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Endemic plant families on islands?
Endemism on islands is quite a common phenomenon, at least at the level of species or genera. Old continental fragments like Madagascar or New Caledonia may even harbour endemic families which went extinct on the continents. I also know of the odd example of Lactoridaceae that comprise only one species which is endemic to the Juan Fernandez Islands.
Do you know other instances of endemic families on islands? What about Hawai'i, the Canaries or Galapagos?

This link (http://lntreasures.com/index.html ) might help you...it doesn't mention particularly about islands...but still I think it's a great site ( if you already don't know about it) for ecologists, like you...

That link is awesome (I didn't know it yet)! +1


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Why don't fish groom each other?
Fish are often plagued by external parasites, which are presumably difficult for them to remove.
There are well known cases where large fish come to coral reefs and allow smaller fish to pick off their parasites. See below a moray eel being "cleaned" by a shrimp.

Some fish, like sunfish, even get cleaned up by birds: https://www.youtube.com/watch?v=U60obmWODLQ
But on land, we have many social animals that solve this problem more directly by grooming each other. How come the fish never seem to do this? Many of them are already social, and I imagine they wouldn't have much trouble digesting the external parasites. Why don't they groom each other?

They probably think that's gross.

All cases of same species grooming I know of involve animals with a certain amount of dexterity. For example (images from wikipedia):

Macaw beaks:

Primate fingers:

Even ponies rubbing each other:

In all of these cases, the animals involved have the right tools for the job. fingers, beaks and prehensile lips can all close in on a parasite and remove it with precision. how exactly would you expect a shark to do this (image from the guardian)?

Sharks can and do rub themselves against rocks to get rid of dead skin but they simply don't have the tools for the kind of detail work that the smaller fish can do for them. The same applies to other fish. I think you will find that at least in most cases, fish that use client species to groom themselves wouldn't be physically able to do the same job themselves. It's all a matter of the right size and the right tools.

Note that this is pure speculation, I have no references to back this up, it just seems reasonable. I would not be surprised if some fish did actually indulge in social grooming, it's just harder for the reasons outlined above.

A good answer, but keep in mind that the question was about fishes in general. I assume that the OP is talking about the more subordinate species of fish.

@VatsalManot yes, but I think it's applicable to all. In order to be able to eat parasites, you need to be small enough to get at them. Presumably, if you're the same species, you will be too big. Still, as I said, this is pure speculation.

As you correctly noted in your answer, symbiosis is a viable solution for the size to size ratio problem.

Something from my imagination: Probably the first fishes were of small size with some of them evolving to be big. The variation in the sizes of the fishes is larger compared to the variation in the sizes of mammals(picture elephants and rats with whales and tiny fish). That being said, if you'd have bank of small fish staying in one place and all grooming each other, a bigger fish would swallow them with one bit(as whales eat). This does not happen on land with, say monkeys, because it would be too big of a load for  a tiger or an eagle to snatch both of them with one move. In conclusion, the ways of predators in oceans(trickier ambush tactics, faster speed attacks) and variations in sizes might have made this more of a disadvantage than an advantage underwater compared to on land.

Regarding predators: Many fish such as herrings already live in large, dense groups - and they do get swallowed wholesale by whales. This apparently is not enough to deter the schooling behavior, though.

But herrings constantly move, they would have to be able to move and groom at the same time.

Perhaps it has something to do with fish slime coats.
Fish are covered in a thin layer of mucus which helps with immune system function, etc. According to these guys at least, who admittedly are not exactly a scientific authority.
Perhaps grooming as a social behavior would disturb the slime coat more often than it would help remove parasites? Or it's dangerous for other reasons? (Some fish are very territorial)
Some(most?) fish are just incapable of grooming other fish of the same size and shape. I mean look at this guy. The moray eel above has a jaw much larger than that of the entire shrimp that is grooming it, so perhaps picking parasites off things with such a jaw is like cutting your fingernails with a meat cleaver?

But the fish still get groomed, by other species. Are you saying that they would loose the layer if a fish did the grooming but not when done by a shrimp or seagull?

You know the more I think about it the more I suspect mouthparts are to blame. A marlin for instance can't groom anything, much less another marlin. They just don't have the right teeth/jaw for it.

Yeah... but then at some point there was a bifurcation, they could have chosen a suitable mouth for grooming or a mouth for other stuff to do. Maybe the severity of having parasites, which I don't know, versus other dangers has something to say in this.

I mean grooming parasites off of other members of your own species can't be a viable food source for your whole species. Specialist mouthparts for eating any other food would be better, so I imagine it's just a thing that might be nice to have, evolutionarily speaking, but ultimately shrimp are "good enough" at it.

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Importance of Double Helix DNA Structure
Gene expression involves transcribing only one strand of DNA molecule. So i was wondering what are some biological advantages of the double stranded DNA?

It maintains a certain structure - and it also holds a second copy of a strand (though reverse complement). This can be used to repair damages.

@Chris — Please make the point about DNA repair into an answer.

The structure allows for the DNA to be tightly packed into chromosomes. It also provides an extremely stable backbone with the negatively charged phosphates pointing to the outside of the molecule. This charge aids in the attachment of other molecules to the strand of DNA.
DNA double helix allows it to be stable and it won't easily destroyed.

Unconvincing answer lacking critical comparison to support your points. You don't explain how dsDNA can be packed more tightly than ssDNA or how it is "more stable".

The most important role of this peculiar double helix structure of DNA is to facilitate replication....in preparation of cell division each of the 2 strands acts as a template thus facilitating precise copying of genes....in the Nature(1953), Watson & Crick also suggested that " It has not escaped our notice that the specific pairing we have postulated immediately suggests a possible copying mechanism for the genetic material"...
Also, the extremely stable structure doesn't allow DNA to mutate rapidly, unlike RNA...thus converting it into an "efficient information storage structure"....
& lastly this double helix structure is also resistive against extreme physical changes...as is evident from Griffith's experiment, where the heat-killed bacteria had their DNA intact...
Also try this link- "Genetic Implications of the Structure of Deoxyribonucleic Acid"- Watson & Crick....as it always helps to learn from the very masters of DNA structure;)

Your first point is valid, but only to a point. It is necessary that a dsDNA is formed at some point as the replicative form, but ssDNA viruses show that there is no need for a dsDNA genome for replication. Your second point is nonsense. It is the phosphodiester bond between the deoxyriboses that is more stable than that between ribososes and the lack of proof-reading that is the difference in mutability. And the third point likewise is nonsense. You don't show the heat resistance is due to the double strandedness. And your final reference is dead.

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Can one use a hemocytometer on a compound upright microscope?
I'm posting this as a follow-up on What to look for when buying a light microscope?. The answerer states that you would need to use a an inverted microscope to count cell in the hemocytometer(counting chamber).
I've read, partly, a book on lab diagnostics tests and it was not written that there. Moreover, they mentioned things about microscopes featuring a compound upright microscope both in words and picture.

Yes, you should be able to! The reason I suggested the use of inverted microscope was because I put a number of other things in the same sentence such as dishes etc. Inverted microscope is used in those cases to reduce the distance between the objective and the sample when looking at the dish with cells. In most cell culture rooms that I have worked in, an inverted microscope is used! Inverted light microscopes also tend to have a phase contrast, which is helpful in viewing cells!

I have now made an adjustment to my response to reflect this point!

@Bez Sorry to bother, but what features would I want to have on my microscope(on a upright compound one) for lab work(urinalysis, blood work, cytologies, histologies, fecals and all other)?

I'm a molecular biologist (fluorescence and cell culture) so I do not know much about urine or blood work analysis microscopy. This is best posted as a new question but please show some degree of research into the question to prevent it from getting a close vote!

Yes it can. You will want to use a thin hemocytometer and the working distance of the objective (20x) needs to be long enough to focus both the cells under the cover glass and the grid under the hemocytometer. Because you are looking at it from the top it would be helpful probably to have some phase on the scope to increase your contrast so that you can more clearly see the grid.
Hemocytometers are most commonly used with inverted microscopes because inverted microscopes are the most convenient microscope for performing tissue culture, and 's a commonly used to count cells when passaging or setting up an experiment etc, as they allow you to view cells in a culture plate. Upright microscopes require that you make a slide.

You can use a hemocytometer(counting chamber) on whatever microscope for transmitted light, regular scope, inverted, whatever. It doesn't make any difference.
But you should keep in mind what a counting chamber is designed for: to count red or white blood cells, reticulocytes, yeast cells, whatever.
They're not designed with having the best possible image in mind. Their dimensions fall far outside the specifications microscope optics are calculated  for.
I measured a few (regular Thoma from the well known brand Assistent): thickness is 4 mm. The standardized coverslips to be used with those are 0.4 mm thick.
There's a very small chance, some minor distortion will be visible in the image ;-)...


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Which is better against genetic mutations? Asexual or Sexual Reproduction?
In terms of genetics, which type of reproduction is better against adverse mutations? I understand a bit of Muller's Ratchet—in which asexual organisms accumulate a number of deleterious mutations in their genomes. However, doesn't the crossover process and corresponding genetic diversity in sexual-reproducing organisms make them more susceptible to these mutations?

Mutations can be caused by much more than just recombinatory events--polymerase fidelity, DNA damage repair, even environmental factors can have a huge impact on DNA damage. While most DNA polymerases have an error rate of around one mutation per billion, there are different levels of fidelity among different polymerases (McCulloch and Kunkel, 2008).
Regarding the fidelity of crossover/recombination events, it is true that these events increase the likelihood of a lethal or detrimental mutation. However, recombination is not a random process. Recombination hotspots are chromosomal locations where the rate of recombination can be hundreds of times higher than other locations. These hotspots are generally in "safe" locations, not in the middle of a crucial gene, etc. There are also recombinase enzymes specific to certain sites of recombination.
As to "which is better", I don't think the answer is as straightforward as you might think. You might think a sexually-reproducing eukaryote with a very high-fidelity DNA polymerase and safe, specific recombination hotspots would be ideal. That situation is generally what we find in nature, so you're (probably) correct. However, at the other extreme, think of a virus*. Viruses have a much, much, much higher rate of mutation than eukaryotes--orders of magnitude higher. This is how a virus survives, basically out-evolving the host's defenses. A high rate of mutation works for a virus, and a low rate of mutation works for a multicellular eukaryote.
*Of course, there is always debate about whether or not viruses are alive. However, they definitely reproduce.


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How do fish communicate?
Fish, as far as I know (of course there may be exceptions), don't have any vocal organs, despite the fact they are proven to be social. So how do they manage to communicate with each other? On land, organisms like the honey-bee have their "tail-wagging dance" and ants have pheromones, so what about fish?

Fish also produce sounds; the difference is that they are put in different positions by the body to sound. The sound produced by fish is about 20Hz and therefore is difficult for humans to hear. However, these sounds can be recorded and reproduced using instruments.
Of course, some fish also rely purely on action to exchange sounds. Some fish use ultrasonic communication, similar to dolphins (although dolphins are not fish).
Some fish transfer information by changing body colour. These fish are usually located in the tropical shallow water. Some fish pass through the water with their fins flapping to communicate courtship information. A few, mostly deep-sea fish, release pheromones.

What do you mean by " they are put in different positions by body to sound"? Also, it would be really great, if you can provide any reference to substaniate your answer>>>

means thier  "tail-wagging dance" will make some noise

can you provide any reference to substantiate your answer???

Please provide some sources for the information you have in your answer.

There are a variety of fish species that produce sounds, including many species of Bocaccio (i.e. rockfish). This article is a great resource for learning more about 'fish choruses', a phenomenon where many fishes produce noise during dawn/dusk hours, much like the dawn chorus we're more familiar with for birds.
One of the most famous examples of fish vocalizations is probably the plainfin midshipman fish (listen here!). In this case, the hum is used to attract females for mating.
As for how these sounds are produced, this interview with a scientist at Scripps Institution of Oceanography says
"Fish make sounds by oscillating their swim bladder, or by rubbing the bones where their fins attach to the body, similar to how crickets make sound by rubbing their legs".

You should also check out Dr. Rodney Rountree's website. It looks old but has lots of useful information about fish sounds.  http://www.fishecology.org/soniferous/soniferous.htm

I second MZiegenhorn's answer and Xavier Mouy's comment that a variety of fish species produce sounds, and I'll shamelessly refer you to our new website FishSounds for an inventory of published research (updated up to the end of 2020 - 2021 update coming soon) on fish sound production, and some example sound clips.
Fishes don't have vocal chords, but they can produce sounds in a variety of ways. In Ingrid Katz's words: "Fishes are known to produce sounds using five mechanisms: 1) swimbladder pulsations, 2) stridulation, 3) hydrodynamic movements, 4) substrate, body and tendon vibration, 5) air release. "
Regarding yazhuo's answer about fish sound production mechanisms, you can check Eric Parmentier's work, such as for example this book chapter:
Parmentier, E. and R. Diogo (2006). Evolutionary trends of swimbladder sound mechanisms in some teleost fishes. Communication in Fishes. F. Ladich, S. P. Collin, P. Moller and B. Kappor. Enfield, NH, Science Publishers: 43-68.
Now that I mention a book chapter, the entire book would be an excellent source to answer the original question, if you are up for the reading.

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Will genetically modified food affect our health?
It's a popular public sentiment that - GM foods like tomatoes (flavr savr) will affect our health.. Is there any logical scientific explanation behind this?

I don't see a personal health question here. The question might not be very profound otherwise though.

this q. is legitimate...slightly debatable...but not at all a personal medical q....

I agree with the above comments. However, I think this question would be a better fit on skeptics.SE. By doing a simple search for "GMO" on skeptics.SE you will get several interesting hits. The question might be considered as a duplicate of other questions on skeptics.SE. I would tend to think this question should be answered following these guidelines

Would improving health count? If GMOs provide larger yields or better nutrient content with less dependence on pesticides or herbicides those would all be good things. Most of the questions I see about GMO only ask about potential negative outcomes.

It's a popular public sentiment that - GM foods like tomatoes (flavr
  savr) will affect our health.. Is there any logical scientific
  explanation behind this?

GM organisms can have different genes and gene expression than natural ones, so they can create more protein or different proteins. Proteins can be toxic, can cause allergy and can catalyze reactions which can lead to toxic products.
To create a GM plant you need dollar millions, so it is not a cheap business. The GMO food regulations are very strict (at least in the EU), so it is unlikely that you will eat a GMO which contains toxic compounds.

Whereas food safety organizations find nothing inherently unsafe in
  the process of genetic engineering, they note that new plant
  characteristics developed in the next wave of agricultural
  biotechnology could present new risks. At the same time, future
  generations of biotechnology may well provide food products with
  higher vitamin or protein content and lower allergenicity, yielding
  benefits to food consumers.

2014 - Agricultural Biotechnology: The Promise and Prospects of Genetically Modified Crops

Despite all the effort to make GMO foods safe, there are issues:

Pesticides associated to genetically modified foods (PAGMF), are
  engineered to tolerate herbicides such as glyphosate (GLYP) and
  gluphosinate (GLUF) or insecticides such as the bacterial toxin
  bacillus thuringiensis (Bt). The aim of this study was to evaluate the
  correlation between maternal and fetal exposure, and to determine
  exposure levels of GLYP and its metabolite aminomethyl phosphoric acid
  (AMPA), GLUF and its metabolite 3-methylphosphinicopropionic acid
  (3-MPPA) and Cry1Ab protein (a Bt toxin) in Eastern Townships of
  Quebec, Canada. Blood of thirty pregnant women (PW) and thirty-nine
  nonpregnant women (NPW) were studied. Serum GLYP and GLUF were
  detected in NPW and not detected in PW. Serum 3-MPPA and CryAb1 toxin
  were detected in PW, their fetuses and NPW. This is the first study to
  reveal the presence of circulating PAGMF in women with and without
  pregnancy, paving the way for a new field in reproductive toxicology
  including nutrition and utero-placental toxicities.

2011 - Maternal and fetal exposure to pesticides associated to genetically modified foods in Eastern Townships of Quebec, Canada

The study of combined effects of pesticides represents a challenge for
  toxicology. In the case of the new growing generation of genetically
  modified (GM) plants with stacked traits, glyphosate-based herbicides
  (like Roundup) residues are present in the Roundup-tolerant edible
  plants (especially corns) and mixed with modified Bt insecticidal
  toxins that are produced by the GM plants themselves. The potential
  side effects of these combined pesticides on human cells are
  investigated in this work. Here we have tested for the very first time
  Cry1Ab and Cry1Ac Bt toxins (10?ppb to 100?ppm) on the human embryonic
  kidney cell line 293, as well as their combined actions with Roundup,
  within 24?h, on three biomarkers of cell death: measurements of
  mitochondrial succinate dehydrogenase, adenylate kinase release by
  membrane alterations and caspase 3/7 inductions. Cry1Ab caused cell
  death from 100?ppm. For Cry1Ac, under such conditions, no effects were
  detected. The Roundup tested alone from 1 to 20 000?ppm is necrotic
  and apoptotic from 50?ppm, far below agricultural dilutions (50%
  lethal concentration 57.5?ppm). The only measured significant combined
  effect was that Cry1Ab and Cry1Ac reduced caspases 3/7 activations
  induced by Roundup; this could delay the activation of apoptosis.
  There was the same tendency for the other markers. In these results,
  we argue that modified Bt toxins are not inert on nontarget human
  cells, and that they can present combined side-effects with other
  residues of pesticides specific to GM plants.

2012 - Cytotoxicity on human cells of Cry1Ab and Cry1Ac Bt insecticidal toxins alone or with a glyphosate-based herbicide

Though GM crops promises to meet the world's food need and eliminate
  the world hunger and starvation, the potent harmful effects cannot be
  overlooked and these need to be taken seriously. The long term impact
  on the society cannot be overruled as it includes the health risk of
  all the people involved be it producers (farmers) or the consumers
  along with the scientists who are working in the laboratory. Hence, it
  is the need of the hour to reach and try for sustainable development
  that meets the needs of humans and the balance of nature maintained.

2013 - Cry1Ab Treatment Has No Effects on Viability of Cultured Porcine Intestinal Cells, but Triggers Hsp70 Expression

I think it is the same story as by food, pharma and plastic industry. The billion dollar profit can be more important than the consequences. Btw. if you check a regular food, which you can buy in the shop, you will find a lot of unhealthy components e.g. trans fatty acids, omega-6 fatty acids, fungicide remnants, etc... which can affect your health as well.
My conclusion is that in most of the cases it is safe, however in rare cases it might have a mild harmful effect. To filter out those cases and their causes we need further studies and better regulation.

Genetic engineering is a technology not a trait.
In general, genetic engineering and genome editing are as safe as conventional breeding and mutagenesis (introducing thousands of random mutations by radiation or chemicals to speed up the breeding process).
The safety of the resulting product depends on what has been changed or how the crops are used. You can obtain unsafe products from conventional breeding, as shows the popular example of the Lenape potato (Wikipedia), which was bred for specific traits while unintentionally increasing its solanine content to dangerous levels.
The same goes for GMOs. Glyphosate resistant crops will increase the glyphosate level in the plant and favor unsustainable farming practices like large mono-cultures and a lack of crop rotation with potential risks for the environment or even human health. On the other hand, Bt-crops have been shown to reduce pesticide use and can therefore be beneficial for health and nature.
Your tomato example is not that much related to farming. The aim was to improve shelf life, which could help to reduce food waste. Similar products are non-browning apples (Arctic Apples). Usually, they work by blocking the activity of an enzyme that normally would degrade the fruit. Of course, there are debates if the enzyme is needed for important processes in the plant and if it would have any negative effects on the healthiness of the product. But usually nothing significant is found.
Furthermore, genetic engineering can also make products healthier by introducing positive traits like increasing vitamin or healthier fatty acids.
Again, the safety of the product depends on specific changes and not on how these changes have been achieved. If we could have all these products with conventional breeding, we would do it. And we probably could, it just takes ages. So, all "negative impacts" of GMOs should really be discussed as "Do we want/need this trait and what are the effects?" and not as "Was it created by genetic engineering?".
Finally, GMOs are the best tested products on the market. While we know very well, what has been modified in these plants, we have no idea which genes have been changed in mutagenesis products. And because of strict regulations and research, approved products can generally be considered to be safe to consume. So far, there is no recorded case of someone having serious health issues from consuming GM-food, while people are dying from their self-grown zucchini (I'm not kidding).

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Criteria for compound action potential thresholds
As opposed to action potential thresholds (which are binary yes/no events), electrophysiological thresholds of compound action potentials are arbitrary. Mostly a certain noise level is picked and when the neural signal crosses this 'threshold' it is said to be 'above-threshold'. I have come across various definitions of this threshold, such as SD-based values (2xSD, 4xSD etc), 'visual' thresholds (a bit iffy from my point of view) among other things. Is there a rule of thumb as to define threshold? Alternatively, a review article, book chapter, or a primary research article with considerable impact explicitly dealing with this matter would be very helpful.

Dr. Izhikevich's book Dynamical Systems in Neuroscience may be a good place to start. However, he takes a odd position that thresholds, from a mathematical point of view, don't exist. This may not be informative for your experiment as the mathematical view of compound action potentials (bursting) is not well connected to actual neurons, and mostly comes from playing with toy models.

Action potentials of single neurons (APs) are the building blocks of compound action potentials (CAPs). While each of the individual APs is a yes-or-no response with a clear-cut defined threshold, CAPs are not. CAPs are build up of hundreds or thousands of neuronal contributions in, e.g., the auditory nerve. Decreased responsiveness as well as desynchronization of the neuronal responses can decrease the amplitude of the CAP.
It all depends on the amount of background noise and stimulus artifacts versus the amplification factor (the gain) whether a CAP can be recorded and identified yes or no. Typically, gross-potential recordings do not allow for single APs to be measured. CAPs are therefore stochastic phenomena and hence the CAP threshold should either be defined by visual examination (subjective), or through noise-dependent threshold criteria (objective). Therefore, unlike AP thresholds, CAP thresholds are arbitrary and heavily dependent on the noise level.

Yes, it's eventually statistical.


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Weird gelatinous substance in highland bog
I recently went walking in the highlands in Snowdonia, Wales and we came across this:

Can anyone explain what it is? My guess was some kind of fungus but I'm not positive. The ground was very water logged and boggy.
It looked a lot like frog spawn, but it's autumn here and we wouldn't see frog spawn until Spring. There appeared to be no animals living inside or around it.
It's often called star jelly and there's a whole wikipedia article on Star Jelly talking about it:

“Star jelly” (also called astromyxin, astral jelly, pwdr sêr, star
  rot, or star shot) is a gelatinous substance sometimes found on grass
  or even on branches of trees.1 According to folklore, it is
  deposited on the earth during meteor showers. Star jelly is described
  as a translucent or grayish-white gelatin that tends to evaporate
  shortly after having “fallen.” Explanations have ranged from the
  material's being the remains of frogs, toads, or worms, to the
  byproducts of cyanobacteria, to the paranormal.[2][3][4][5] Reports of
  the substance date back to the 14th century and have continued to the
  present day.

How did it feel on touching???

Surprisingly solid. when I poked it, rather than my hand going into it, a lump fell off.

It could be a fungal formation. If you look carefully there's one mushroom just left bottom of it and it also looks kinda soggy, for lack of a better word. So if there was a lot of moisture, too much of it for a bunch of mushrooms that often grow together out of same hypha, they could decompose into a jelly-like see-through substance as the cellulose soaks in water. Digestive enzymes that snails and slugs (gastropods) release when feeding off them might have also helped with that process. I've seen similar before, it's not limited to Welsh highlands.

Could be algal secretion, fungal growth, bacterial formation, animal's secretion, etc many thing.

There appear to be no animals? Insects are also animals, in the boggy environment insects could live.

So the One show did a magazine piece on this the other day; a scientist did some DNA analysis of some of it.
The conclusion was that it's frog jelly (full of frog DNA). Apparently frogs have glands full of the components of the jelly in sacks in their bodies, when the sacks come into contact with moisture it expands massively (same process that allow them to produce frog spawn). When a frog is eaten (by a bird or fox) the jelly expands on contact with any moisture. The animal eating the frog either vomits it up or doesn't eat it in the first place and voila.

Why did you cross out a whole section? If it is not correct, please remove it. Otherwise leave it, as it was.

Do all frogs make this jelly or just some? i.e Can we narrow down what species this came from?

All frogs. It's the jelly they produce to make frog spawn, so I'd guess only females. They definitely had the DNA of the frog, so you could likely discover the frog species from that. They also said that the DNA in places had been contaminated with predator DNA, hence the conclusion that the frog had been eaten.


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What kind of animal can do this?

When I was moving to another house, I found this plastic bag on the top of the cabinet of my old house. It looks like someone cut it all with a scissor, but no one have access to my bedroom, and it was not me.
I don't thing it could be rats. That bedroom was very tiny and closed, there's no way for a rat to enter.
The house is very near a university with a little "forest", there are many types of mosquito and little flying animals, but I can't imagine which could do this.
I'm just curious. (and not sure if "zoology" is the correct tag here, but I had to choose one)

How old is this bag? How is been exposed to light for a long time?

@Chris about 2 years old. Exposed to lamplight from 19h to 22hs (when I was home), and not directly exposed to sunlight. The cabinet was on the same wall as the window, and it's top (where this bag was) was higher than the window. But a little sunlight was entering the room during the day, through the glass window. Not directly, as the windows was close to another wall outside.

Then I would suspect this is due to decay of the material of the bag. I have seen similar bags which sat on shelves for years and literally fell into pieces when touched.

Although your plastic bag tears are most likely due to light damage as @Chris mentioned above, there is a type of ant that chews its way through plastic, rubber and other manufactured polymers: Monomorium pharaonis, the Pharaoh ant.

It is capable of destroying many manufactured materials and is a great example of budding, a method by which new ant colonies form. They are very invasive and difficult to control.


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Do ants feel pain?
I have watched video on youtube where guy pours molten aluminium into fire ant colony to make casing. In the comments below there's huge discussion on is that a right thing to do. I am on the side that one should not exterminate colony of living things to get aluminium shape of questionable artistic value.
Main argument on the opposing side is that ants do not feel pain - therefore it's ok. I have done some reading around and opinions differ greatly.
Do ants feel pain?

There have been no studies that I can find addressing this issue.

I think they feel pain. Afaik. we are talking about fire ants which are invasive species, so it is better to kill them.

Not directly related to the question: I had seen the NatGeo episode on that guy. I don't think he does it for artistic value. He does it to study the architecture of ant nests. Ethics depend on ant species and their effect on environment.

Possible duplicate: http://biology.stackexchange.com/questions/19446/can-insects-feel-pain

Whether they feel pain or not the artist is still killing living organisms for art, and on purpose. This seems to be a bit of an ethical question. Is killing things for enjoyment (of art) ok?

@TylerS.Loeper we kill living organisms for art all the time, several pigments are made from dead organisms, you kill living organisms just by being alive. In the case of fire ants the artist should be killing them whether or not they produce art from it, since the fire ants are destroying the native ant species and the only way to help the problem is killing them. Art is just a side benefit.

I believe every living organism (even single cell ones) experience pain somehow, because it is important to stay alive. The scientific answer depends on how you define pain...
Related articles:

Evidence suggests that some, if not all, invertebrates have the
  potential to suffer through current practices that do not take into
  consideration that invertebrates may experience something like pain
  and stress and have the capacity for advanced and unexpected cognitive
  abilities.

2013 - Invertebrate welfare: an overlooked issue

Genetic analysis of nociceptive behaviors in the nematode
  Caenorhabditis elegans and the fruit fly Drosophila melanogaster has
  led to the discovery of conserved sensory transduction channels and
  signaling molecules. These are embedded in neurons and circuits
  that generate responses to noxious signals. This article reviews the
  neurons and molecular mechanisms that underlie invertebrate
  nociception. We begin with the neurobiology of invertebrate
  nociception, and then focus on molecules with conserved functions in
  vertebrate nociception and sensory biology.

2004 - Invertebrate Nociception: Behaviors, Neurons and
Molecules

Just to mention fire ants you possibly meet are invasive species, so you should not protect them.

The red imported fire ant, Solenopsis invicta Buren, is an invasive
  pest that has become widespread in the southern United States and
  Caribbean after accidental introduction from South America in the
  1930's. This species, which has diverse detrimental impacts on
  recipient communities, was recently discovered in Australia and New
  Zealand and has the potential to colonize numerous other regions.

Figure 1 - fire ants worldwide - source

Hi inferno, every species at some point was invasive... lol

@MatasVaitkevicius Interesting thoughts. :-)

@MatasVaitkevicius I think it is somewhat different nowadays because most of these species would be localized to a region or would spread much slower without (un)intentional help from us.

In short, scientists usually conclude that pain is unlikely to be found in insects in the way it is defined in humans, but this is difficult or impossible to test directly.
In humans, pain is often described as a "subjective experience involving a class of sensations with which is associated a characteristic 'negative affect and aversive drive'". So to simplify, pain is defined as a sensation that causes negative emotions and reduces the behaviors that an individual was performing before or during the stimulus. Note that with this definition, it is hard to differentiate pain from fear or response to an unpleasant but non-painful stimulus.

Eisemann, C. H., Jorgensen, W. K., Merritt, D. J., Rice, M. J., Cribb,
  B. W., Webb, P. D., & Zalucki, M. P. (1984). Do insects feel pain?—A
  biological view. Experientia, 40(2), 164-167.

To put this more clearly, pain in humans is defined as resulting in a "a protective stimulus-avoidance response".

Fiorito, G. (1986). Is there “pain” in invertebrates?. Behavioural
  processes, 12(4), 383-388.

Fiorito (1986) notes "Venom used for incapacitation of prey probably does not inflict
pain, as it may be disavantageous because pain may increase struggling on the part of the prey: it is indeed when venoms are painful that they can function in defense.". This is probably the argument most commonly employed to support the idea that invertebrates don't feel pain: insects can't do much about injuries or intoxications so feeling pain is unlikely to be adaptive because it is unclear how it could elicit a response that would increase their survival.
Many invertebrates are autotomic which means they can voluntarily detach legs or antennae (like a lizard's tail) to avoid being captured by a predator, in this case it is hard to imagine an insect experiencing a pain that would be comparable to the level of pain of a human loosing a leg, because it would incapacitate the insect and reduce its chances of survival. Insects could instead have a direct stimulus to behavior response without any conscious emotions or feelings, comparable to a very simple computer program: "if pressure on this leg; drop the leg".
However, there is at least one case known in ants of wound treatment that would suggest this argument is not valid at least for this species of ants:

Frank, E. T., Wehrhahn, M., & Linsenmair, K. E. (2018). Wound
  treatment and selective help in a termite-hunting ant. Proceedings of
  the Royal Society B: Biological Sciences, 285(1872), 20172457.


text:
Does muscle get bigger by increase in size of individual cells or increase in number?
Somewhere in the back of my mind, I have the claim that a muscle never increases its amount of cells but, if the muscle gets bigger, it's simply because individual cells get bigger.
The book Anatomy Trains on page 36 cites "Changes in sarcomere length and physiological properties in immobilized muscle by  Williams et al" when it makes the claim :

Stretched, a muscle will attempt to recoil back to its
  resting length before giving up and adding more cells
  and sarcomeres to bridge the gap.

Is that true? Do muscles increase the number of their cells in that way?

This is what we currently know: http://www.gssrr.org/thesis/10.pdf . It suggests that both hypertrophy and hyperplasia happens. You might find the answer about whether stretch causes hyperplasia.

@inf3rno - I got to page 22 without seeing hyperplasia. Might you direct me to where in this paper hyperplasia is given as a means to increase muscle mass in adults?

@anongoodnurse page 7 - "One look at the current state of professional bodybuilding adds substantial evidence to support that hyperplasia actually occurs given the fact that bodybuilders keep adding substantial muscle mass that could not be otherwise gained through the mechanism of hypertrophy. There appears to be a threshold that governs hypertrophy and once the ceiling of adaptation has b een met, other mechanisms for growth such as hyperplasia must be considered (Engel & Franzini - Armstrong, 2004)." - I don't have the time now to read further that's why I did not wrote an answer.

@anongoodnurse ctrl+f and "hyperplasia", I run over the text, it says that by the adaptation of untrained people is due to hypertrophy, which has a threshold. after that threshold it is most likely that other mechanisms work, like increasing fiber length, or increasing cell numbers. it claims that currently there is no proof, because we lack of studies on professional bodybuilders.

@inf3rno - "One look at the current state of professional bodybuilding adds substantial evidence to support that hyperplasia actually occurs given the fact that bodybuilders keep adding substantial muscle mass that could not be otherwise gained through the mechanism of hypertrophy." I have any number of reputable papers in peer-reviewed journals that refute this. Even this thesis parer does not emphasize that theory (and muscle builders are not scientists).

@inf3rno - if one looks hard enough, one can find evidence for almost anything. This is one such example. If you look at the body building 'literature', you'll see the same claim.

@anongoodnurse "I have any number of reputable papers in peer-reviewed journals that refute this." - I checked the links in your answer, but found nothing that rules out muscle cell hyperplasia. Do you have a study which have the conclusion that hyperplasia does/can not happen in muscle?

@inf3rno - yes. Just about any in the links in my answer. Rule out hyperplasia? They all state it does not happen. Just like you will not find  paper ruling out ovaries splitting in two before conception of twins. There is no evidence for either.

@anongoodnurse Yes, it did not happen in those experiments, but it might happen by different conditions. I think I can agree with your answer, usually hyperplasia does not happen.

A quick survey of the above info points to measured stress and overload can cause the natural body responses into growth :)

The "back of your mind" is correct: "if the muscle gets bigger, it's simply because individual cells get bigger."
Growth of muscle can occur in three ways:

by an increase in muscle cell numbers
by an increase in muscle fiber diameter
by an increase in fiber length.

However, growth in cell numbers is limited to the prenatal and immediately postnatal period, with the animals and man being born with or soon reaching their full complement of muscle cells.

[G]rowth occurs by either hypertrophy of the existing muscle fibers by adding additional myofibrils to increase the muscle mass or by adding new sarcomeres to the ends of the existing muscle fibers to increase their length. Both of these mechanisms occur during the growth process. Growth in the girth of the muscle fibers... may be stimulated by development of stress creating an unequal pressure with splitting at the Z-band and development of additional SR and T-tubule systems. This adds to the diameter or girth of myofibers without any hyperplasia. The growth in length occurs at either end of the fibers and results in addition of new sarcomeres. In both cases, new myofibrillar protein must be synthesized and deposited in the muscle cells.

Adding or removing sarcomeres and myofibrils is determined by exercise, that is, the degree of force a muscle can generate which is in turn dependent on the degree of overlap of the thick and thin filaments. Thus, the amount of tension would control the number of in-series sarcomeres and the number of myofibrils in a single muscle fiber.
Nutrition is also known to play an important role in muscle growth, but growth (that is, increase in girth) cannot occur without exercise.
The exact roles of GF and IGF-I are not completely clear.
Muscle size does not increase by the addition of new muscle cells:

The results show that the increase in muscle cross-sectional area from childhood to adult age is caused by an increase in mean fiber size. This is accompanied by a functional development of the fiber population: the proportion of type 2 fibers increases significantly from the age of 5 (approx. 35%) to the age of 20 (approx. 50%), which, in the absence of any discernible effect on the total number of fibers, is most likely caused by a transformation of type 1 to type 2 fibers.

Activation of satellite cells, a claim made by body builders, is mis-represented by them. The satellite cells seem only to aid severely damaged muscle cells to heal, not to increase in number.
Muscle growth and exercise
Muscle hypertrophy
Growth and development of human muscle: A quantitative morphological study of whole vastus lateralis from childhood to adult age
Regulation of muscle mass by growth hormone and IGF-I

A tissue can undergo two types of quantitative growth:

hypertrophy - cells increase in size
hyperplasia - cells increase in number

There are tissues that grow as a result of one of the above processes and there are tissues that grow because both processes happen.
A Google search for muscular growth yields as first result Muscle hypertrophy. And this is the process that happens to muscle tissue of an adult body under physical exercise.
But muscle tissue can undergo hyperplasia too if stimulated by specific hormones like IGF-1 and human growth hormone (Wikipedia:Hyperplasia).
Muscle hyperplasia can occur also under physical activity in animals but this hasn't been proven for humans (Antonio J, Gonyea WJ. 1993). Stretch overload seems to be the most important trigger of hyperplasia (Kelley G., 1985).


text:
Can we harvest energy from plants?
This is a cross-cutting question but I think its core is about biology. Our society's need for energy is dramatically growing and we are messing up with our environment to answer them. Maybe another way to proceed would be to use the primary energy source that is the sun in the same way as it has been used throughout the ages: photosynthesis.
I know the energy effiency is not as good as a solar panel's but it could clearly be compensated by volume. I found surprisingly little information about harvesting energy from photosynthesis which is why I began to wonder where we are at today.
Thanks!
Edit
I meant transforming the chemical energy generated by photosynthesis into electrical energy. For instance, the first algae powered building was unveiled at the International Building Exhibition hosted in Hamburg. This is a whole different approach.
The most basic example of what I would like to talk about seems to be the algae powered lamp that has (apparently) been developped. In other words, it seems that some sort of plant solar panels are under development and I don't understand how it's done.

Yes, planting trees and burning them afterwards is a way to harvest energy from plants that's with us since millenia.

We can't currently use that energy directly, and if your question is "how can we indirectly extract the energy captured by plants" the answer is "see almost all of human history" (e.g. agriculture, burning wood, even fossil fuels)!

Do you have a link to this house?

@jonrsharpe Apparently, it is possible (cf the algae powered building, or algae powered lamps), which is why I find it surprising that there is so little information about it

@Chris If you Google algae powered building, you'll find some links (I'm not sure which link would be the most relevant to share)

Hmm, they claim that the growth of the algae produces heat - something I actually doubt. Similar systems (albeit without algae) are used as solar heating systems. They work pretty nicely.

@Chris I might have misunderstood how this building works, but what about a more simple example? Could you look up the algae powered lamp and tell me what you think about it?

If you want to use plants as glorified solar panels it's not a good idea, the best photosynthesizers are around 10% efficient at converting solar energy to chemical energy, modern solar panels can reach about 20% efficiency pretty easily. If you consider the energy lost when converting plant matter to electricity your efficiency gets even worse.

@user137 Does it actually matter that we don't get the best efficiency if we get energy that 1. didn't require digging up scarce resources to build and 2. has been proven sustainable over time in exchange?

@Thibault Solar panels are mostly silicon, which is abundant. Furthermore, old solar panels can be mostly recycled. And anytime you use plants for energy you get into the food vs fuel debate. We only have so much farmable land, and population is expected to peak around 2050 with over 9 billion people. How do you feed all those people AND their stuff? You need to get your electricity from other sources, such as solar, wind, or nuclear, not plants. Keep in mind climate change could reduce farmable land and crop yields by that time too.

@user137 I was pretty sure that rare earth elements were need for solar cells but I find one thing and its opposite on the internet right now... I need to check that out in depth. About the food vs fuel debate, I'm not talking about replacing farms with plants to produce energy, I'm talking about putting "plant solar panels" where there were none before (roofs, walls, roads, ...). Hence, I would get my electricity from the sun with the extra advantage of taking the whole ecosystem into account by using plants to do so.

@Thibault I was talking about solar panel which heat water - like the bioreactors with the algae do, not about those which produce electricity. They claim that they put the algae in thin layers of glass on the outside of the building where the sun reaches them. They then say that they circulate the medium with the algae to the inside and it gets heated by the growth of the algae to about 40°C. And this is the point that I doubt - my interpretation from similar heating systems is that the heating up is done by the sun and the algae are a nice addition. They want to dry them and use further.

Some friends of mine are working in a lab that hopes to genetically engineer plants to produce more efficient biofuels. I don't fully understand the work they're doing but they're apparently at the "proof-of-concept" stage just trying to show that they can produce specific high-energy compounds in high-enough volumes to warrant further research

The most basic example of what I would like to talk about seems to be
  the algae powered lamp that has (apparently) been developped.

I think you misunderstood the idea. That lamp uses bioluminescence and not electric power. Normally living cells don't like to give you energy. The trick we use is anaerob fermentation. Without the presence of oxygen (good electron acceptor) they cannot extract more energy from compounds like ethanol, etc... so they get rid of them. After that we can "burn" these compounds with oxygen and get a lot of energy. So currently there is no solution which uses sunlight and microbes to produce electricity directly, however it might be possible.
There are many ways to use photosynthesis in order to produce energy.

The simplest way to burn the plant itself when it has grown enough. You can burn wood, energy plants (e.g. energy grass), etc... and use a generator.
A more sophisticated approach to ferment biomass and produce methane, ethanol, etc... which you can burn. This works very well by starch (e.g. corn bioethanol), and there is active research about cellulose conversion.
There is active research about artificial photosynthesis as well.

You can feed microbes with electric power coming from a photovoltaic system (solar panel), so they can produce ethanol, methane, etc... This might be better than storing energy in batteries.
You can use electric power coming from solar panels to split water. After that microbes can use the hydrogen as electron donor to fix $CO_2$, so they can create ethanol, etc...
You can use light to split $CO_2$ into $CO$ and $1/2O_2$. You can use $CO$ in biological systems to create ethanol, etc... You can use $CO$ in shift reaction to create $H_2$. It is a new technology to use copper nanoparticles to convert $CO$ into ethanol in a completely artificial system.

You can use a photovoltaic system instead of photosynthesis if you need electric power instead of chemical compounds.
Related articles:

2011 - Light Absorption Enhancement in Thin-Film Solar Cells Using Whispering Gallery Modes in Dielectric Nanospheres
2010 - Powering microbes with electricity: direct electron transfer from electrodes to microbes
2008 - The microbe electric: conversion of organic matter to electricity
2011 - Electrosynthesis of Organic Compounds from Carbon Dioxide Is Catalyzed by a Diversity of Acetogenic Microorganisms?
2011 - Metal centers in the anaerobic microbial metabolism of CO and CO2
2014 - From Ionizing Radiation to Photosynthesis
2012 - Biological conversion of carbon monoxide to ethanol: effect of pH, gas pressure, reducing agent and yeast extract.
2014 - Electroreduction of carbon monoxide to liquid fuel on oxide-derived nanocrystalline copper
2009 - Molecular Approaches to the Photocatalytic Reduction of Carbon Dioxide for Solar Fuels
2014 - Comparison of CO2 Photoreduction Systems: A Review
2013 - Leaf-architectured 3D Hierarchical Artificial Photosynthetic System of Perovskite Titanates Towards CO2 Photoreduction Into Hydrocarbon Fuels
2009 - Water-Gas Shift Reaction Catalyzed by Redox Enzymes on Conducting Graphite Platelets

It is not possible to do this directly. Indirectly, it is possible, this is actually done by harvesting fruits - they contain the energy of the sunlight conserved in chemical compounds like sugars or starch and their cellular structures. The basic process for this is photosynthesis.
The products from the fields are used technically to produce gas by fermentation, which then can be burned to produce electricity. Read reference 1 for more details.
What is also done is the use of sugar cane (done widely in Brazil) or corn to produce ethanol which is then used in the fuel of cars. See references 2-4.
Besides these technical processes, there is of course still the possibility to simply burn whole plants or the wood of trees, which is also the result of the fixation of sun energy.
References:

Biogas Production from Maize Grains and Maize Silage
Ethanol Production Using Corn, Switchgrass, and Wood; Biodiesel
Production Using Soybean and Sunflower
Ethanol fuel in Brazil
Corn ethanol

Then I don't quite understand what has been done here http://blog.ted.com/2013/10/02/a-streetlamp-powered-by-algae/ I might be daydreaming but if this technology was enhanced, and scaled, it would be marvellous

@Thibault I'll have a look at it.

I found surprisingly little information about harvesting energy from
photosynthesis

Photosynthesis does not produce energy as such, it produces sugars/carbohydrates/chemical energy, which the plant then converts into energy via respiration.

You can burn the sugar to produce heat. But this is basically what your doing when you burn a plant. So no, photosynthesis cannot be used (directly) to produce electrical energy.

In a Standford university research they did successfully harvest electrictity from photosynthesis:

The Stanford research team developed a unique, ultra-sharp
nanoelectrode made of gold, specially designed for probing inside
cells. They gently pushed it through the algal cell membranes, which
sealed around it, and the cell stayed alive. From the
photosynthesizing cells, the electrode collected electrons that had
been energized by light and the researchers generated a tiny
electrical current.

But it goes on to say:

Ryu said they were able to draw from each cell just one picoampere, an
amount of electricity so tiny that they would need a trillion cells
photosynthesizing for one hour just to equal the amount of energy
stored in a AA battery. In addition, the cells die after an hour.

So this is be no means practical at the moment

I can highly recommend Prof David MacKay's online book http://www.withouthotair.com/
where puts things into perspective. You can find him on YouTube and TED too.
e.g. http://www.withouthotair.com/c18/page_103.shtml "Can we live on renewables"
POWER PER UNIT LAND OR WATER AREA
Wind            2 W/m2
Offshore wind   3 W/m2
Tidal pools     3 W/m2
Tidal stream    6 W/m2
Solar PV panels 5-20 W/m2
Plants          0.5 W/m2
Rain-water
  (highlands)   0.24 W/m2
Hydroelectric
  facility      11 W/m2
Geothermal      0.017 W/m2

Table 18.10. Renewable facilities have to be country-sized because all renewables are so diffuse.
So it doesn't look good for plants  as direct energy source (except for food) (in UK at least)...(or most renewable things for that matter).
Essential reading for anyone interested in energy.

this is more of a comment than an answer.

i didn't have enough points to comment. Then I got 100 more so maybe i do. Nor can i format comments

Ok - It's kind of annoying that it needs more than 1 point to comment...

I'll definitely read that, thanks. It does put things in perspective.

Another alternative is using plants to generate biomasse using photosynthesis and letting bacteria convert that into electricity.
There is research being done about this method and you can read more about it on the following websites:

http://www.plantpower.eu/
http://plant-e.com/technology.html

I'm totally not an expert on this but read a news report on this only yesterday.  I wouldn't mind and even appreciate if someone would integrate this into a bigger and more complete answer.

That sounds more like what I expected. As @Zombaya said, could elaborate on this and integrate it in a more complete answer?

Everyone's looking at photosynthesis for direct energy conversion, but it's not the only approach. Another function of most plants is to pump water up to altitude, to serve its own needs.
Tap into that - picking plants where the sap is watery, not inconveniently sticky like maple syrup, resinous, or likely to congeal into rubber, and you have at least hypothetically, the potential for micro hydro power...
I'm making no claims for energy density or efficiency.


text:
Confusion regarding niches in evolution theory
This is the definition of a niche from Crash Course:

An area of the environment that requires a special set of skills or traits to extract food and reproduce.

Obviously, this version of the definition has been dummed so that it appeals to mass audiences, but after some research, I believe that the general concept remains the same.
Here is what I've learnt about species living in a niche:

The more the competition, the slower the evolutionary process.
Lack of competition provides an ideal environment rapid evolution.

But these points seem non-intuitive to me, because:

Why would a increased competition slow down the evolutionary process? Shouldn't it speed it up, as different species will try to evolve the fastest in order to beat adversaries?
Why does a lack of competition promote rapid evolution? Won't it slow down the evolution, as there is no reason to evolve?

I know that there is a logical reasoning behind this, and I would very much like to understand it.

My source is Crash Course, specifically this  video. I've found it to be extremely reliable over the past, and highly doubt that they are supplying incorrect information. If anything, it is probably my inability to understand the concept.

what is the source for your definitions?

I've updated my question to answer your question.

having watched the video (and developed quite a headache, why don't these presenters stop for breath??) I think the key is in the context they are talking about, mass extinction events have cleared out bunch of niches, suddenly then species which weren't filling a niche before because they were being competively excluded can fill a gap if they evolve rapidly enough, see ~8:40 in the video

I think part of the confusion is that these terms are very loosely defined.  Also this discusses evolution in terms of taxanomic radiation, e.g. macroevolution at large spatial and temporal scales.
Problem 1 is that you haven't been clear about what kind of competition, inter or intraspecific competition?  These will have opposing effects generally which can counter balance each other [1]
[2].  When a species is free from interspecific competition, but under high intraspecific competition, that will promote an adaptive radiation, which concurrent morphological changes.  The most famous example of this would be Darwin's finches as studied by the Grants [3].  With a lack of interspecific competition, the finches exhibited rapid morphological divergence.  Following the logic of this, you'll see that lack of competition will lead the kind of rapid taxanomic radiation the video is discussing, especially over a longer time scale.
However increased interspecific competition will have two effects. It will reduce the number of available niches for an existing species to expand into [4], this generally will drive specialization of a species, which tends to limit genetic diversity which will lead to less "raw material" for evolution to work with. This specialization though is also technically evolution.  However with fewer niches, the new species tend to arise via replacement of existing species in an existing niche, as opposed to an adaptive radiation.
So you can see how actually both conclusions are right depending on the type of evolution and competition being considered.
More interspecific competition -> More specialization (one type of evolution), less adaptive radiation (another type of evolution)
More intraspecific competition -> More adapative radiation, less specialization.
I hope that helps answer your question.


text:
How can I get brighter DNA bands?
I amplified my DNA with real time PCR. The amplification curve shows good amplification but not a single band is observed in my gel after gel electrophoresis. What would be the possible reasons?
I am attaching a photograph of my gel below. My ladder opened correctly but not a single band can be observed:

In which cycle did your sample come up? Are you sure it is your wanted product and not a primer dimer (which are visible on the gel)? What is you expected product size for your PCR product? How much DNA from your qPCR did you load on the gel?

almost at 30th cycle.yes these are primer dimers. i load about 5ul of pcr products in my gel.

my product size is 170 base pair

Do you know that you have product besides the primer dimers? How does the melting curve look like? There you should see two melting peaks - one for your product and one for the primer dimers. Besides that, 30 is relatively late, so there is not much template. You could of course precipite the whole PCR reaction and then concentrate it to see the product.

yes there are two melting peaks.but i quantify my pcr products with nanodrop method; quantification shows that signifacant amount of amplified dna is present

The top of the gel looks really red, are you using too much ethidium? Sometimes the background can obscure faint bands, and you can avoid that putting a small amount of ethidium in your DNA loading buffer instead of the entire gel.

will u please send me the recepie for gel preperation may be there will be a problem in my gel preperation method

i used 5ul of ethidium bromide

@tanzeela For which volume of gel?

@tanzeela Did you clean-up your product before measuring it on the Nanodrop? If not, you will measure residual dNTPs which will give you a too high reading.

Can you put a pic of amplification curve. Another thing. It would be good if you can resize your image so that they dont exceed 500×500px

@chris for 2% gel

@tanzeela I mean how much of your gel did you make - 50ml, 75ml....?

@chris for 50 ml

As you can see from the bottom of the gel, the brightness of the bands have reduced even for the DNA ladder/marker. The main reason for this is that when you are running an agarose gel containing EtBr, due to the positive charge of the EtBr, the stain runs to the negative chamber, against the direction of the DNA migration as @Chris has pointed out! Although some of the DNA will stain but the rest of the EtBr will migrate towards the top of the gel (where the DNA is loaded).
A quick remedy for this is once you ran your gel is to soak your gel in a separate container containing your stain and running buffer such as TAE. I do this for one hour and that makes a huge difference!! Also make sure you regularly change the buffer in your agarose gel running apparatus and don't use the same buffer for a long time since again as @Chris has correctly pointed out there is a reduced conductivity in the older buffers when they heat up so migration does not work as well! Obviously this response assumes that you have a good degree (amount) of DNA in your gel bands, which can be calculated by nanodrop once you extracted the DNA using an extraction kit, or whatever method you normally use. I hope this helps!
This answer is more suited to the title of the question since after reading the main question a bit more carefully I'm slightly confused! So do you see anything at all or your product is far too faint? could you tell us where on the gel, relative to the ladder you expect to see this band? are they the ones at the button of the gel, below the loading buffer?

Your assumption about the Ethidiumbromide is wrong. In solution it is charged positive so it runs to the kathode and against the running direction of the DNA. Some of the EtBr will intercalate into the double helix and stain it (although weaker the further the DNA migrates), the rest migrates as long as the power is on. This is why it is usually recommended to stain gels which run very long afterwards, as this increases the staining.

@Chris Ah, but I was told it is the pH effect that causes this since in my apparatus containing old running buffer this is worse than when made freshly and when I use the buffer in the positive chamber side of the apparatus and sock in EtBr, it doesn't stain. But I could be wrong! I can edit my response if thats best?

No, the pH has almost no effect on this. You will loose conductivity in older buffers as well when it heats up, so the migration is not working that good anymore. You could add EtBr also to the lower buffer reservoir, but this can get messy.

@Chris ah interesting! thanks! I shall edit my response!


text:
Can Anyone Identify This Bug
I am looking for someone to identify this bug:

I'd like to have a closer image, but at first glance, it looks like some sort of weevil

Can you tell us where you found the insect?

This is definitely some species of grain weevil. If you can provide more about it's size, location, where you found it (e.g., what type of food), and whether or not you've seen it fly, then someone should be able to give you an exact ID.

It is an ormányosbogár species. :D
Curculionidae in Latin. I don't know the exact species, but it is common here in Hungary.
It is something like Mecinus janthinus, but it seems like shorter. Probably Mecinus pyraster or another Mecinus species.

Figure 1 - Mecinus janthinus - source

I think it is Sitophilus granarius aka. wheat weevil, but it is hard to decide because of the poor quality photo...

Figure 2 - Sitophilus granarius - wheat weevil - source

The second one looks better, it fits the ratio of the original image better, your first image has a thorax that looks too short.

@user137 Yepp, I think too that it is the second one.

Note that Curculionidae is a very species-rich family though (e.g. 780 species in Germany, >500 in Sweden, ~60000 known worldwide). Without size, location and a better picture I don't think this can be determined to species.

@fileunderwater I agree, better photo needed, or DNA sample :-)

This is definitely Sitophilus granarius [wheat weevil].It is a common pest in India, as it mostly attacks wheat grains stored in sacks.When we buy plain grains of wheat from shops we can see these pests inside and there may be plenty of them drilling the wheat and leave the empty crest of wheat behind.

You should provide evidence with your answer - it's part of writing a good answer, see the help pages.


text:
Confusion over role of current/potential in Nervous system?
I am taking a course on the nervous system and I am do not have any physics background. Therefore, I would like to know, what are we precisely talking about when we talk about current in the nervous system?
At the same time what are we talking about when we talk about potential (i.e membrane potential or action potential.
I once heard an analogy about waterfall and water comparing current and potential (voltage), can someone elaborate on that for me.
Also, I know that electrical activity is the flow of electrons. Therefore does that mean that passive current in an axon/nerve is a flow of electrons? And is it also a flow of electrons when we have action potential.
Thank you in advance for all the help.

Current flow is the movement of charged particles (ions in this case). The membrane potential is the charge difference across the cell membrane. Usually there is more negative charge inside the cell than out, so the membrane potential is said to be negative. When ion channels open, typically positive ions (Na+, K+) will flow into the cell as they are flowing from a medium that is approximately uncharged (extracellular space) into an environment that is highly negatively charged. By analogy, the positive ions can be viewed as water flowing down a gradient (waterfall). Electrical activity is not a flow of electrons per definition, especially not so in nervous tissue where it is ions that move (it is indeed electrons in electric circuits and the likes). During an action potential, therefore, it is not electrons that are moving across the cell membrane, but ions, most notably Na+ and K+, but also Ca+, Cl- among other charged particles.


text:
Does the cellular response to every receptor work the same way?
I heard somewhere that activating any receptor results in the same intracellular response (signaling) which involves NF-κB. If that is true, I hardly understand how the cells distinguish between different types of stimulis coming from different types of receptors. I guess I am missing the point... :S

Figure 1 - signal transduction - source

If you check this picture about signal transduction. What you can see that there are about 10 arrows pointing to the inside of the nucleus, and there are about 10 receptor categories involved. Afaik. there are much more genes in the nucleus, so how is it possible to regulate the expression of so many genes with only a few signaling pathways?

I don't have an answer other than to say that signal transduction is an immensely complex interaction of many different proteins. The schematic you posted represents idealized pathways and omits a lot. Also, how a cell responds to a signal (ie which genes become activated) is largely dependent on the state the cell is already in.

Short answer: No, it's not like this. First, there is a broad variety of different receptors and then there is a wide variety of different receptors within one class. GPCR are not all the same for example, their G$\alpha$-parts are not the same. The same is true for RTKs, which are grouped on homology, but have different ligands for example. I can write a more comprehensive answer later, as this is a complicated topic.

In concur with @Chris: no

It's a complicated answer. More than 200 cell types, each type of cell inherits a unique expression of receptors, internal and external. Diffusion of signals through the plasma membrane and/or nuclear compartment may act directly as cofactors, activators, etc. The specific sequestration, and pattern of expression of external receptors also influence what signals become bound and relayed. The cell will also have a motif of internal/cytoplasmic/nuclear proteins expressed that complex or become directly activated by interaction with any of the above, etc. So the currently expressed set of internal, and external proteins determine not only how the cell interprets the signal, but also how they respond.
As for the actual genetic material, you'll find inherited motifs like DNA methylation, histone acetylation patterns etc. influence what parts of the DNA can actually be accessed. Per the above schema of signaling pathways, the signals received by each individual cell differ based on the actual cell type. In any case there are patterns of activators/repressors, enhancers/silencers that are switched on or off by these signals. Some journals are also introducing evidence insoluble receptors like EGFR+ligand can actually internalize and translocate to the nucleus and act as transcription regulators.
The final note, is that due to alternative splicing and transcription of proteins that promote or repress splicing sites, in a combination with the above concepts a cell can regulate for thousands of genes. This is a very general answer, however. The concept to take home, though, is that differentiated cells have their own specific motifs they express that make "reading" different signals possible, and also makes differing responses to what could be the same signal possible. These motifs also allow for the accurate expression of the relevant portions of the genome (not all genes are expressed at all times in all cells).

I heard somewhere that activating any receptor results in the same intracellular response (signaling) which involves NF-κB.

I don't think all receptors activate NF-κB (Pro-growth signals activate it, mostly).

how the cells distinguish between different types of stimulis coming from different types of receptors.

The cell need not, sometimes, know where and how the signal came from, unless it has to interact back to the origin of signal (as in case of neural synapses). Some pathways such as growth and inflammation can be triggered by many kinds of signals; the responses generally converge to a common pathway (If all that cell has to do is to boost up inflammation, then it would be costly for the cell to keep a unique pathway for each kind of trigger.)

there are much more genes in the nucleus, so how is it possible to regulate the expression of so many genes with only a few signaling pathways?

Some genes are co-regulated because they fall in the same pathway. They collectively comprise what is known as a regulon.
Also, it is possible that multiple signaling pathways have a different response in combination compared either of them individually. Such mechanisms exist in differentiation pathways during development (Can't think of an exact example; will provide one in a while).


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How does the cell regulate different metabolic pathways?
I heard somewhere that cells use different nucleosides bound to triphosphates e.g. ATP, GTP, CTP and other modified compounds: NADH, NADPH to distinguish between different metabolic pathways and so they regulate where they use up the energy. I heard that kinases play an important role in the regulation. Is there a connection (I guess there is if I check NADPH)? Is this regulation mapped? I mean is there a simple map which contains the main processes and the energy carrier and regulatory compounds?
I am looking for something like this map (of receptor responses), but for metabolic regulation:

Figure 1 - signal transduction - wikipedia

So it possibly contains mitochondria, O2, CO2, flows, ATP, NADPH, etc... I understand that different cell types can have different energy producer and consumer organelles and it is not possible to create something that is universally true, so I would be satisfied with a map of your favorite human cell type.

That's going to a large image. Is there some specific metabolic pathway(s) you're looking for?

You can check this out, though it doesn't show regulation: http://www.sigmaaldrich.com/technical-documents/articles/biology/interactive-metabolic-pathways-map.html?cm_sp=Insite--Academic--MetabolomicPathways

There's also this: http://www.genome.jp/kegg/pathway/map/map01100.html     Your best bet is probably a textbook like Lehninger.

@canadianer Nope, I am looking for a simple sketch with the important processes, materials without the details (so no enzymes). Just an example from prokaryotes: the photosystems create NADPH and ATP, which can be used anywhere it is needed, e.g. by carbon fixation. Prokaryotes can use other sources of energy which are transformed to NADH and ATP as well. Thanks for the links.

Metabolic regulation is usually mediated by enzymes.

Also, isn't that first link exactly what you're looking for? The enzymes are included only as EC numbers.

The picture that you attached is not directly related to the question and can be confusing. Either put up a dummy network or a simpler diagram. As it is right now, words are sufficient to explain the question.

I heard somewhere that cells ………………………… so they regulate where they use up the energy.

Yes NADP/H is primarily employed in anabolic pathways such as fatty acid synthesis, while NAD/H is employed in catabolic pathways such as glycolysis.
I don't think there is a general rule for other "energy-currency" molecules (pyrimidine triphosphates are not used except in some rare cases such as glycogenesis).

I mean is there a simple map which contains the main processes and the energy carrier and regulatory compounds?

You can search for the term "metabolic network". It would be too huge so it is better to look at specific sub-networks. KEGG is a good site for finding metabolic networks. There are other representations like hive plots, to visualize very huge graphs.

Our body maintains a very delicate balance between the concentration of metabolites and substrates. If a pathway is not regulated, excess of a particular metabolite can disturb the whole process. Let's take cholesterol metabolism pathway for example. there are various means by which the cells control the production of cholesterol. For example AMP controlled kinase protein detects weather the concentration of ATP is high or not, if its low then the cell does not proceed with the production of it, by inhibiting the enzyme that catalysis the production of mevalonate. Other way is through transcription factor that is present  called SREBP. Sterol Regulatory Element Binding Protein regulate multiple genes that are involved in metabolism of cholesterol. Various protein denaturing components are present that upon receiving signal cleaves the intermediate's in the metabolism of cholesterol.
There are n-number of pathways in our body and all are regulated by a complex network of signals that regulate them.


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Comparative leg sizes
When I was a child, my father showed me the classic essay "On Being the Right Size", J. B. S. Haldane.  It talks (among other things) about how large animals need stockier legs to support their weight.  I weigh about the same per leg as a 350 lb deer, but my legs are closer in diameter to those of a 1500 lb horse. Why?

Nice question. :-) I guess he was wrong or was talking about averages and not individual species...

@inf3rno:  he was clearly talking about averages, based on the body mass increasing with the cube of linear dimensions and the weigh bearing capability of legs increasing with the square.  I suspect the answer is humans stress their legs in ways that deer and horses do not, so it is advantageous to have stronger legs, but that is why I asked.

There is no way your legs are close in size to a horse.

@canadianer:  they are not as long, but in diameter they seem close.  I haven't been that close to horses, so I may be off.  When I asked a farrier this question he seemed to  think it was close.

If you can get access, check this out: http://link.springer.com/chapter/10.1007/978-1-59745-132-1_2  And then there's the musculature…

@canadianer:  No, all I get is a horse skull.  Not too useful for this.

You need to view the chapter, not just the look inside. Qualitatively, the horse femur appears ~2.5 times the diameter of the human femur. Same for the tibia.

@canadianer:  That makes the area ratio close to the weight per leg ratio.  I'm surprised.  Thanks.  That would be a reasonable answer.

I suppose it answers your specific example of horses and humans, but there might be merit in someone actually discussing the biology of weight to leg size ratios. Seems interesting and would be more in the spirit of your question.

@RossMillikan Maybe by a pony it is so long, but an average horse has about 2 fold longer leg than a human...

@inf3rno:  yes, I was more interested in diameter than length, because that sets how much weight a leg can support.  More length makes it more prone to break in buckling, but that would argue for more diameter for the longer legs.

There is an interesting relationship between the length of an animals femur, the thickness and the mass of the thickness. A point that should be taken into account is that bones can different densities and so might be able to support varying amounts. The muscle in you leg also does nothing for the support of you weight it is (basically) all in the bone. Really looking purely at the leg won't tell you much you need to strip back the tissue and get you measurements straight from that. Given the different gate strategies of various animals this can lead to differing levels of muscle surrounding the leg and could be confounding your answer.
Walter Lewin a professor of physics at MIT did a lecture series where in the first lecture he went off on one about the relative sizes and thickness of animal femurs and it is really interesting (http://www.youtube.com/watch?v=PmJV8CHIqFc - between 11 minutes and 22 minutes). The short answer was that the ratio between the thickness and the length stays similar relative to the length.


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Do hairs in the ear respond to things like shampoo?
Shampoo and conditioning products make claims to be the end all be all in hair care. I doubt that they are so advanced "growth formula/anti-breakage/oily treatment". Have any of the claims been shown to be valid? Assuming a positive response do they have application for restoring the hairs used for hearing?

You are mixing up hair cells and hair. Hair cells in the cochlea (wiki) have tiny stereocilia (subcellular organelles) that sense vibrations approaching the atomic scale. These are then translated in hyperpolarizing or depolarizing currents that drive the spiral ganglion cells of the auditory nerve. The 'hairs' on the hair cells will not readily benefit from shampoo I'm afraid. If you should want to test it, the shampoo should be intracochlearly administered in the scala media of the cochlea - so even if shampoo is beneficial it would be hard to utilize it without surgical intervention.

thanks for clearing up my misunderstanding i have had that for a while now


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How to translate a blood type used in Eastern Europe?
What are the I-IV blood type descriptions shown below (commonly used in Eastern Europe), and how do you translate them into the ABO-system?

What do you mean by translate?

@WYSIWYG: Convert it to the system used in the West: http://www.redcrossblood.org/learn-about-blood/blood-types

I still don't understand. Isn't it already clear from the image?

@WYSIWYG: What's this (I), (II), (III), etc. stuff? I guess that's what I'm asking.

I think this description is wrong. Blood type used to be described as AB-I, A-II, B-III and O-IV plus Rh Positive or Negative.

You should provide references for your answers. The article linked to in my answer describes two numerical systems: one created by Jansky (which is what is shown in the question and referred to in my answer) and one created by Moss (which is what you are describing).

It is a direct correlation between the ABO blood groups and the Roman numerals.
 O: I

 A: II

 B: III

AB: IV

This numeric system was pioneered by Jan Jansky of Czechoslovakia in the early 20th century. Apparently it is still used in some former Soviet states.
Erb IH. 1940. Blood Group Classification (A Plea for Uniformity). Can Med Assoc J 42(5):418-421.

I can't upvote it (not enough rep.) But thanks for the info!

@MikeF you should be able to accept it by clicking the check mark.

What would O+ in the US be in the UK?


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How to separate peptide on SDS PAGE?
I want to separate 1600 Da peptide on SDS PAGE, on 20% GEL I didn't get any band, How can I separate on PAGE? Can I use 25% SDS PAGE?

Didn't you get any bands because you sample run off the gel or because of other problems?

@Chris,yes,because of sample run off the Gel.

Well you could turn down the power or reduce the time. What are you trying to separate it from?

Then the answer is simple: Don't run the gel for too long. Sounds simple, but is not necessarily so. Your samples either run with or even before the blue line of the bromphenol blue. o if you run your gel only until 2/3, this should work.

"Can I use 25% SDS PAGE?" - I assume the protein is already saturated with SDS, so it would not make any difference...

@inf3rno I doubt it. 20% is already hard to handle as the high percentage gel get very brittle.

Image is of an 18% Tris-tricine small-peptide SDS-polyacrylamide gel stained with coomassie blue dye [source].

Your peptide is 1.6 kDa; it would not run off in 20% gel if you don't run it for a long time. Also, try to prevent heating up of the gel (you can run it in a cold room or in front of an A/C vent).  However, it is better to use other techniques such as chromatography. You can also try dialysis if other unwanted peptides are much larger.
Protocol for Tris-Tricine SDS-PAGE.

If band is below the dye front it might not stain very well.  Tricine gels are best for such small proteins, and you might might just run until dye front is only half way down the gel. It is also possible that your protein does not stain with conventional coomassie-based stains.  Maybe try a silver stain.


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Why is the DNA codon table "equal" to the RNA codon table
Before anything else please pay attention of the double quotes on the "equal" in the title - I know they are not equal, but you will understand in a bit.
If I look at the DNA codon table here or in wikipedia, and at the RNA codon table here or in wikipedia, their only difference is that the former has thymine (T) whereas the latter has uridine (U). But I am not understanding how all other nucleotides are the same. Bear in mind that transcription reads DNA from 3'->5' and translation reads mRNA from 5'->3'.
Look at this example, focusing on the 3'-TAC-5' of the antisense strand.

The 3'-TAC-5' codes for Tyrosine according to the DNA codon table. However, it transcribes and translates  3'-TAC-5' -> 5'-AUG-3' -> Methionine.
Now focus on the corresponding codon in the sense strand, 5'-ATG-3', which codes for Valine according to the DNA table (it is read from 3' to 5'). This codon transcribes and translates 3'-GTA-5' -> 5'-CAU-3' -> Histidine, not Valine and not Methionine.
So my questions are:

Why do DNA codon tables show the correspondence between codons and amino acids in the sense strands (5'-ATG-3'), if the only way to go from ATG to Met as in the figure is to consider the antisense strand?
I can see that the AUG codon translates to Methionine, and it is translated by reading the 3'-TAC-5' codon in antisense strand, whose corresponding codon in sense strand is 5'-ATG-3'. But this last one is read from 3'->5', so it reads 3'-GTA-5' -> 5'-CAU-3' -> His.

I am guessing I'm getting many things wrongly in this... Maybe on the way that I'm reading  the tables: I always take into account that transcription is read 3'->5' and this is the order I take to read DNA tables.
Thank you and sorry if I was confusing.

Translation is done on the mRNA, not on the antisense strand, and it is done from 5' -> 3'. The first codon is AUG. This is a start code, and codes for methionine. Check this illustrated explanation out, too.

Yes, I understand why AUG translates to Methionine. My question is on why do people refer to the ATG codon coding for Methionine if ATG -> UAC -> His. But I think the main message was that I was reading the tables as polimerase would, and this is not the right thing to do :)

eh, now I understand that :) I was reading 5'-ATG-3' -> 3'-UAC-5' -> His because I was looking for the nucleotide order according to the transcription/translation order

I can understand your confusion but it all makes sense. The basic idea is that what we call the "antisense" strand is actually the one being transcribed. However, since that is in effect a mirror image, it is much simpler to think in terms of the sense strand.
To take a very simple example:
5' ATG 3' <-- sense strand
3' TAC 5' <-- antisense strand

The antisense strand will be read in a 3' to 5' direction:
3' TAC 5' <-- antisense strand
5' AUG 3' <-- mRNA

Since the mRNA is a mirror image, it has the sequence of the sense strand. It is this mRNA that is then translated and this is read in a 5' to 3' direction. So, AUG is translated as Met. To illustrate, have a look at this image from Wikipedia (click on it for a larger version),

In the image above you can see the growing polypeptide (protein) chain snaking its way through the ribosome. The flying blue things are tRNA molecules and the black chain at the bottom is the mRNA being translated. You can't really see it very well in this image but if you look at the original you can clearly see it is moving from the right towards the left. The right hand side is the 5' end and the left is the 3'. Or, in a more static version (adapted from here):

So, the antisense strand is read, transcribed to RNA (which has the sequence of the sense strand but with T converted to U) and it is this mRNA which is read (in a 5' to 3' direction) to produce the protein.

Thank you! But this raises another question in my mind. It seems kind of a "waste" to have the sense strand there if only the antisense is transcribed. Is the sense strand doing nothing more than stabilizing the DNA and wouldn't the same be achieved by having mRNA alone instead of DNA?

@Sosi no, the double strands are essential for many things including i) DNA replication ii) error repair (the "right" sequence can be inferred from the opposite strand iii) most importantly, genes can be found on both strands. The sense/antisense is only with respect to a given gene. What is the sense strand for geneX can be the antisense for geneY.

Thank you! I see, I was misinterpreting and thinking that the sense strand was always the sense strand :)

Genetic code and codons are always used with reference to RNA. When talking about DNA, the the sense strand of a gene is considered its sequence. The anti-sense strand though is the template for mRNA synthesis, does not represent the gene.
DNA-codon table has simply U replaced by T. Apart from a wikipedia article, I don't find the term being popularly (not colloquially) used elsewhere.

Maybe you'd like to add something about the reading of those tables not having to do with the reading direction of the polymerase? This seemed to have been my problem

@Sosi The reading of those tables is directly related to the direction of the polymerase. The polymerase reads 5' to 3', translation happens in that direction too, and that is the direction the tables are read.

@Sosi as I mentioned The anti-sense strand though is the template for mRNA synthesis, does not represent the gene. The direction of RNA polymerase movement is not a factor here.

@JasonC: Just for clarification — RNA polymerase reads 3'→ 5' but produces 5'→ 3'.

@WYSIWYG that is exactly my source of confusion: if it is reading a 5'-ATG-3' strand from 3'->5', it would be reading GTA. But despite "walking" the DNA strand in the 3'->5', it still reads it ATG that's it?

@Sosi.. No RNAP reads a 3'→ 5' strand (with 3'-…-TAC-…-5') and produces a 5'…-AUG-…-3' mRNA. And note that RNA synthesis does not start at ATG (it is the protein synthesis).


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Does vitamin D form crystals in the blood with calcium and magnesium?
I read on a vitamin-D product (2000NE) that I should not use calcium and magnesium with it, because it can result crystal formation in the blood. I googled, but find anything about this. Is it true?
(Somehow I doubt it, but I don't know the exact mechanism how vitamin-D works by building bones. Afaik. there are osteoblasts and osteoclasts which constantly build and degrade the Ca-Mg-PO4 depos, and I assume vitamin-D is just a cofactor of an enzyme or it is required to produce a hormone. I never heard of Ca/Mg - vitamin-D cross-reactions...)

Since vitamin D leads to the absorption of calcium, it can lead to hypercalcemia and calcium precipitation! This is true specially in patients with hyperphosphatemia (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2486454/)

Vitamin D does not bind to Calcium. It is a pre-hormone which is converted to calcitriol. Calcitriol has an intracellular receptor (VDR) that, as a heterodimer with Retinoid-X receptor, regulates gene expression.
I guess the "should not be had together" is because of possible over-absorption of Calcium. There are commercially available supplements (e.g. 1, 2) that have Vit-D + Ca + Mg.

Additionally both are present in milk, if I remember correctly.

The exact words were "it forms crystals in the blood with calcium or magnesium" (in Hungarian ofc.). I guess it was just a bad joke of a frustrated worker, I don't know...


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Do mosquito repellent sprays work on all insects?
I would like to know the mode of action of mosquito repellent aerosols. Are these specific to mosquito or are other insects affected too?

Are you specifically interested in the aerosols. The sprays are sometimes insecticidal as well.

The most common active ingredient in insect repellents is N,N-diethyl-3-methylbenzamide (other name: N,N-diethyl-m-toluamide; abbreviated DEET). It provides protection against mosquitoes and many other insects. After various interesting hypotheses, it is currently assumed that mosquitoes simply smell DEET directly and avoid it.[1]

Could you add some references to your answer?

Citronella oil is also used as an insect repellent and is seems effective on mosquitoes[1] and head lice[2] as well. Though I was not able to find information on the mode of action, just the effectiveness of citronella.
Wikipedia also says DEET is effective for fleas, ticks, and chiggers (though this lacks a references). Anecdotally, I know the Off brand of repellent is useful when the dogs get fleas to avoid getting all bitten up (Off contains DEET I believe).


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Is the nuclear envelope present in G1 of interphase?
Is the nuclear envelope present in G1 of interphase of eukaryotic cell? If so how does a method like Calcium mediated transfection get DNA past the nuclear envelope?

That is a very good question. I have done calcium phosphate transfections on primary hepatocytes, so I know it works on non-dividing cells, but I don't think there's a clear answer yet. The calcium ions released from the particles may help trigger nuclear envelope disintigration and allow plasmid DNA to enter. I'll try and find and find links to a couple papers I've read about it.

Alright, Paper 1 and 2 by Dana Olton are about Calcium phosphate nanoparticle transfection and intracellular trafficking. Leaf Huang has several papers about lipid coated Calcium phosphate for DNA delivery in vivo, 1, 2, and 3. And here is a paper about parvoviruses and how they enter the nucleus, which involves Ca.

To answer the question about nuclear envelope in G1 phase, yes it exists. The nuclear envelope is reformed at the end of Telophase after the 2 copies of the DNA are pulled apart, but before the two daughter cells are separated by cytokinesis. We can see the new nuclear envelope in these images:

Image from here

Nuclei visible near end of cytokinesis, centrosome still visible. Image from here.
As for how DNA gets into the nucleus without cellular division I don't have a good answer and I'm not sure anyone does right now. The nuclear envelope is a major barrier for non-viral gene delivery.


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Where do I purchase a fly with the collagen tagged?
Where can I purchase a fly with tagged collagen?  My senior undergraduate research paper is observing the collagen in larvae with normal diet compared to larvae with an experimental diet.  I need flies that have the protein tagged so I can observe the collagen under a fluorescent microscope.  Instead of using an expensive antibody (my budget is $300) to tag the protein, my advisor suggested purchasing stock flies that already have the tagged protein.

try bloomington (http://flystocks.bio.indiana.edu) if you work with Drosophila.

There are some more places other than what Bez has already mentioned.
See here.
However, tagging collagen may be a problem. Collagen undergoes a lot of post-translational modifications including hydroxylation and end clipping. It forms a unique structure (triplex) and adding tags may compromise its structural integrity. You can try Masson's trichome stain instead, which is used to stain collagen — a very cheap alternative.


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DNA polymerase I exonuclease activity
Does DNA polymerase I in bacteria use forward or reverse exonuclease activity to remove RNA primers? One of my books says it uses 5' to 3', but another says it uses 3' to 5' exonuclease activity.
Update: I know RNase H can remove the primers, but the exonuclease activity of pol I can also remove them.

Googling your question showed that it is RNAse H that removes the RNA primer. DNA Pol I has both 3'-5' as well as 5'-3' exonuclease activity for proofreading and nick repair activities, respectively. See the wiki on Pol I

From wikipedia:

In the replication process, RNAse H removes the RNA primer (created by Primase) from the lagging strand and then Polymerase I fills in the necessary nucleotides between the Okazaki fragments (see DNA replication) in 5' -> 3' direction...

And elsewhere in the same article:

Pol I possesses four enzymatic activities:

A 5' -> 3' (forward) DNA-Dependent DNA polymerase activity, requiring a 3' primer site and a template strand
A 3' -> 5' (reverse) exonuclease activity that mediates proofreading
A 5' -> 3' (forward) exonuclease activity mediating nick translation during DNA repair.
A 5' -> 3' (forward) RNA-Dependent DNA polymerase activity. Pol I operates on RNA templates with considerably lower efficiency (0.1–0.4%) than it does DNA templates, and this activity is probably of only limited biological significance.

So the answer to your question is neither. RNAse H removes the primers, and the exonuclease activity of DNA Pol I is irrelevant to primer removal, although it turns out it can operate in either direction depending on the context.