Firstly, how does this fit with the ATP consumption of actin treadmilling that has to be expected? (it has to fit in the 10% for thymocytes?) What else can one expect to find in these 10%?

Actin treadmilling for neurons I expect to be a pretty big part of energy expenditure. They recycle neurotransmitters and rearrange their dendrites and things often, and all that has a cost. Thymocytes are just blobs, so they don't have to spend as much energy on the cytoskeleton. http://www.genome.jp/dbget-bin/www_bget?cpd:C00002 is a list of some of the things ATP does in the cell. Where and how the ATP budget is spent is going to vary a lot from cell type to cell type. Muscles and nerves do a lot of ion pumps, glands do synthesis, etc.

A significant amount of heat generated by the cell does not come from the hydrolysis of an NTP. ATP is generated by a H+ gradient in the mitochondria, and this gradient is created by mechanisms which rely only in part by ATP.  Most of the energy stores in our bodies are not in the NTP pool. This is why CO₂ and urine are used to measure energy expenditure during physical exercise. On the scale of individual cells, it is a challenge to conceive a protocol which would account for all confounding variables. However, on the scale of a human, confounding variables in energy use are easily controlled. If you are interested in the energy expenditure of a single biological process, this would seem a better project rather than quantifying all processes simultaneously.

Thanks for your answer. In the paper I mention above indeed, there's a lot of cell-scale respiration which is not accounted by ATP processes but attributed to "proton leakage", and I understand that this is linked with heat production. Anyway, what I'm interested in is really the cell-scale energy expenditure, within which I'd like to particularize ATP-based energy. Then, specifically, I am interested in energy consumption by myosin (in nonmuscle cells).

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text:
Why does a housecat (or other predator) play with it's food before killing and eating it? Does it make the food taste better?
I've read a couple people theorize that a cat playing with a mouse causes the mouse's body to be flushed with adrenaline before the final kill and that this adrenaline makes the meat more tender/easier to digest/more nutritious etc.
Is there any evidence to support the idea that by playing with it's prey the cat is making it taste better or easier to eat?

Animal Planet is quoting researcher Dennis C. Turner who claims this is an instinct which is supposed to tire the prey:

Cats, rather, wear down prey to avoid sustaining injuries. They're motivated by self-preservation, just like most other animals, and they know what could happen if they aren't careful. Mice and rats, for example, can deliver nasty bites that can cause injury or spread disease. Birds, for their part, are able to scratch and peck. So, what's a cat to do? Rather than playing with their prey for amusement, cats tire out their victims to the point where they're too worn down to fight back. And after that, the cats will feel better, and safer, about finishing them off, according to researcher Dennis C. Turner. So while it might look like a display of cruelty, a cat playing with its prey is just an (admittedly harsh) example of animal instinct in action [1].

Karen B. London (animal behaviorist) agrees:

Actually, the way that cats let go of and then recapture their prey is not a way for them to have fun, but rather a way for the cats to protect themselves from serious injury. Cats kill their prey by breaking the spinal cord with a strong bite to the neck. If a cat must let go of the animal in order to grab it on the neck, that cat is risking escape or retaliation by their prey [2].

Playing (not only with prey) also gives cats experience and improves their ability to make judgments [3].

References:

Animal Planet. Why do cats play with their prey? Available from http://curiosity.discovery.com/question/why-cats-play-with-prey (accessed 27.07.2014)
Karen B. London, Ph.D.. London Zoo: Why do cats play with their food? Available from http://azdailysun.com/lifestyles/pets/london-zoo-why-do-cats-play-with-their-food/article_46a97775-232d-5e56-b0ea-dd1c8782b062.html (acessed 27.07.2014)
Perfect Paws. Predatory Behavior of Cats. Available from http://www.perfectpaws.com/help3.html#.U9TLpON_tJk (accessed 27.07.2014)

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Why are particulate matter toxic to humans?
There are many studies on fine particles (PM2.5) and their fully negative effect on human health. There doesn't seem to have any positive aspect of inhaling particles, except very particular ones, but most often people smoke, and release all sort of unwanted and toxic PM2.5, same goes with for fuel combustion.
At a huge dose, we die within minutes, like in a gas chamber, at small dose below this hazardous health risk level, is it still dangerous to us? If yes, why aren't we equipped to fight them, I guess this smoke concentration and pollution level is very recent on human evolution scale, but at the lowest layer of life, bacteria may develop to break and eat toxic particles, does it happen it our blood? Is it hard to explain to a non-biologist like me?

Particulates can accumulate in the aveolae in the lungs. This leads to inflammation and tissue damage and scarring. This reduces the available surface area for gas transfer. Low level exposure over long periods is harmful. Asbestos workers are well known to get sick, but miners can get black lung or silicosis from inhaling mining dust, and farmers can get lung disease from inhaling dirt that gets blown up as dust. This damage usually isn't seen until they are in their 50s or 60s.

Interesting. For the 3 examples you gave, is it high level exposure? What level is it for someone using his bike everyday, with part of the itinerary inside traffic? thanks


text:
Genetically improved *Leucaena leucocephala* seeds
I am looking for fast growing Leucaena leucocephala seeds. Now, I am cultivating Leucaena leucocephala which can grow 6 meters in a year. But I am looking for a genetically improved seed which can grow up to 10 Meters in a year.

I am not saying it is off-topic. But can you repost this on: http://gardening.stackexchange.com/


text:
Scale up of Bacterial growth from 250mL to 1-5L?
I am currently growing up a specific strain of E.Coli with a knockout in 40mL of growth medium (LB) in a 250mL shaker flask... My ultimate goal is to scale up this process to a 1-5L large scale setup for the lab. But for now I'd like to quantitatively characterize this 250mL scale using Monod Kinetics so that the mathematical model can be used to build the aforementioned bio-reactor.
Currently I am making two growth curves of the E.Coli in the current 250mL flask. One is OD vs. time and the other g.Dry mass vs. time. The idea of doing so is to ascertain the $\mu_g^{max}$ (maximum specific growth rate). However, I am stuck as to how to find the saturation constant (Ks). I am also stuck on how to measure the sugar concentration ([S]) at each time-point that I would measure the OD. The idea behind these two variables is to use the equation(s):
$D = \mu_g^{max} . \frac{[S]}{Ks + [S]}\\
D^{\ max} = \mu_g^{max} . \frac{[S^{\ max}]}{Ks + [S^{\ max}]}$
Am I looking for the right variables and/or using the right equations?
Thanks again for your help!

Are you aware of Lineweaver-Burk plot for enzyme kinetics??

No I am not... only Michaelis menten and monod

Michaelis-Menten:
$V=V_{max}.\frac{[S]}{Ks+[S]}$
Lineweaver-Burk:
$\frac{1}{V}=\frac{Ks}{V_{max}[S]}+\frac{1}{V_{max}}$
Plot $\frac{1}{V}$ vs $\frac{1}{[S]}$; find the slope and intercept of this plot.
Depending on what you consider as primary substrate (glucose??) measure the concentrations using appropriate assays. Glucose sensors (based on glucose oxidase) are available or you can do conventional biochemical assays (DNSA) for glucose and other reducing sugars. To find the growth rate, measure OD at different time-points and get the differences of OD in a time interval. A better method would be to make a scatter-plot of OD and time and fit a polynomial function. Get rate by taking the tangent of the curve at that time-point.


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What is LD50 for 25i (25I-NBOMe)?
Firstly I would like to apologise if this is not correct place to ask this question, as it can be seen more as chemistry and not biology question.
I was looking around for data on psychedelic substance called 25i (25I-NBOMe) . It was fist synthesized in 2003 and is somewhat 'new'. I have found some data on overdoses and they are few, however I could not find any specific data on mortality to dose rate nor on LD50 (Dose where 50% of people would die). Wikipedia is quiet in this regard.
Judging by the dosage it being active in sub-milligram doses (600–1,200 µg) it should not be very lethal compared to most, should it?
Where could I get data on LD50 for 25i (25I-NBOMe)?

Wiki is not quiet. It explicitly says the LD-50 has not been determined.

@daniel I know I have read that article before posting, but thanks anyway.

Cimbi-5 or 25i (25I-NBOMe) is a class 2C psychedelic drug.(wiki site.)

Lethal dose or LD50 of "Cimbi-5" is still unknown.
Though you can predict approximate the LD50 by structure computationally.

Hi Das, I have registered moments ago to http://preadmet.bmdrc.org/ but can't see controls on toxicity 'drawer' nor on Chrome nor IE. If you have access to this tool could you do the prediction or help me on making it work on my machine. Thanks.


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Periods of Heavy Speciation
I have a set of microRNA ages with corresponding labels suggesting which clade they first emerged from. For instance, for hsa-mir-1, let's say, it would have an age of Eutheria. I have several peaks in the distributions of my age. One idea I had was to check to see if these peaks correspond to periods of intense specialization. For instance, the Eutheria clade saw a vast diversification of species relative to other clades. I'd like to determine this from a more computational perspective rather than Googling each clade.

Can you clarify what exactly your question is? You want to phylogenetically classify using microRNAs??

My guess (as your question need heavy editing!!) would be MiRdup.

MiRdup Goals:

Validation of pre-miRNAs predictions
Prediction of mature miRNA

Abstract: MicroRNAs (miRNAs) are short RNA species derived from hairpin-forming miRNA precursors (pre-miRNA)
  and acting as key post-transcriptional regulators. Most computational
  tools labeled as miRNA predictors are in fact pre-miRNA predictors and
  provide no information about the putative miRNA location within the
  pre-miRNA. Sequence and structural features that determine the
  location of the miRNA, and the extent to which these properties vary
  from species to species, are poorly understood. We have developed
  miRdup, a computational predictor for the identification of the most
  likely miRNA location within a given pre-miRNA or the validation of a
  candidate miRNA. MiRdup is based on a random forest classifier trained
  with experimentally validated miRNAs from miRbase, with features that
  characterize the miRNA-miRNA* duplex


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bacterial cell wall degradation in humans
can human degrade the D-amino acid present in bacterial cell wall, I'm confused about it i have read somewhere that human can do so.If yes than why we need antibiotic to kill bacteria???If it is not so than why??

Humans have at least one enzyme which can break down D-amino acids, the D-amino acid oxidase (DAAO). They are able to break down these amoino acids, interestingly D-serine seems to play a role as a neurotransmitter. For more information have a look at these papers:

Physiological functions of D-amino acid oxidases: from yeast to
humans.
Human D-amino acid oxidase: an update and review.
d-Amino-Acid oxidase and its physiological function

We still need antibiotics, since only a small part of the bacterial cell wall is composed of D-amino acids. The cell wall is made of monomers from N-acetylglucosamine and N-acetylmuramic acid which are crosslinked by small peptides (these are short amino acids chains) to form the peptidoglycane polymer. A part of the amino acids in the crosslinking peptides are D-amino acids. I am not sure if the DAAO is able to attack these peptides in the polymer. Additionally most of the enzyme in the human body is present in liver and kidney, indicating that it breaks down D-amino acids that are transported there by the bloodstream.


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Does a non-extinct gliding species of bird exist?
According to wikipedia was Archaeopteryx rather glider than capable of active flight. As a hunting strategy it crawl up to a tree (or other high positioned place) and glide from it to a prey.
Most of the modern birds are capable of active flight. Does anybody know if a (purely) gliding species of bird exist in present?

That's really not how Archaeopteryx hunted, maniraptorans have really abysmal climbing ability, and Archaeopteryx shows no improvement on that. The current consensus is that Archaeopteryx was an active flier, albeit a poor one.

There is a classification of birds called Soaring birds.
Soaring Birds

In definition, some land birds, such as vultures and certain hawks,
sustain flight for long periods without flapping their wings. They
take advantage of updrafts produced when the wind blows over hills and
mountain ridges or make use of rising columns of warm air called
"thermals."
Vultures stay within thermals by flying slowly in tight circles. They
have short, broad wings and a low wing loading (ratio of bird weight
to wing area) that allows them to remain aloft and to be highly
maneuverable at slow speeds. [1]

List of soaring birds

Birds of Prey

Buzzards
Condors
Eagles
Falcons
Harriers
Hawks
Kites
Osprey
Secretary Bird
Vultures

Passerine

Chough

Cranes

Sandhill

Sea birds

Albatrosses
Frigatebirds
Gulls
Herons
Pelicans
Petrels
Shearwaters
Storks
Terns

Extinct

Argentavis

Buzzard

Chough

Sandhill

Albatrosses

(source: scienceviews.com)
Argentavis[Extinct]

(source: mnn.com)
Update:
Most similar morphology to Archaeopteryx is found in Hoatzin (Opisthocomus hoazin) like claws as hands as they hold the branch when they are small.

(source: pbworks.com)
Source:
[1] Soaring Birds by Paul R. Ehrlich, David S. Dobkin, and Darryl Wheye.

Hi @Devashishish Das!. Thank you for your answer, howerver I can not accept it. I am looking for "pure" gliding species (WITHOUT ability of active flight).

@LadislavNado: Are you sure? Soaring Birds Are gliding birds. Moreover, flight pattern of  Archaeopteryx is still under research.

Thank you @Devashish Das for updating your answer! Opisthocomus hoazin is a great example!!! If you in future find another similar species, please add it. Many thanks again, I will use Opisthocomus hoazin for my popular science lecture where I wil make acknowledges to you ;)

I think this might be a better approximation of the most current consensus for the comparative size of Argentavis to humans than the one you've used?

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Can non-carbonated energy drinks boost alcohol intoxication?
I just read news article about

banning caffeine in alcohol drinks and
about that energy drinks increase the urge to drink alcohol.

Energy drinks cause sugar intoxication - answer about it here in the thread Decreasing the alcohol proof and faster in hangover, why?.
Sugar dehydrates faster as well as causes a cascade of hormonal changes that are more immediately troubling than the alcohol.
I want to understand why energy drinks boosts you to drink more alcohol.
This suggests me that

malaise (caused by energy drinks) can be improved shortly by alcohol drinks

by some unknown mechanisms to me; and this can be the reason why people like to drink more alcohol after energy drinks.
I think that the mechanisms are related to some cascade which I do not know.
This mechanism can lead to improvement in the dehydration very shortly

by acting on the membranes of the cells
or by stabilising the architecture of the endothelium i.e. stabilising the hormonal changes.

My conjecture is that the alcohol can affect on the secretion of the substances from endothelium (EDRF, EDCF).
There are three types of substances secreted by the endothelium

NO
Endothelium hyperpolarising factors
Endothelins

So sugar intoxication causes changes in the endothelium architecture which alcohol intoxication reverts shortly back which boosts people to drink more alcohol to recover from the malaise caused by the energy drinks.
How can non-carbonated energy drinks boost alcohol intoxication?

This is not very broad. If I am not wrong this phenomenon is attributed to caffeine.

A very well-written question, so I'm sorry if my answer is a bit too simple. Perhaps it will attract attention of somebody with a better answer.
I think the effect could be mainly caused by the fact that sugary drinks slow down alcohol absorption. So while those who drink just alcohol already know they've had enough, those who have had a couple of energy drinks still feel fine and continue drinking, not knowing that they are about to become even more inebriated.
Also, the stimulants in energy drinks can somewhat reverse the sedative effect of alcohol, leading to higher overall activity of the person and thus faster drinking.


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Viagra for pain management
Not all men who take Viagra experience any sexual side effects about 40% have no change of sexual abilities on the pill. However like many women the drug in such cases cause a strong pain reduction without any considerable side effects. Also in some cases is able to eliminate persistent nausea and increase oxygen flow through the lungs.
Could Viagra be used for cancer patients or others who need to manage pain?
Update:
Roles for Sildenafil(or Viagra) in Enhancing Drug Sensitivity in Cancer

Amazingly there is a paper on this: Roles for Sildenafil in Enhancing Drug Sensitivity in Cancer


text:
Is there any completely Computation Drug ever launched in market?
I am working in bioinformatics(part of it in Drug Designing) for years, still if I have no idea about it. As it is too hard to prove (Pass all Clinical trials) and get FDA Approvals.
So, My question is there a drug available in market, which is actually designed computationally?

Yes, there are a few. Mostly they are designed in combination with X-ray crystallography of the target which should be inhibited. Then molecules are designed which fit specifically into these targets.
The oldest example I could find is Dorzolamide which acts as a carbonic anhydrase inhibitor. See here: "Application of the three-dimensional structures of protein target molecules in structure-based drug design."
Some more examples are names in the Wikipedia article on drug design.
While looking for an example, I found these articles, which also look interesting:

Molecular Modeling and Computer Aided Drug Design. Examples of their
Applications in Medicinal Chemistry
Computer-based de novo design of drug-like molecules
Recent advances in computer-aided drug design

I am also not sure, to what extent the modern small molecule inhibitors like Vemurafenib (PLX4032) and others are designed using computers. At least to some extent this should be true.

Thanks Chris, this was the question which almost stopped getting my current job!!(Though I got it finally). Still there are 4-5 drugs as per my boss. So, if you find them, sure add to the list.

Have a look at the Wikipedia page I linked. There are some more examples listed (although I haven't checked all of them).


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Is pork poisonous?
Besides religious prohibition, there are several non-religious arguments against eating pork. A few of which are:

Pigs and swine are so poisonous that you can hardly kill them with strychnine or other poisons.
Swine and pigs have over a dozen parasites within them, eg tapeworms, flukes, worms, and trichinae. There is no safe temperature at which pork can be cooked to ensure that they will be killed
The swine carries about 30 diseases which can be easily passed to humans

I would like to hear some scholarly verification regarding these points. Simple Yes-No-Yes will be enough, elaboration is welcome, though.
Thank You

These "non-religious" arguments all seem to be found in religious contexts.
The whole "pigs are immune to poison" thing may have stemmed from the fact that pigs can successfully kill and eat poisonous snakes. But so can people.

Pigs and swine are so poisonous that you can hardly kill them with strychnine or other poisons.

This is a non-sequitur. An animal being poisonous does not imply that it resists to poison, nor the reverse is true.
In any case, to the extent of my knowledge pigs do not produce any specific poison. Obviously, if you could provide a more specific claim, this could be tested a bit more in depth.
The second part, instead, is plain false. You can definitely kill a pig with strychnine.
Both the Merk veterinary manual and Diseases of swine, 9th edition report an oral lethal dose of 0.5-1 mg/kg.
For comparison, the CDC reports a probable lethal oral dose of 1.5-2 mg/kg for humans.

Swine and pigs have over a dozen parasites within them, eg tapeworms, flukes, worms, and trichinae.

Sure, pigs do have parasites. Chapter 55 of Diseases of swine is specifically on parasitic infections.
Now, do ALL pigs have them? The answer is no, some parasites are more common than other, and the amount of parasites depends on the health status of the farm.
For instance:
Northern Europe (Roepstorff et al. 1998)

In Denmark (DK), Finland (FIN), Iceland (I), Norway (N), and Sweden (S), 516 swine herds were randomly selected in 1986-1988. Individual faecal analyses (mean: 27.9 per herd) from eight age categories of swine showed that Ascaris suum, Oesophagostomum spp., Isospora suis, and Eimeria spp. were common, while Trichuris suis and Strongyloides ransomi-like eggs occurred sporadically. Large fatteners and gilts were most frequently infected with A. suum with maximum prevalences of 25-35% in DK, N and S, 13% in I and 5% in FIN. With the exception of the remarkably low A. suum prevalence rates in FIN, no clear national differences were observed. Oesophagostomum spp. were most prevalent in adult pigs in the southern regions (21-43% in DK and southern S), less common in the northern regions (4-17% adult pigs infected), and not recorded in I. I. suis was common in piglets in DK, I, and S (20-32%), while < 1% and 5% were infected in N and FIN, respectively. Eimeria spp. had the highest prevalences in adult pigs (max. 9%) without clear geographical differences. I. suis and Eimeria spp. were recorded for the first time in I, and I. suis for the first time in N.

USA (Gamble et al. 1999)

To determine Trichinella infection in a selected group of farm raised pigs, 4078 pigs from 156 farms in New England and New Jersey, employing various management styles, were selected based on feed type (grain, regulated waste, non-regulated waste).
[...]
A total of 15 seropositive pigs on 10 farms were identified, representing a prevalence rate of 0.37% and a herd prevalence rate of 6.4%. A total of nine seropositive pigs and one suspect pig from six farms were tested by digestion; four pigs (representing three farms) harbored Trichinella larvae at densities of 0.003-0.021 larvae per gram (LPG) of tissue; no larvae were found in six pigs.

China (Weng et al. 2005):

The prevalence of intestinal parasites was investigated in intensive pig farms in Guangdong Province, China between July 2000 and July 2002. Faecal samples from 3636 pigs (both sexes and five age groups) from 38 representative intensive pig farms employing different parasite control strategies were examined for the presence of helminth ova and protozoan oocysts, cysts and/or trophozoites using standard techniques. Of the 3636 pigs sampled, 209 (5.7%) were infected with Trichuris suis, 189 (5.2%) with Ascaris, 91 (2.5%) with Oesophagostomum spp., 905 (24.9%) with coccidia (Eimeria spp. and/or Isospora suis) and 1716 (47.2%) with Balantidium coli. These infected pigs were mainly from farms without a strategic anti-parasite treatment regime.

However, note that Boes et al. 2000 reports higher percentages.

The prevalence of helminths in pigs was investigated in five rural communities situated on the embankment of Dongting Lake in Zhiyang County, Hunan Province, People's Republic of China, in an area known to be endemic for Schistosoma japonicum. The helminth prevalences identified on the basis of faecal egg count analysis were: Oesophagostomum spp. (86.7%), Ascaris suum (36.7%), Metastrongylus spp. (25.8%), Strongyloides spp. (25.8%), Trichuris suis (15.8%), Globocephalus spp. (6.7%), Gnathostoma spp. (4.2%), Schistosoma japonicum (5.0%) and Fasciola spp. (1.3%).

Kenya (Nganga et al. 2008):

A total of 115 gastrointestinal tracts (GIT) from 61 growers and 54 adult pigs were examined between February 2005 and January 2006. Seventy eight (67.8%) had one or more helminth parasites, of which thirty six (31.3%) were mixed infection. Ten types of helminth parasites encountered in descending order of prevalence were, Oesophagostomum dentatum (39.1%), Trichuris suis (32.2%), Ascaris suum (28.7%), Oesophagostomum quadrispinulatum (14.8%), Trichostrongylus colubriformis (10.4%), Trichostrongylus axei (4.3%), Strongyloides ransomi (4.3%), Hyostrongylus rubidus (1.7%), Ascarops strongylina (1.7%) and Physocephalus sexalutus (0.9%).

There is no safe temperature at which pork can be cooked to ensure that they will be killed

False. Proper cooking, as well as freezing (but see below) are effective in killing worms.
The CDC suggest:

The best way to prevent trichinellosis is to cook meat to safe temperatures. A food thermometer should be used to measure the internal temperature of cooked meat. Do not sample meat until it is cooked. USDA recommends the following for meat preparation.
For Whole Cuts of Meat (excluding poultry and wild game)
Cook to at least 145° F (63° C) as measured with a food thermometer placed in the thickest part of the meat, then allow the meat to rest for three minutes before carving or consuming.
For Ground Meat (excluding poultry and wild game)
Cook to at least 160° F (71° C); ground meats do not require a rest time.

Also

Curing (salting), drying, smoking, or microwaving meat alone does not consistently kill infective worms; homemade jerky and sausage were the cause of many cases of trichinellosis reported to CDC in recent years.
Freeze pork less than 6 inches thick for 20 days at 5°F (-15°C) to kill any worms.
Freezing wild game meats, unlike freezing pork products, may not effectively kill all worms because some worm species that infect wild game animals are freeze-resistant.
Clean meat grinders thoroughly after each use.

The swine carries about 30 diseases which can be easily passed to humans

Again, sure pigs can carry diseases that can be passed to humans, but proper storing and cooking of meat is effective in getting rid of the great majority of bacteria.
Finally in 2012 Public health England reported food poisoning caused by red meat as accounting for 17% of all food poisoning incidents, with pork accounting for 3%. By comparison, poultry accounted for 29% of food poisoning events (although people eat more poultry than red meat).
Similarly, the CDC report on the Attribution of Foodborn Illness (1998-2008) puts red meat accounting for 12%, pork as accounting for 5.4% and poultry 9.8%.

Just a summarizing note: The primary reason to be careful with pork is for tapeworm- Taenia solium. Most pathological form of the disease is neurocysticercosis (mostly because it is difficult to cure compared to gut infection).

@WYSIWYG: good point. Taenia can be quite problematic especially in poor countries where it is more prevalent.

@nico ... thanks. you may find more here. as you said: if you could provide a more specific claim...  i would like to add: Farmers will often pen up pigs within a rattlesnake nest because the pigs will eat the snakes, and if bitten they will not be harmed by the venom

First: There is no biological reason to not eat pork. These bans (Jewish and Islamic) are based on religious rules, so this is more a cultural, not so much a biological answer.
The reasoning that pork meat would deteriorate pretty fast in warm climates is true, but it is also true for all other sorts of meat (like cattle, goat or sheep). Besides cultural reasons (think of India, where cows are holy) there is another reason according to the antrologist Marvin Harris.
In his book "The Sacred Crow and the Abominable Pigs" (you can find a chapter on pigs here and another interesting article on that topic here) he says that feeding habits are important, too. While goats, cows and sheep can be fed a grass only diet, this is not possible for pigs. They need a grain-based diet (where they compete with the humans for the food) or at least rich woods to survive. As these were depleted by the humans in the middle east, pigs couldn't be held sustainable.

Joseph Campbell also points out that pigs are across many cultures very strongly associated with mother deities.  So it would make sense that the Jews, with their strong rejection of female deities, would deem the animals most closely associated with them to be off-limits.  Also remember Cain and Abel.  The God of the Bible just doesn't much like farmers, he prefers herders.  Farmers keep pigs, not herders.


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Where do flies go?
Where are flies attracted most? Apart from food odours, of course. Why do they seem to be attracted by hot and humid places? Do they prefer shades or light? Why do they tend to get inside very easily?

As far as getting inside, they are small, and they can get in through openings you don't notice, or just sneak in when you open the door.

It's more of a comment.


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Why is too much glucose harmful?
I learned the citric acid cycle in biotechnology school and how cells work; about ADP and ATP and how the Cellular respiration (C6H12O6 + 6O2 -> 6CO2+6H2O) works.
I am interested in understanding why exactly too much glucose is harmful, e.g. when having diabetes.
What happens inside the cells so that the organs get damaged over time? Why can't the cells not simply "ignore" the needless glucose or convert it into energy?

High intracellular glucose.
Affects: all cells that do not depend on insulin to take in glucose. Examples: neurons [1], kidney cells, retina cells.
Causes: high extracellular glucose (in most cases hyperglycemia)
Effects: promoting necrotic cell death through $H_2O_2$ (peroxide) formation, which may participate in the development of diabetic vasculopathies and associated disease [2].

High extracellular glucose.
Affects: extracellular matrix, cardiac muscle
Causes: lack of / low levels of insulin, insulin resistance
Effects: enhances collagen production thus affecting kidney by thickening glomerular basal membrane [3, 4]. It promotes cardiomyocyte metabolic stress and altered glucose handling [5]. It is also a potential mechanism involved in cardiac glycogen accumulation [5].

Diabetes mellitus involves:

high extracellular glucose, leading to:
high intracellular glucose in cells that do not depend on insulin to uptake glucose;
low intracellular glucose in cells that depend on insulin (muscle and fat tissue).

References:

David R. Tomlinson and Natalie J. Gardiner. Glucose neurotoxicity (2008). Available from http://didattica.uniroma2.it/assets/uploads/corsi/140868/Glucose_Neurotoxicity_-NATURE_Reviews-Neuro,_Jan_2008.pdf (accessed 27.07.2014)
RnCeus.com. Glucose Homeostasis (2012). Available from http://www.rnceus.com/dmeds/glucose.html (accessed 27.07.2014)
Takeuchi A, Throckmorton DC, Brogden AP, Yoshizawa N, Rasmussen H, Kashgarian M. Periodic high extracellular glucose enhances production of collagens III and IV by mesangial cells. Am. J. Physiol. 1995 Jan;268(1 Pt 2):F13-9. PubMed PMID: 7840239.
Ayo SH, Radnik RA, Garoni JA, Glass WF, Kreisberg JI. High glucose causes an increase in extracellular matrix proteins in cultured mesangial cells. Am. J. Pathol. 1990 Jun;136(6):1339-48. PubMed PMID: 2356864.
Kimberley M. Mellor , Upasna Varma , David I. Stapleton , Lea M. D. Delbridge. Cardiomyocyte glycophagy is regulated by insulin and exposure to high extracellular glucose. American Journal of Physiology - Heart and Circulatory PhysiologyPublished 15 April 2014Vol. 306no. H1240-H1245DOI: 10.1152/ajpheart.00059.2014

An excellent answer - it really should be accepted.

The glucose can react with proteins, damaging them.  This is called glycation.  Note that glucose is the preferred body fuel and has a 10 fold lower ability to cause glycation than fructose.
http://en.wikipedia.org/wiki/Glycation

Perhaps worth adding that the level of glycated haemoglobin is used as a way of monitoring how well diabetes is being controlled over the long term.

Protein is also insulinogenic, so presumably the body tries to keep it under some level in the blood. Would the same things happen with excess amino acids as you've mentioned?

Too much glucose leads to the formation of advanced glycated end products, which deposit in tissues like glomerulus and cause disease like diabetic nephropathy.
Also glucose is osmotically active, so when it starts appearing in urine (because of its high levels in blood), it leads to polyuria, following which the lost water is recovered from body tissues, leading to dehydration and increased thirst.

Glucose transports from the blood into the cells via facilitated diffusion. This means that glucose goes from higher concentrations (in the blood) to lower concentration (in the cell). Therefore, if you have super high glucose concentrations in the blood, you will have a ton of glucose in the cells. Glucose will oxidize by itself, thus it will contribute a lot to the oxidative stress experienced by the cell.
To answer your question of why they cannot "ignore" it, it is because it simply goes down its concentration gradient via facilitated diffusion.
To answer your question of why they can't convert it to energy, well they can, but too much metabolism of glucose will also generate an excess of reactive oxygen species.
In conclusion, high glucose in cells generates a lot of oxidative stress, which of course, is bad.

This answer has things backwards. In diabetes the failure of the insulin response to high blood sugar means that the glucose carriers are not recruited to the cell membranes. This results in a decreased capacity for glucose uptake and so blood sugar stays high. Also, glucose does not "oxidise itself".


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Age of shells on beach
As a child I watched tiny fiddler crabs living in conical shells, and many years later I find that people study fossil turritellids. So now I wonder: how old are shells, typically, that you see on beaches? Do they wear out after a year of sand abrasion? 100 years, a million? Is it known?

Might be able to do carbon-14 dating on the shells to determine the average age of shells on a beach. I do not know if this has ever been done, but it probably has. No clue where to look for this data.

Apparently it's tricky to radiodate seashells that have stayed in the sea. There's exchange with carbonate from the seawater, etc etc. There are a lot of worn out seashells that you can find on beaches. Conceivably you could do some kind of statistical analysis based on the amount of filled versus empty seashells and the age of the filled ones. (If seashells take one critter-lifetime to decay, you should see roughly equal numbers of live and dead shells) Most seashells are only a couple years old, using the dating method below.

Mollusk shells found on typical east coast (US) beaches can range from days old (the animal that made the shell died recently) to thousands of years old.  Some shells in our state, North Carolina, have been dated as 40,000 years old.  A high number of "seashells" found on east coast beaches are from mollusks that lived in the marsh on the back side of the island.   The presence of these shells on ocean beaches provides evidence of island migration - the island has moved landward over the marsh until what was once the marsh is now the ocean shore.  Once buried in the sand, the shell is well preserved until erosion uncovers it.  Occasionally, fossilized shells are washed up on beaches after having been dislodged from offshore limestone deposits - these shells can be millions of years old.
-Richard -
Carolina Ocean Studies

Ages of shell as a piece can be checked or counted.

Procedure:
1) Examine the shell's ridges with a magnifying glass.
2) Tabulate the number of ridges. You can approximate by number of cell per unit length.
3) Divide the total number of ridges by 365. Each day the little mollusk
 earns a new ridge, thus total will give you its age.
But, that is age of one shell. If you are asking the age of all of them in a beach, my guess would be as old as the beach.
Read more : http://www.ehow.com/how_6331956_tell-age-seashell.html

that is interesting but I wonder about the shell, not the animal. If the animal lived ten centuries ago, is it possible that the shell still exists? I call that shell 1000 years old.

@BobTerrell: Then surely the shell would be as old as the beach. Moreover, carbon dating would the last resort.

The shells you find on the beach are from molluscs (mostly bivalves and gastropods) not insects, which are arthropods.


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Verifying Protein Folds
I have recently begun using Folding@Home and I am curious how people are prevented from cheating the system. It seems to me that unless the final result is easily verifiable users could submit bogus folds in order to quickly gain credits. Is it in fact the case that the final results of calculating a protein fold are easily verifiable?

What I think might be happening is the same set of sequences is sent to multiple computers, and the incoming results are compared a number of times before they're declared valid. So, for example, the same sequence could be sent to 50 computers, and a certain threshold need to match (say, 20 of them) before they're marked as valid. Then, if any other computer submits a different result, it's marked as invalid and not counted.

That is what happens. These distributed computing platforms send out duplicate jobs for computation and the results compared after all are returned. It is also possible to get a sense of confidence in the fold prediction by comparing sequence homology to what is already known for solved protein structures.

Besides duplication as verification there are numerous other computational methods to ensure that the result is valid. Proprietary software is used for folding at home so one can safely assume that they check hashes on processors and files regularly. If integrity is broken (by a crash, memory corruption or God forbid injection) the software client side and server side trashes the result. One can imagine that faulty hardware or other problems can result in a ban from the servers.


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If penis reconstruction from a clitoris is possible why isn't penis enlargement possible?
I don't understand why, if a penis can be reconstructed from a clitoris for sex change, surgical penis enlargement is not possible.

Do you have a reference for your assertion that surgical penis enlargement is not possible?

@MattDMo there are options for surgical penis enlargement but they give maybe half an inch where as well I mean it's just no comparison to what they enlarge in a sex change

www.mayoclinic.org/healthy-living/sexual-health/in-depth/penis/art-20045363?pg=2

That's an interesting article. I though I had heard of implants to increase girth and help maintain erections for those with micropenis and injuries/other medical issues, respectively, that were similar in character to breast implants (i.e., they aren't resorbed by the body like a fat transplant).

@MattDMo silicon in such regions spells disaster it's painful it is eaten by the body and may cause other ailments

Micro penis is a disorder that is correctable with testostone otherwise nope

If you look at urological sites for female-to-male reconstructive surgery the procedures often involve significant skin/tissue grafts and/or prostheses. See, e.g. this interesting and somewhat graphic site.
Penis enlargement (see this site) for cosmetic purposes often entails less drastic measures, such as detaching the ligaments that keep part of the shaft inside the body or grafting (relatively small areas of) tissues to widen the penis. Weights are used to keep scar tissue from drawing the penis back into the body after surgery.
The seriousness of sex re-assignment surgery would seem to make it inappropriate
for a patient who wants a cosmetic versus a morphological change.
There is a huge urological literature on these topics but I think the above give an indication of why the two situations might call for different sorts of surgery.


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About molecules and their shape
When a molecule is being used in some biochemical process it has a certain 3-d structure. Is this maintained throughout it's usage or can one specific molecule change it's 3-d shape while it is being 'used' in the process. Can a specific molecule in all it's interactions in a cell say , take on 4 or 5 distinct 3-d shapes??

It's too broad. But as per enzymes and basically proteins it happens.

All molecules have a 3D shape. This is referred to as it's conformation. Most molecules have certain degrees of flexibility. For example, single bonds usually allow free rotation, while double bonds don't. Cyclic structures have less freedom, but can still twist into several shapes. This can be important because some molecules bend into a certain conformation and then fit into protein binding sites they normally couldn't fit into. And it's not just small molecules, proteins, RNA, and DNA fold into specific shapes, and often must be unfolded, twisted, or bent in order to carry out their function. Protein dynamics is an active field of study. A great example is the ATP synthetase, which has a large rotating portion and acts a lot like a motor.


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What kind of microscope for ML/biological research?
I am a computer science student, focusing on machine learning applications. I have been always interested in biology but I lack any training in it. Now, I had an idea that I could introduce myself to biology more by buying a microscope, and doing some small (still serious, if possible) experiments.
Now, the problem one I am facing is what kind of microscope should I get? Preferred answer would outline what kind of research is possible to do with such and such microscope, and what is the typical price range for the system.
If there are any safety (e.g. does any of the UV leak from fluorescence microscopes?) or ethical concerns I would like to hear about them too. Thanks!

Initially I can invest about max. 1000€ ($1300) but if it need be, I can keep saving more.

There is a similar question, which I have provided an answer for (http://biology.stackexchange.com/questions/5470/what-to-look-for-when-buying-a-light-microscope/17313#17313)

Put it this way: if I come to you and ask "I am a biologist wanting to learn about ML. Should I learn about linear regression or about classification trees?". Surely you would reply "depends on what you want to do in the end". This is exactly the same situation :)

:) I see. Could you answer my comment in the answer below, where I outlined some possible materials for study (food, blood, plants, wine)?

This really depends on the application you have in mind. As with other precision instruments there is a huge range of qualities and applications.
If you just want brigth field illumination and look at relatively big things ( approx 100 microns) then you could find something decent for the price you mention if you buy used.
But if you want more complex imaging techniques like confocal microscopy or fluorescence microscopy to image smaler strutures and cell imaging then your budget is probably not enough. There you probably won't get a decent microscope for less than 2500 Euro.
I think you should figure out what you want to do with your instrument not just buy one and then get started.

Ok, I see. Thank you for the good advice! What kind of microscope I should I get if I wanted to study for example a) plants, b) blood, c) liquids such as wine, d) food?

A simple bright field microscope should be enough. Best look for one with Köhler illumination and x10, x20, x40 and if possible x100 objectives.

I agree with @Jeremias Brand's answer.
Pretty much you will have to forget about fluorescence microscopy... you can probably find some dusty old one on eBay in your price range, but it probably won't be any good.
However, the good news is that seen that in your comment you mention

a) plants, b) blood, c) liquids such as wine, d) food?

transmitted light (white light) would be perfect for a start.
eBay is surely a good place for finding used objectives at a cheap price. You may end up with a good collection of objectives for less than 100€.
That is surely tempting, and it may actually be OK as a start.
However, I personally think that it is better to own a good lower magnification objective than a cheap high-magnification one, so be always be a bit wary about offers that look too good to be true (especially for new piece of equipment).
I would strongly suggest getting a binocular microscope (so with two eyepieces), rather than a monocular one. Makes life much easier.
Also, be sure to have a camera attachment. While a camera may not be strictly necessary, especially at the beginning, it's better to have an attachment so that you can add one in the future, if you feel the need of taking pictures. Although many microscopes have specialized attachments for microscope cameras, you can get away with using your own normal camera, or even your cellphone, if you position it correctly (may need some DIY depending on the situation).
This page has very detailed explanations on how to connect a camera to a microscope.
As for your samples, plants are a very good and easy thing to start observing. Onions are probably one of the best samples to start with.
You may also want to stain your samples. Probably the easiest thing to get is methylene blue, which should be a few euros for 20-30 ml. However, fountain pen ink works as well.
Whenever you use chemicals, remember to look for their safety data sheet (MSDS). Methylene blue is pretty safe to work with, provided you don't swallow it (doh...) and use gloves (standard latex gloves are OK). Be careful because it stains and can be a bit messy, which is true for pen ink as well!
Crystals are also pretty cool to watch under a microscope: take a coverslip, put on a drop of sugary or salty water and wait for it to dry!

With all respect I think the accepted answer underestimates the quality of current inexpensive instruments. What I have found comparing images on my recently acquired $400 scope to those produced by top-end Nikons is that it produces images which are aesthetically less appealing but nearly identical in detail.
Mostly I have used it for fungi, which are well-suited for optical magnifications. To get the full benefit you need a PC to run the imaging software, so that expense must be factored in. Here is I think a pretty clear  image of Aspergillus (tape mount) showing concave spores.

When I hit the Lotto I will get a $7000 scope but I am really amazed at what I can see with this very inexpensive scope (and there are several similar brands available).
Another example--here is a high-end google image of Trichophyton sp. showing the diagnostic macroconidium. Everything that is wrong and right with the inexpensive scope can be seen by comparing the photo below:

The color is a bit garish (the blue stain is intentional) and there is always a background color as opposed to a neutral field). But the detail is very good. I had borrowed a scope from a friend and did not hesitate to buy.
The claim that one is restricted to objects of about 100$ \mu$ is incorrect. I bought a decent calibrating slide and here is a snippet of an image showing Penicillium spores. The small divisions are 10 microns. I didn't bother to calibrate the slide but the order of magnification is amply supported by the sorts of structures I have seen.

Again, the clarity and aesthetic appeal of images captured with a $7000 scope cannot be achieved, nor can you do good phase-contrast or florescence. But the functionality is really pretty amazing.
Below is a group of very small Penicillium from potato dextrose agar. The spores are not much bigger than 1 micron in diameter. It's not a crisp image but conveys a good sense of what an intact structure looks like.

Amateurmicrography.net has some nice images that can give you an idea of what different scopes can do.
Edit: added an image 7/31/14.

I have mixed feeling about this. Sure, you can see stuff with a small microscope, but sometimes you want crisper images than those you posted (and maybe with less fringing). But I am probably spoiled by using expensive scopes :P

@nico: Yes indeed, I really get envious when I see a crisp image with minimal distortion. In time I will move up for just those reasons. The cheap scope is also good for getting experience spotting structure in a cluttered field and preparing slides, but ultimately there is no alternative to a good quality scope.

obviously there are many factors to consider. I wouldn't spend 2000 euros on a microscope if I just want to give it a try... better to start with a cheap one and see whether you like it, then move on if you really want to get serious. Unfortunately there are certain microscopes you just cannot afford to buy, but then get a job in an imaging lab if you want to play with those toys! It's lots of fun!

Very popular microscopes for bio work these days are the inverted style, These allow you to view samples without preparing slides.
http://en.wikipedia.org/wiki/Inverted_microscope
http://www.biotechequipmentsales.com/equipment-for-sale/details/564/14/microscopes/nikon-eclipse-ts100

If you have to prepare samples or not depends on what you want to see. Can you work out your answer a bit more? Actually it is more or less two links.

Although what you say is correct, remember that mounting, especially if using specific microscopy mounting media increases the quality of the image. See for instance: http://www.microbehunter.com/the-importance-of-mounting-medium-refractive-index/


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How are new staining protocols designed for microscopy?
How are new staining protocols designed for microscopy? Is it manual work or does it rely on computer simulations?
Say for example I thought the H&E staining does not bring enough contrast. How would I go about producing The Superb H&E Staining Protocol (not necessarily using just hemalum and eosin Y)?
Looking this from a mathematical point of view, the staining is some operator O applied on image I to produce enhanced image E. While clearly the operator O depends on the particular type of specimen, what I want to see, etc., there are surely some general principles guiding the search for finding an appropriate operator O? What are they?
Since the question is on hold, maybe I can try to put it even more clearly. How was the H&E staining invented? What was the process for its invention? I don't see why it would be unclear what I am asking. Dear biologists please take a more interdisciplinary approach.. If the question really is not answerable as such, please explain why. There's probably an answer in that.

About what new staining protocols are you thinking? And what kind of simulations do you think of?

Added example to the question.

Put on hold now after I added the requested example? Duh.

At least I still don't understand where you want to go.

The reason why could be an answer. Clearly I have little knowledge on the topic.

I mean, H&E staining was developed for a reason. That reason I believe is contrast (indirectly resolution). Surely there are means to make things even better? If you need to stain your specimen, and there is no known way how to do it well, what will you try to do then?

The question is what you want to stain and how. A newer method would be fluorescence micropscopy with specific antibodies coupled to fluorescence dyes. You can also couple the dyes to proteins which bind to cell surfaces.

Ok. I was trying to view this from a generic point of view. For example, if I google "a new staining *" I may find multiple scientific papers, mostly behind paywalls unfortunately. I understand that the protocol varies case-by-case (depending on what I want to do), but probably there are some general principles? For example, if you want to solve an optimization problem in mathematics, you need to model the problem, but need not to reinvent how to minimize a function. Similarly, I am trying to understand the general background for particular staining protocols.

As far as i understand staining, you have to primarily know what it is that you want to observe since most of the time, the sample of interest can not be seen unaided. Once you determined, what the nature of the sample is i.e. protein, or lipid or a specific structure, then you think of molecules/dyes that are known to interact/bind to it, preferably in a specific manner, providing a good contrast against the background. For example for staining DNA, you use DAPI. So its highly dependent on the nature of the molecule/structure you want to observe!

Are you particularly interested in HE stain?

This answer addresses the question of how stains were developed historically, which may bring into perspective your overly modern assumptions.
Most of these older (but stil very usefull!) staining techniques, such as haematoxylin (or rather haematein), cochenial/carmine etc. were inspired by the work of textile dyers of that era, starting somewhere in the middle of the 19th century.
It was more a question of trial and error, coïncidence and luck, rather than it being a case of systematic, structured research, starting from the well known molecular structure of the dye and the sample to be stained... Most of the time those were still -at least partial- mysteries.
You should keep in mind, that many of the protocols still in use, were developed in an era when the dye industry as well was still in its infancy, so to speak. Standardization of dyes, Biological Stain Commission and all that, came later. Biologists, histologists etc. used what worked for them. At that time, at that place, with that lot of dry dye powder. Much inspiration, the right idea at the right time and a fair amount of luck. Up to well into the 20th century.
As an illustration: in 1917-1918 there was a shortage on haematoxylin in the German histopathological labs, due to the allied blockade. A lab worker, Fraulein Wilhelmina Schmidt, inspired by the impossibillity to remove elderberry stains from her hands, wondered if it would be possible to use elderbery juice as a substitute for haematoxylin. As there wasn't really an alternative, it was tried. Elderbery juice was concentrated by boiling, diluted with an alum solution and tried. It turned out to work very well.
The story went unnoticed until 1949, when an article on it was published in the German “Zeitschrift für die Wissenshaftliche Mikroskopie”. In the article, the author, Grüber, pointed out that, even after more than 20 years of storage, the slides were still vividly stained, not showing any trace of fading.

I think this is a useful answer, but I have edited the first sentence as it seems to me that site policy does not allow answers that explicitly claim not to be answers.

I have noticed that indigo dye doesn't seem to dissolve in anything. Wonder if that would make a usable stain, or if it would totally stain everything blue. But the natural precursor to indigo is a glycoslyated molecule, similar to X-gal, maybe the precursor could be used in a manner similar to beta-galactosidase staining.

Do you mean indigo carmine, CI 73015 (synthetic)/ CI 75781 (natural)?


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Where do the 31 spinal nerves start/meet?
Which part of the brain is the first place (from top to bottom) where all 31 pairs of spinal nerves (on each side) meet? Or if they all start at one place - where is that?
Nominally, the beginning of the spinal cord is the medulla oblongata, but perhaps the spinal nerves or some sort of "root" of every nerve start at the Thalamus?

They don’t meet.
Some framework:

Spinal nerves contain motor, sensory, and autonomic fibers. Each of these have different pathways.
Spinal nerves don’t go to the brain. Rather, they synapse in the spinal cord with other neurons which in turn go to the brain (sometimes requiring one more synapse).
In the case of motor neurons, we talk about upper and lower motor neurons. In the sensory system, we talk about first order and second order neurons. Explanation below.

Regarding sensory (afferent) neurons:

Touch and limb position sense are mediated by the dorsal column-medial lemniscus system. The first order (primary sensory) neurons from the spinal nerves, synapse on a second order neuron in the dorsal column in the medulla. There it decussates (i.e. courses to the contralateral side) and ascends via the medial lemniscus to the thalamus. There it synapses with a third neuron that courses via the internal capsule to the primary somatic sensory cortex.
Pain, itch, and temperature sense are mediated by the anterolateral system. These first order (primary sensory) neurons synapse at the spinal level they enter. The second order neuron decussates at that level and courses rostrally via the anterolateral column, ending up in the thalamus. There it synapses with a third neuron that courses via the internal capsule to the primary somatic sensory cortex.

Conclusion: It takes three neurons (inclusive) to get from the spinal nerve to the primary sensory cortex in the postcentral gyrus of the parietal lobe.
Regarding motor (efferent) neurons:

Limb muscles are innervated by circuits beginning in the primary motor cortex. These upper motor neurons descend to the medulla, decussate here, and continue caudally via the lateral corticospinal tract. At the level of the spinal nerve, they synapse with neurons in the lateral ventral horn. These are the lower motor neurons that become the spinal nerve.
Axial/girdle muscles are innervated by circuits that also begin in the primary motor cortex. These upper motor neurons synapse in the midbrain, descend, and decussate at the appropriate spinal level. They synapse there with the lower motor neurons that exit the spinal cord and end up in the muscles.

Conclusion: It takes two neurons (inclusive) to get from the primary motor cortex in the pre-central gyrus of the frontal lobe to a spinal nerve.
In the cortex, these circuits also don’t all come together. They are actually quite diffusely organized across the sensory and motor cortices. Here is a representation of the sensory cortex.* It is a schematic of the post-central gyrus with pictures to indicate where the signals from various body parts end up. The motor cortex is similar. (Google homunculus if interested.)

In addition the pathways described for cognitive perception and control, there are others that help with sub-conscious control of movement (e.g. those involving the cerebellum and basal ganglia), sub-cortical perception of pain signals (e.g. amygdala), and even spinal reflex arcs that never reach the brain. Not all circuits that begin or end in the spinal nerves are destined for or originate from the cortex
This is already considerably over-simplified, and the autonomic system is more complex yet and is not confined to spinal nerves, so I won’t detail it. These signals originate in and feed back to an entirely different area of the brain (mostly hypothalamus). Similar to the motor and sensory systems, at least one synapse is required to connect the brain to the peripheral nerve.
Conclusion: they don’t meet.

Reference:

Martin, John. Neuroanatomy: Text and Atlas. McGraw-Hill Medical; 3 edition (March 27, 2003)

*The source of this image is: http://www.mindtrippingshow.com/mind-trip-of-the-week-17-how-do-we-feel-the-world

Thank you very much. This is exactly the type of answer I was looking for. And though technically they don't meet - what I meant was that (according to your answer) they meet at the somatic sensory cortex / primary motor cortex. Do I understand correctly that the muscles aren't affected by the Thalamus, and the limb muscles - not even by the midbrain? And that sensory perception is not affected by the midbrain?

If I understand correctly - Though the cerebellum doesn't act as a relay for these messages (both afferent and efferent) -  doesn't it communicate with the rest of the body through the spinal cord (again, both afferent and efferent)?

@user133943 I have edited the answer to address your second comment. Regarding the first, the nerves don't really meet, but the circuits (partially) head to the same area, so I'm glad I was able to provide some useful info. As for the thalamus, the midbrain....everything is affected by everything, and the sub-circuits are really too complex to describe here (or for me to remember - I'd be copying from my neuroanatomy text; I suggest you just buy a copy for yourself if interested!).

I am not sure whether I grasped the gist of your question appropriately, but let me provide some clarifications.
$\text{Nerve}$ is simply a collection of axons. Therefore, all the spinal nerves are just bundles of assorted nerve axons.
Now, the origin of nerve is slightly ambiguous as far as its meaning is considered. It can mean the physical origin, the place where the particular branch of nerve starts off from a main trunk or some other nervous organ. It can also mean the location of the cell bodies the axons of which comprise the nerve, the functional origin.
Now coming back to the question, the physical origin of the spinal nerves is not common. Each pair of spinal nerves originates from a specific segment of the spinal cord via two roots, the dorsal and the ventral. Therefore, each nerve originates separately and different spinal nerves cannot be traced back to a common physical origin. (The cauda equina, is actually a collection of several spinal nerves which move dorsally and periodically gives of the nerves out of the vertebral column. Although the nerves comprising the Cauda Equina, second lumbar nerve onwards, appear to have a common origin, they actually originate from their own specific segment and then move caudally as a bundle to overcome the developmental constraint of spinal cord being shorter than the vertebral column, necessitating the caudal movement of nerves within the column to emerge at appropriate points)
The functional origin is a bit more complicated. This is because each spinal nerve has a variety of nerve fibres. There are some sensory fibres with cell bodies in the dorsal root ganglion, there are motor fibres with their cell bodies in spinal cord, there are sympathetic fibres with cell bodies in the series of collateral or the sympathetic ganglia, connected to the spinal nerve via gray and white ramus communicans. There can also be cell bodies located directly in medulla which passes nerve fibres in cranial nerves as well as through its branches into the sympathetic ganglia and ultimately into the spinal nerves. Sacral nerves also contain parasympathetic nerve fibres functionally originating in the CNS. Thus, considering the functional origin, though each spinal nerve has a lot of origins, there is a slight convergence of origins for different nerves. The sympathetic ganglia and the spinal cord are two places where the origins of different spinal nerves may coincide or be structurally and functionally integrated.  But it must be kept in mind that this is a very limited convergence. There is an appreciable uniqueness to the functional origin of each spinal nerve and hence we cannot say that they "meet".
IMAGE

Thank you for your answer. However, it seems that you understood the question differently than how I meant it. For example, you wrote: "Each pair of spinal nerves originates from a specific segment of the spinal cord via two roots" (yes, I have read your whole answer. This is just an example). I'm asking "Which part of the brain...". and "Nominally, the beginning of the spinal cord is the medulla oblongata..." - I want to know which part of the brain "decides" to send a "message" through the spinal cord. (or receives, of course...). But thanks again.


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What happens to lactic acid I eat?
Let's say I drink some Kefir Milk, what happens to the lactic acid in the Kefir Milk that has entered my digestive system?

First, there are two different isomers of the lactic acid, the L(+)- and the D(-)-form. Both differ in the position of the OH-group in the molecule:

Both turn polarized light in different ways, the D(-) to the left and the L(+) to the right. The physiological form of lactic acid for the human body is the L(+) form, which is taken up in the gut and then metabolized by the L-Lactatdehydrogenase to form pyruvate and NADH.
For the D(-)-Lactate is has been thought the the D-Lactatedehydrogenase is only present in some lower animals and bacteria and that this lactate isoform is mostly excreted. This seems not to be true and there is some D-Lactatedehydrogenase in humans (and other mammals) as well.
See these publication for more information:

D-lactate in human and ruminant metabolism.

Lactic acid has been found to act as a fuel for the muscles. Refer to:  http://www.nytimes.com/2006/05/16/health/nutrition/16run.html?_r=0

Most athletes consider lactic acid their enemy, and think that training helps eliminate the metabolic waste product from their muscles so the muscles will function longer and harder. But UC Berkeley physiologist George Brooks has found that training actually teaches muscle cells how to use lactic acid as a fuel to get more bang for the buck. With training, mitochondria grow, take in more lactate via a shuttle and burn it to generate more energy.
"I gave rats radioactive lactic acid, and I found that they burned it faster than anything else I could give them," Dr. Brooks said.

You may also refer to http://www.eatmoveimprove.com/2009/11/the-truth-about-lactic-acid/ for details on lactic acid metabolism.

Hi, thanks. But what happens to it when it's in my stomach? Will it ever get to my muscles or will it simply pass through my digestive system?

where can I buy some of that radioactive lactic acid; is that at GNC or what

lactic acid undergoes radioactive dating in the lab


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Why doesn't Fenoxaprop-P-ethyl damage cool season lawns?
For controlling bermudagrass, Cynodon dactylon, a serious perennial grassy lawn weed in my area, I use the herbicide Fenoxaprop-P-ethyl. It kills the bermudagrass rather well, without damaging the cool season lawn grass in the least.

I believe Fenoxaprop-P-ethyl acts by inhibiting the synthesis of fatty acids in the meristematic tissues of the weedy grasses (designed especially for bermudagrass).
How does this mode of action not affect the 'good' grasses (the fescues, bluegrasses, and ryegrasses popular in my area)?

Will get to this question hopefully before end of bounty :) interesting stuff!

A number of studies have been done that investigated resistance to Fenoxaprop-P-ethyl and related compounds. Most of these studies focused on resistance in crops (e.g., maize) or black grass. One of these studies (Kay et al., 1999) was particularly interesting as it focused on several possible mechanisms of herbicide resistance in Alopecurus myosuroides (Black-Grass). I quote from the abstract:

[...] Resistance at the whole-plant level correlated well with reduced acetyl Co-enzyme A carboxylase sensitivity (target site resistance) in two of the populations (one from the United Kingdom and one from Germany) but enhanced metabolism appeared to be the primary mechanism of resistance in the majority of the other populations. [...] We suggest that resistance in Lincs E1 may be explained by multiple resistance mechanisms—the expression of both insensitive acetyl Co-enzyme A carboxylase and an increased rate of detoxification. However, resistance in the population Clay from the United Kingdom could be explained neither by target site insensitivity nor by an enhanced rate of metabolism. These results provide conclusive evidence that a single resistance mechanism alone cannot explain insensitivity to fenoxaprop-P-ethyl in European resistant black-grass populations and that additional, as yet uncharacterized, mechanisms must also be present.

So based on these data, I think several mechanisms may play a role in the cool season lawn grass resistance (a species name may help to specify my, admittedly, broad answer).
Interestingly, Fenoxaprop-P-ethyl is an acetyl CoA carboxylase (ACC) inhibitor (Kay et al., 1999). Note that Haloxyfop (as mentioned in your question "How does Haloxyfop control young grassy weeds in fields of broadleaved crops?") is also an ACC inhibitor. From the answer on that question it appears that ACC inhibitors inhibit cell membrane formation and that monocots (grasses) are most susceptible and dicots less. Dicots are less sensitive because they have two ACC types at their disposal, one being insensitive to ACC inhibitors. Not surprisingly then, Bermuda grass, being a monocot is killed by this herbicide. Interestingly however, other monocots seem to survive, such as the cool-season lawns you mention.
I was not able to find conclusive evidence as to why some monocots survive ACC inhibitors. An educated guess is that resistance can be conferred by mutations in the ACC enzyme (Letouzé & Gasquez, 2001) that make the enzyme less sensitive to the herbicide. These mutations can be caused by repeated exposure to these herbicides, whereby strains become resistant to the material, much like the way in which (multi-) resistant bacterial strains emerge after repeated exposure to antibiotics.
References
Kay et al. Pesticide Biochem Physiol 1999; 65:169–80
Letouzé & Gasquez, Theoretical Applied Genetics 2001; 103:288-96


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How can a plant resist glyphosate (Roundup) herbicide?
In my area, the most common weeds that strongly resists (N-(phosphonomethyl)glycine) (glyphosate) are the horseweed, or mare's tail, Conyza canadensis, and Canada thistle, Cirsium arvense There are several other weeds with similar resistance. I use the brand Roundup on jobs where a complete kill is necessary. However, I sometimes have to go through again, with glufosinate, to control these weeds. I'd prefer not to, as the glufosinate lingers much longer in the soil.

Glyphosate inhibits an enzyme used in the synthesis of the aromatic amino acids tryptophan, tyrosine,  and phenylalanine. It is taken in by the stomata in the leaves, and is moved throughout the plant to all the points of growth, acting fastest on those plants which are undergoing fastest growth.
I can't seem to find an article on how the weeds mentioned can tolerate this treatment. How do these weeds resist the glyphosate?

I found a paper investigating the mechanism of glyphosate resistance in Conyza canadensis. They used 31P NMR to investigate the fate of the glyphosate in vivo. What they found is that the resistant plants are able to transport glyphosate into the vacuole:

The following view of horseweed resistance to glyphosate emerges from
  the data presented herein. Glyphosate enters the cytoplasm of both R
  and S plant variants at the same rate. Within hours, however,
  glyphosate begins to occupy the vacuole in the R but not the S
  biotype. The identical pH values of R and S vacuoles speak against the
  possibility of a pH-driven process. This, coupled with the
  preferential movement of glyphosate from the cytosol to the vacuole in
  R tissue but not in S, suggests the presence of a transporter for
  glyphosate either specific to R or at a substantially greater
  concentration in R than in S tissue.

Another paper titled "Two non-target mechanisms are involved in glyphosate-resistant horseweed (Conyza canadensis L. Cronq.) biotypes" found a different mechanism for glyphosate resistance in addition to the sequestration into the vacuole.

Glyphosate was metabolized faster in the R (C004) biotype than in the
  S biotype. The herbicide disappeared completely from the R (C004)
  biotype by conversion into glyoxylate, sarcosine and
  aminomethylphosphonic acid within 96 HAT.

The resistant plants seem to be able to metabolize glyphosate more effectively.
It is of course not guarenteed that these are the only mechanisms for glyphosate resistance, there are likely more variations.

This answers concession to the diversity of evolution and the humble state of human endeavors is awesome.

authors: Деррик Морган


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Why doesn't the herbicide 2,4-D damage lawn grass?
I sometimes use 2,4-Dichlorophenoxyacetic acid to control broadleaved weeds in lawns. It is selective, and quickly kills the dicot weeds, while other plants are unharmed.

2,4-D is a synthetic auxin, a class of plant hormones. It is gets taken in through the stomata on the leaves, and is transported to the meristems of the plant. This causes uncontrolled, unsustainable growth, and the plant wilts, and dies.
Why doesn't this affect most monocotyledons?

According to this link from Purdue, the seed of the answer is this:

The herbicide is used to kill broadleaf weeds, which are dicots, while monocot grasses, such as sorghum and corn, are more resistant. That's because grasses inactivate 2,4-D inside the plant, while broadleaf dicots do not.

But on the other hand, Song 2014 has this to say about 2,4-D:

However, the underlying molecular mechanism of how auxinic herbicides selectively kill
  dicots and spare monocots is not
  understood yet (Grossmann 2000; Kelley
  and Riechers 2007; McSteen 2010). The mechanisms of auxin biosynthesis, transport,
  and signal transduction
  are conserved in monocots and dicots make this question more complex (McSteen 2010). Early research has
  proposed that the selectivity of auxinic herbicide is because of
  either limited translocation or rapid degradation
  of exogenous auxin, altered vascular anatomy, or altered perception of auxin in monocots (Monaco et al. 2002;
  Kelley and Riechers 2007). Auxin transport is influenced by plant vascular
  systems (Mattsson et al. 1999;
  Scarpella et al. 2006). The difference in vascular tissue structure between dicots
  and monocots may contribute
  to the selectivity of auxinic herbicides. In monocot
  stems, the vascular tissues (the phloem and xylem) are
  scattered in bundles, and lack a vascular
  cambium; in dicot stems, the vascular tissues are form
  ed in rings and
  possess a cambium.

So in other words, we don't know yet. It seems to be very strongly tied to auxin transport, but we do not have the full mechanism of action; since auxin is such an important plant hormone, and the pathway is therefore highly conserved (that is, the genes tend to be nearly identical on the parts of the sequence that affect the phenotype), the general conclusion is that the pathway itself is not affected, but an accessory pathway clears up auxin in levels excess of any normal amount in monocots.
Edit: Whoops, got the author's first/last names mixed up.

The specificity of 2,4 D may be due to either limited translocation or rapid degradation ,altered vascular anatomy or altered perception of auxin in monocot

Welcome to Biology.SE! Your answer doesn't appear to be adding anything to the existing answer and lacks supporting references. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then edit your answer accordingly. Thanks!


text:
Facultative Cannibalism?
I heard about Larger cats eating the cubs. Is it some kind of facultative cannibalism or they can eat there own kind like that?
What are the facultative cannibalism present in animal kingdom?
What is the genetic origin?

+1 Spawned a related question on Pets Will neutering a male cat stop it from killing kittens?

Lions
Lions are a classic example of cannibalism. To understand why this occurs we have to understand their mating system.
Males have a harem of females and males fight in order to access a harem (Note: females may also take part in the battle depending on which male they prefer). When a male takes over a new harem, he kills the young ones of the previous male if these young ones are still dependent on their mother. The reasons are:

The mother is not fertile while she is taking care of a young baby while the male would appreciate that the female is ready to raise his own kids.
The mother needs to invest quite a lot of energy to feed/milk their young while the new male would prefer this energy to be invested in his own offspring.

In short, a male kills the young ones when he takes over a new harem because these young ones do not carry his genes and prevent this new male to optimally pass on his own genes as the offsprings of the previous male consume time and energy from the females of the harem.
And well… once the offsprings are killed, it would be a shame to waste all this good and fresh meat. Better to eat them!
In the cases of lions, cannibalism does not result from food shortage but from "not wasting food". I think that the "not wasting food" hypothesis is the most explanation for cannibalism (I am not sure though). I guess that most often the "not wasting food" occurs after death due to competition as it is the case in lions.
Other Examples
There are many cases of cannibalism in the animal kingdom. Chimpanzees eating other chimpanzees and bear eating other bears. In the tiger salamander, there are cannibal morph and normal morphs. In this species cannibalism is very frequent as in nature one offspring over 5 is eaten through cannibalism (if I am not mistaken). Cannibalism is very common in prairie dogs as well (Reference). In Dragonflies cannibalism represents 95% of the total mortality (Reference).
Sibling sharks eat each other in their mum's womb. Here is a video on the subject. This type of cannibalism is called siblicide.
In Praying mantis the female may eat her mate after copulation. This is referred to as sexual cannibalism. The subject is slightly controversial, please have a look to the wiki article for more info.
In many species (including the dragonflies example above) the old individuals eat the young. This is referred to size-structured cannibalism.
Fillial cannibalism is a type of cannibalism when the adults eat their own offsprings as it is the case in the prairie dogs example I cited above.
Have a look to the Wikipedia links for filial cannibalism, sexual cannibalism and siblicide, they go further than my answer.

Wow!! Can you add something about Siblicide too?

I don't know much about all that. I'd suggest you to have a look to the wiki articles I linked in my answer and eventually come up with a more accurate question on another post as this post was fairly broad.

My first thought of why siblicide may evolve in sharks is: It seems a good solution for the parents to make sure that the only offspring they want to produce will carry very good genes. It is like producing a "pre-selected" offspring. r-strategy species don't do that. They let selection act later. But that makes sense that siblicide occurs in sharks as they perform some parental care and they don't want to lose energy for unfit kids. according to my hypothesis the question might then be "Why don't everybody does that?" But I really don't know much. I just had fun formulating a hypothesis!

@Remi.b the video you linked says that the oldest embryo eats the young ones as soon as its teeth are sharp enough. So not that much selection going on, except for the possibility that an older embryo with retarded development could be eaten by a younger sibling with normal development. But there isn't a bunch of embryos hunting each other at once.

It's a dangerous strategy for the species. Some embryos might develop particularly fast and then be strong enough to kill/eat their fellow embryos. That doesn't say much about their fitness as adult sharks. E.g. imagine if all the geek kids got killed by their football-loving classmates? Who would run the Internet? Siblicide probably leads to fast evolution into a niche (more siblicide). Allowing the siblings to live longer and compete for mates and offspring probably leads to more stable/fitter/more adaptable outcomes, at the expense of slower evolution.

Cannibalism in praying mantises is not a required part of copulation, this is a myth, as they can successfully mate without the male dying. It is speculated that sexual cannibalism is due to other factors such as hunger, increased aggression in the female due to invasive observation at the time of copulation, or a few other factors.

@Remi.b Your comments makes it seem that you believe that a species has conscious control over evolution or that the mother shark has control or influence on this type of behavior of the embryonic sharks within her. This is just NOT how nature works.

Ha ha seems that I would have better to remain silence on possible explanation of the shark siblicide. I have to confess that it was a quick thought. @TecBrat No, I didn't any of these naïve mistake. I am just saying that the parents may want to make sure that their unique offspring is fit to carry the parents' gene further.

@rumtscho Indeed this is interesting and is a counter-argument to my hypothesis. However, developmental time might be a proxy for fitness. Similar mechanisms exist in bees. The first queen to hatch will usually be able to kill all the other before they even hatch.

@winterblood Ok, thanks for the comment. I edited my post to indicate that it seems to be a myth. If you have a reference, the answer could be definitive. Thanks

The wikipedia article you linked for the praying mantis covers most of this in the first two paragraphs of the  Reproduction and life history section.

@winterblood Thanks! Seems indeed that the subject is controversial. Feel free to edit my answer if you want to improve it.

@winterblood Making any generalisation about cannibalism (other than that it often happens) in praying mantis copulation isn't currently scientific. Research has only been carried out on a few species.


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How to operate a microtome?

In the picture above (Source: Amazon.com, United Scientific MCT001 Hand Microtome) we can see a microtome. How is it operated?

Also, are these still used in everyday biological research? Teached for students?

Interesting picture. My guess is that this is a historic piece of equipment, but still seems to be available. The guys next door (who cut sometimes for us) use a cryomicrotome like this.

The imnstrument is shown here upside down. If it is turned around, it looks like this:

The glass disc are placed around the middle tube. The operation principle can be seen in this image:

The specimen is placed in the tube in the middle and pushed out by turning the knob at the bottom. The minimal increment for this kind of microtome is 10 micrometers. The razor knife is used to cut the slices of the specimen.
An operation manual can be found here.

Also, are these still used in everyday biological research? Teached
  for students?

It's a hand microtome allright. As Chris explained, these are used to section thin slices of plant tissue, to be examined using a transmitted light microscope. They're still availlable from several sources, for example from Euromex in The Netherlands. I still have one of those, but it's years ago I used it:

Those are hardly used anymore in research, but they are still being used by amateur biologists/botanists/microscopists.
The only uses I can imagine in research would be to use it to section a sample to see whether or not it is interesting enough to be processed and sectioned using more contemporary techniques, such as paraffin embedding followed by rotary-/sledge-/base sledge microtomy. Or perhaps in the study of life processes.
Depending on the skills of the operator (including his skills to sharpen/strop his knives!) and the nature of the sample, slices as thin as 20 µm can be sectioned, using a hand microtome.
That's often thin enough to make for a more or less acceptable botanical slide, temporary or permanent, but as kind of a norm, "regular" paraffin botanical/histological/histopathological/... sections for light microscopy are sectioned these days at any thickness between 2 - 10 µm.
That's not possible with this type of microtome.
The impossibility to section samples at a thickness thin enough to make for really clear microscopic images has burdened scientists for ages.
It wasn't untill 1883 that an American mechanic, Adam Pfeiffer, came up with a usable machine to make that happen. Pfeiffer worked further on the idea provided by two others, Cowles and Richards, who made a first prototype in 1879.
In 1886, Charles Minot, an American as well, came up with the first really usable rotary microtome.
That "Minot-microtome" is up to the present day, the workhorse in the botanical, histological and histopathological lab.
It's an interesting story, but the rotary microtome is based on a fundamentally different concept, compared to a hand microtome.
The real offspring of the hand microtome is the (base) sledge microtome, as it mimics more or less the movements of an operator using a hand microtome. But without all those impossible to controll variables.
This is a base sledge microtome, I finished restoring only a few weeks ago. It's the legendary Jung Heidelberg Tetrander II. The Tetrander was put on the market in 1910 and some of those are still in use. They're used to section large and hard samples (hard wood, bone, teeth, ...), which can't be sectioned using a rotary microtome.
At the time it appeared on the market, a popular joke amongst German histotechnicians was, that it was named "Tetrander" because it took four man to handle it... In reality it was named "Tetrander" because it was designed by four German scientists, amongst them the legendary Paul Mayer (yes, that Mayer's hemalum staining solution guy).
This one (it is operational) is capable of sectioning samples as large as about 5cm * 7cm (ca. 2in * 3in), section thickness adjustable between 1 and 50 µm.
Larger, motorized models are capable of sectioning things as hard as a concrete bloc, having the size of a modest tree. And that's no exageration...


text:
What is wrong with this analogy: Individuals are to alleles what governments are to individuals
I'm an amateur when it comes to genetics, I'm hoping to learn something from the corrections. I am taking epigenetics into account (kind of); all 3 entities are susceptible to external physical influences.
Kind regards,
Frank

In this analogy, what is a gene?

Alleles are passed down (to individuals) and created by individuals (although not fully under their control). But individuals are not passed out or created by the governments (I suppose), although individuals are influenced by the governments and they can influence governments, whereas individuals can not necessarily influence the allele of the gene they already have unless you take epi-genetics into account. Also, the creation of an allele is not entirely influenced by individuals due to independent assortment and chromosomal crossover, but individuals can more or less influence governments.