Experimental Analysis: What are possible reasons for this increase in N₂O production? My professor wanted us to each conduct an experiment for class on something we thought would interesting. My experiment was very simple, but I'm not sure how to interpret my results. (Please note that this is not for homework – I'm just genuinely confused and trying to understand the data.)

Basic method:

Take soil samples, add varying concentrations of Roundup and water equalling a total of 50ml, seal in airtight jars, incubate for 7 days, run through a Gas Chromatograph, and record the rates of production for CO2, CH4, and N2O. Overall, there was the Control and then three treatments, for a total 8 jars because each had a duplicate:

Control (Roundup: 0, H2O: 50ml),
T1 (Roundup: 10ml, H2O: 40ml),
T2 (Roundup: 25ml, H2O: 25ml),
T3 (Roundup: 50ml, H2O: 0).

I expected the Control to have the highest levels of production, followed with a decrease in production for T1, followed by T2, and then T3, with T3 being the lowest because all microbial activity was inhibited by the massive dose of Roundup.

However, the results were a bit surprising.

In general:

The Control rates were the highest, as expected.
T1 showed a decrease in production, as expected
T2, again, showed a decrease in production, as expected.
And then T3 showed a significant increase in production.

Here are some graphs to illustrate this in more detail:

This is a new field of science for me, so forgive me if I'm missing something obvious, but my natural intuition is certainly not helping me out on this one. What are some possible causes for this increase – in particular for the N2O/denitrification? Or at the minimum, are there any particular resources I can take a look at to better understand why this happened?

Edit

This is my brain on paper, so forgive me again for any ridiculous things I say. But, could it have something to do with the denitrification process such that more gas is given off as N2O because the microbes responsible for processing the N2O into N2 have died. So in the previous Treatments 1 and 2, the N2O was lower because the N2O was being converted into N2 (but we never recorded the N2), but in the final treatment, no conversion occurred, so the N2O appears to go up, even through the microbes are functioning even less.

Thoughts?

This may have no correlation to your project but many insecticides, bacteriocides, and herbicides need a "solvent" or "transfer medium" such as water to be effective. Even when using ethanol in the laboratory against a variety of bacteria 100% ethanol becomes almost ineffective.

I would take a look at running round-up again by itself versus 95% roundup 5% water, and 90% roundup and 10% water and I am sure you may seem some results that will aid your experiment.

Good Luck!


bi-directional transcription experiment We suspect a bi-directional transcription event is happening at a locus in our organism where two genes are directly adjacent to each other. The annotation data is not well established. The intergenic distance is probably less than 200 base pairs.

The two genes are expressed in opposite directions towards each other. Base on the preliminary transcriptomics data, it seems like one gene is over transcribing (3' UTR perhaps?) into the adjacent gene, possibly resulting in some kind of transcriptional regulation of the adjacent gene.

Here is a rough diagram of what we think might be happening:

------------------------==========gene A================>----------------------

----------------------------------------<====gene B=====-----------------------

Of course we need to first confirm this by designing primers to see if this over transcription is actually happening.

If this is happening, we intend to do some knock down experiments. We have no transgenesis available in our organism, only RNAi by dsRNA. It is possible to specifically knock down geneA by introducing dsRNA to the 5' region of geneA that does not overlap with geneB. Perhaps this will lead to ectopic/over expression of geneB.

Is there anyway to knock down geneB specifically without knocking down geneA? It looks like designing dsRNA for geneB would knock down both A and B.

How well is gene A annotated? Do you have the gene A sequence (after post-transcriptional modifications)? If you do, you can order it from a company like DNA2.0 and they will synthesize it for you for like $0.35/base. Then you can transform the cells with this plasmid and do a knockout of gene B by inserting some sequence at the ~200bases overlap.

Also, I guess you can transform the immediate transcript (without modifications). It will also be modified once it is in the cell. But it will be longer and more expensive to synthesize, but there are a few methods you can use to do that.

Let me know if this idea appeals to you. I can give you more info if you are interested.


Standard notation for dominant and recessive allele I'm reading through some science that could come up in my GRE equivalency.

I've never been much of a biologist, more of a chemist/geologist....though it does interest me massively!

I'm just seeing this question in a textbook....

Q) Assume eye colour in humans is controlled by a pair of alleles of a gene where the allele giving brown eyes is dominant to the allele giving blue eyes. Both parents of a blue eyed man, John, were brown eyed. He married a brown eyed woman, Sara, whose father had brown eyes and mother blue eyes. Sara had a blue eyed sister. John and Sara had a brown eyed child.

Fill in the boxes and circles on the family tree below to show the genotype of each individual.

I just wanted to ask how exactly we mark out genotype in science? Do we use D's and r's?

Thanks!

[H]ow exactly we mark out genotype in science? Do we use D's and r's?

General rule

The general rule is to indicate the dominant allele with a upper-case letter and the recessive allele with a lower-case letter.

The most commonly used letter is the first letter of the alphabet. The two possible alleles are a and A and the four possible genotypes here are therefore aa, aA, Aa and AA. Only aa has blue eyes in your example. Note that it is very common to merge together Aa and aA (that is to not consider whether the A allele was inherited from the father or from the mother) and just call it Aa.

More than 2 alleles OR no clear dominance relationship

It is quite common to use A1 and A2 as well but when doing so, we don't implicitly indicate a relationship of dominance. This notation also has the advantage to be able to deal with cases where there are more than two alleles segregating in the population (A1,A2,A3). Note that in reality perfect dominance is quite rare.

More than 1 locus

When dealing with more than one locus, we generally use A/a for the first locus, B/b for the second locus, C/c for the third etc... However, in general when dealing with several loci, authors don't have identical loci ad therefore they directly name them and use appropriate letters. For example, in models of recombination under control of a modifier locus, the modifier locus can often take the values M and m, while a random linked locus under purifying selection would take the letters A and a.


Where can I find the list of all tendons in the human body? https://www.healthcentral.com/article/aging-can-take-major-toll-on-womens-tendons (mirror) claims that:

  There are about 4,000 tendons throughout the body.

This claim is echoed by a fair amount of websites but I couldn't find any
decently trustworthy source.

Where can I find the list of all tendons in the human body?

I have only been able to find a list of skeletal muscles of the human body so far. I'm surprised that there are 4000 tendons even though they are only ~640 muscles: most muscles that I am aware of are attached to fewer than six tendons (FYI: Why some muscles have more tendons than others?).

Your best bet is the Terminologia Anatomica, which is the international standard for anatomical terminology.

The 1998 edition is freely available. It lists only a few named tendons though, which is consistent with my experience as an anatomist: very few tendons are named separately from the muscles to which they are connected. Central tendon of the diaphragm, conjoint tendon, and calcaneal tendon are a few.

Otherwise, it's just "tendon of biceps brachii" (which actually has 2 tendons at one end and one at the other).

4,000 seems like a too high number to me. 2x the 640ish muscles plus some extra for multi-headed muscles and those with internal tendons or aponeurotic tendons seems like a more reasonable estimate.


Do animal cells have vacuoles? I overheard a rather heated argument about whether or not animal cells have vacuoles.

One person said that they do, but they're much smaller than vacuoles in plant cells.

The other person said they don't. While there is something there that acts similar to a vacuole, it's slightly different. The person also noted that the only websites that say that something as a vacuole aren't credible sites (ie. not University sites, etc...)

I'm really curious as to which it is: Do animal cells have vacuoles or not?

They are both right.

Animal cells do have vacuoles, but they are smaller, larger in number (plant cells usually have just one or a few large vacuoles) AND serve a somewhat different purpose than those of plants.

A vacuole is basically a membrane-covered compartment (vesicle) filled with molecules, that shouldn't, right now, be in the cytoplasm. For plants, this means long-term storage of water and waste products, which cannot be removed from the cell due to the cell wall. For animals it means mostly taking part in exocytosis and endocytosis - they are much more dynamic structures.

And about some half-professional sources, here is a bit from Molecular Biology of the cell which in fact calls plant vacuoles "a kind of specialized lysosome".


Does the human hand have 27 degrees of freedom? I have counted the degrees of freedom in my hand over and over and I keep getting the number 19.

Suppose each finger has 3 degrees of freedom. Then 5 * 3 = 15. The wrist can rotate around or back and forth so that contributes to 4 degrees of freedom. In total the hand has 19 degrees of freedom.

From a cursory google search, I can notice that it is commonly agreed upon that human hand has 27 degrees of freedom. Can someone provide a good reference and explanation for this?

Keeping in mind that I know nothing about this, I will try to explain why the hand can be modelled with 27 degrees of freedom. This is just my interpretation of this paper, which says:

  The human hand has 27 degrees of freedom: 4 in each finger, 3 for extension and flexion and one for abduction and adduction; the thumb is more complicated and has 5 DOF, leaving 6 DOF for the rotation and translation of the wrist.

  To accurately model the hand, a complete model of the muscles, tendons, bones and a neurological control structure is necessary. The dynamics of such a complex model are still poorly understood, forcing the use of simplified models. Current models are too simplified for our purpose so we turn to recent work from the medical community to motivate assumptions used in a new model that we propose here. We use a 27 DOF model of the hand with the following sim- plifying assumptions:
  1. The thumb is independent of the other fingers.
  2. Adduction/abductionofthefingerjointsareindependent.
  3. Motion frequency does not affect joint interdependence.
  4. Both hands have the same interdependence model.
  5. The posture of the wrist and the rest of the arm do not
  affect the underlying interdependence structure.

Incidentally, this implies to me that there are different models of the hand with different assumptions that use a different number of degrees of freedom.

Anyways, take a look at this hand:

[source]

And now, follow along with your own hand!

finger (4 DOF): each finger has 2 interphalangeal joints between the distal, middle and proximal phalanges that allow for flexion/extension (2 DOF); each finger also has a metacarpophalangeal joint between the proximal phalanx and the metacarpal that allows for flexion/extension as well as abduction/adduction (2 DOF)
thumb (5 DOF): an interphalangeal joint between the distal and proximal phalanges allowing flexion/extension (1 DOF); a metacarpophalangeal joint between the proximal phalanx and metacarpal allowing flexion/extension and abduction/adduction (2 DOF); a carpometacarpal joint between the metacarpal and trapezium allowing flexion/extension and abduction/adduction (2 DOF)
wrist (6 DOF): between the carpals and radius allowing flexion/extension, abduction/adduction and supination/pronation (3 DOF); I think when the authors refer to translation of the wrist, they are simply saying that hand can be moved in all planes of 3D space (ie up/down, side to side, forward/backward - 3 DOF)

Since we have 4 fingers, they give 16 DOF. Adding the 5 DOF of the thumb and 6 of the wrist, we get 27. Please nobody question my reasoning. Thank you.


Why is inhibition of inhibition (reciprocal inhibition) such a common motif in cell signalling? In transcriptional regulation, you often find that positive signals proceed by inhibiting or destroying a protein that is in turn inhibiting or destroying the effector protein. This can be seen in the retinoblastoma - E2F signalling pathway, and many others. I was wondering if there was any direct biological utility, and if so what this utility was.

This feels like a my philosophical question...

Direct regulation of proteins would have to have biological utility - such a gene has to be driven by positive selection to adapt that ability.  The question is more about learning what might be driving its role.

I would hazard that protein deactivation and degradation would be important to make sure that these inhibitors could be down-regulated fast enough - if they were left to degrade via a general pathway, the specific signal would not be available for too long a time.


Black squirrel in France? I saw a nearly jet black squirrel in ardeche today,  carolinensis have invaded the UK and Italy, however I didn't find news about their arrival in France. Was that black squirrel really a Canadian species?

Yes, Sciurus carolinensis has been invasive in France, Italy and Switzerland for quite a few years already (Bertonlino and Genovesi, 2003).

Note that the "original" distribution of S. carolinensis is over eatern Canada and USA. Not Canada only.


What’s this bug? Sign of an infestation? Found crawling up the side of my washing machine. [WA] Just spotted this bug on the side of my washing machine after putting some dirty clothes in the hamper and transferring a damp load to the dryer. I’m hoping it came in from outside somehow, and isn’t some type of vermin (I live in an apartment and I’m probably the cleanest resident in the building. I’m also paranoid about household pests.) It’s very small, photographed against a damp paper towel. Please tell me this is not a baby roach?

Don't worry, it is definitely not a roach. It is a true bug, Hemiptera. Not a household pest.


Do all plants grow roots when separated from parent? Recently I bought my very first plant.

I thought it was doing well because it remained green, sometimes a yellow leave but all of my acquaintances which do know about plants told me not to worry, and remove the yellow leaves.

Until yesterday,
suddenly
a branch of the plant fell off,

I looked at it and it had rot through the whole stem of that branch and broke off.

Quite displeased of course,

Now, the branch is still alright, I guess, the leaves are still green,

now what am I supposed to do?

For now I planted the branch in the pot of the main plant,
I'm intending to get a separate pot for the branch and plant it again,

But I wonder, do all branches of all plants grow roots when put in ground?

If not it's not worth the effort to buy another pot of course,

Could someone help me out?

Dear respected person,

I am not a professional botanist, but I adore gardening, and would like to help you as much as I can from my humble garden experience.

As far as I have experienced, not all plants have stems which root when put in the ground. For instance, I have a plant called Bouganville Tom Thumb (I apologise for any spelling error). I once decided to clone this Tom Thumb variety by cutting its stem off and then burying its base in potting soil. I even tried rooting hormone powder (from a gardening store) but it did not root, even after a whole month.

On the other hand, I had a plant called Petunia whose stem I cut off on purpose to maintain the plant's shape and threw the stem into the soil. The stem shriveled, and I thought it died and left it there. However, to my surprise, I found the stem all fresh after 2 weeks only to find that it had rooted into the soil from side of its stem. Another plant called Jade Plant can be cloned by putting its leaf in soil.

I think it really depends on the type of plant whether its stems will root or not and how long the stem will retain its rooting potential after being cut.

If possible, you can try the following. Put the cut stem in a small plastic pot (they are very cheap) with soil and see if it roots (leaves will begin growing). If it does, transfer it into a larger pot later once it has grown. Wait for it to grow big enough to spread its roots thoughout the pot, then shift it into a big pot.

I believe if a plant roots, then all stems of that plant will root. Plus, congratulations on your first plant.


Why don't mosquitoes target the visible blood vessels under the skin? We can see numerous veins under our skin. Why don't mosquitoes suck blood from those vessels?

Why don't they use better option?

For a mosquito, there is really no benefit to targeting those visible blood vessels. Mosquitoes take only a small amount of blood, and their proboscis is going to be a limiting factor anyways.

However, mosquitoes also aren't just blinding sticking their proboscis into the extracellular space. They actually do target individual vessels, and scientists have actually been able to video the process. Capillaries are good targets because they are found in all the tissues, so the mosquito doesn't need to find a surface vein.

See the videos with the original paper here: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0050464 (in the "Supporting information" section)

There are also versions on YouTube, like here:
https://www.youtube.com/watch?v=MbXSPacvuak

Choumet, V., Attout, T., Chartier, L., Khun, H., Sautereau, J., Robbe-Vincent, A., ... & Bain, O. (2012). Visualizing non infectious and infectious Anopheles gambiae blood feedings in naive and saliva-immunized mice. PLoS One, 7(12), e50464.


What is two-start or zigzag model of 30 nm chromatin fibre? I read some webpages describing the two-start model but could not get it. I'll be obliged if someone helped me understand the topic.
The websites I have been through are:

1.http://www.nature.com/nrm/journal/v13/n7/fig_tab/nrm3382_F4.html

2.http://www.mechanobio.info/topics/synthesis/go-0006323

3.http://www.fastbleep.com/biology-notes/41/118/1272

From the MB Info Wiki you linked:

  In the one-start solenoid model, bent linker DNA sequentially connects each nucleosome cores, creating a structure where nucleosomes follow each other along the same helical path [4, 7]. Alternatively, in the two-start zigzag model, straight linker DNA connects two opposing nucleosome cores, creating the opposing rows of nucleosomes that form so called “two-start��? helix.

This means that in the one-start model each nucleosome is connected to the one adjacent to it, and this is a continuous cycle. Meaning that it is more like a phone chord.

The Zig-Zag model instead proposes that each nucleosome is connected to the nucleosome approximately opposite to it (parallel), and is a pattern that is continuous through out the chromatin fiber. This is more complicated to understand but imagine it being more like lacing on a shoe.It goes from a hole on one side to a hole on the other side parallel to it but not in the same plane as itself.

To move to the third nucleosome (and pack as tightly as possible) instead of it being directly below the 1st one it is slightly off to the side and not exactly parallel to the 2nd nucleosome.

However the 4rth nucleosome will be exactly parallel to the 3rd, and thus the same amount of degrees off-center from the 2nd nucleosome as the 3rd nucleosome is to the 1st, maintaining the pattern.

This forms a more 3-D tubular strucuture than an actual shoelace on a shoe would (which is more flat like a plane but serves for visual cue).

A 2D step-by-step representation of this would be like the image below:

Here is a model of final figure I made to help explain this:

In the MBI figure each "Green" nucleosome is connected to an opposite slighty lower "Purple" nucleosome and that purple one is connected to yet another green one that is slightly off center to the first green nucleosome:

In Theory (Not sure if correct):
This may mean that when this fiber "unwraps" it would act less like a spring coming undone(where the whole structure would start to unravel due to how it's linked) and instead each sequential nucleosome being pulled away from the fiber after the one its connected to has moved and experiences full tension.

For the ZigZag model imagine you take a piece of paper and fold it many times as if it were an accordion. Then hold the paper folded up in one hand. Take your opposite hand and pull the paper from one end slowly unfolding it. You'll notice that each fold comes out sequentially while the rest of the structure stays intact until the fold before it flattens out so the tension can pull it. At least that is what would happen in my mind. I could be totally off base.


Has any large-scale origin-of-life simulation/experiment been done? I have been thinking a little about the origins of life, and was further inspired by this question: How did the first self replicating organism come into existence?

I can accept that we don't quite know exactly how, but has any large-scale/long-term simulation been carried out?

There have been experiments but they seem to have been on a small scale. As an example, according to the Abiogenesis page on Wikipedia, some experiment which spontaneously formed peptide structures was carried out by Sidney Fox during the 50s and 60s.

What would be really interesting is if there had been some experiments or simulations carried out during a very long time, plausibly allowing for extremely low-probability structures to form. I doesn't matter whether this simulation/experiment has been carried out in a lab or as a computer simulation. There is of course the interesting but old "Conway's Game of Life" simulation, but according to my search efforts nobody has really tested it on a very large scale and in 3D.

Again, I'm looking for something extensive, like a decades-long single lab experiment or a simulation that has been run for years.

What you are possibly thinking of is large versions of the Miller Urey Experiment where a mixture of reducing gasses carbon dioxide, ammonia, nitrogen and the like are subjected to electrical arcs in a closed flask reaction, resulting in some biological molecules being produced.

Opinions have changed - Miller Urey did get the atmosphere wrong and so their finding of amino acids is not necessarily, but variations of this experiment continue to be done, with different conditions in the reaction vessel which reflect typical or even unusual conditions.  I've found some nice collections and reviews. There continues to be an enthusiastic effort even today.

Looking over several of these overviews, it's clear that many different conditions are being tried - reactions on mineral surfaces, examining chemicals on meteorites, near volcanic vents, different kinds of radiation.  What I don't see is anyone going to a huge tank.

I think that this might not have been tried (perhaps someone else will find a counter example), but if it were not me, I would probably not try longer experiments either.

There's some good reasons for this, if true.

Firstly all the published descendants of the Miller experiment have produced biologically relevant compounds after a few days.  Extending the experiment a few orders of magnitude may not prove anything new.

Secondly, the longer a reaction is run the more likely the sealed containers and heaters and other apparatus has to fail, causing you to restart or include contaminants that would ruin it.

Thirdly, one is not going to run an experiment that will ever come close to reproducing the time spans or volumes over which life emerged on earth - that was perhaps a few hundred million years over the area of the planet.

That's not to say you won't find out something new - an extra week could produce a new set of compounds or even a replicating system - we don't know if we haven't done it, but the nature of science is that you have a little time and money for a project like this and you would like to prove feasibility  - 'it could have happened this way'.  By selecting the conditions and doing a series of modest experiments which allows some to fail so that you can find something new.

I would say the observation of other planets and analysis of meteorites are getting closer to your idea - they are huge systems and been going for billions of years.  Titan is especially promising.  They just aren't the same conditions as Earth.

In brief, nothing is both affordable and perfect in proto-biotic research.


How to grow bacteria? We have this science experiment on how to grow a bacteria, our teacher told us to use gelatin, beef stock, and sugar as an alternative for agar. I am confused on  why we need gelatin, beef stock, and sugar in growing a bacteria. What ingredient is in those 3 materials that can aid in growing bacteria?

There are several requirements for bacteria to grow.

A carbon source - Sugar
A nitrogen / amino acids source - Beef stock
Gelatin is there to hold everything in place, it doesn't provide any nutrients.


Insect identification It is found in my apartment in Finland. I had to kill it to stop it from getting away before looking for the camera, but it looked pretty much the same alive and intact. It's length is about half a centimeter, and the younger ones look darker. It is often found in dark. Since their appearance, I often notice red and slightly itchy bug bite in the morning. The question is what is this insect?

It reminds me of silverfish, a common wingless house insect.


Why don't we have two hearts? The human body is amazing. But there seems to be some evolutionary changes that appear to not make sense regarding redundancy.

While not necessarily the primary reason for their existence, the human body has a great deal of redundancy.

Two eyes.
Two arms.
Two legs
Two ears
Two nostrils
Two lungs
Two kidneys
Two sets of teeth
A very large liver that can work in part.
Two brain hemispheres that can (to some degree) do the work of the other.
An appendix that is not critical.

But why do we not have two hearts? It would seem like a good idea to have two smaller hearts, together they work above optimally, but survival would be possible with one.

It is not about redundancy. There are evolutionary and developmental  reasons why we have two eyes or two legs and one heart. However just to give you short examples, two eyes are better than one because of our binocular vision while we have two legs because of its locomotor energetics.


Definition of nucleotide-associated proteins and RNA-polymerase associated proteins Nucleotide-associated proteins and RNA-polymerase associated proteins, I found those two terms in an article but I didn't understand what they mean exactly, is there any relation between those terms and DNA-binding proteins ?

The article : DNA supercoiling-a global transcriptional regulator for enterobacterial growth?

In short:

Nucleotide-associated proteins are DNA-binding proteins that bind DNA. RNA-polymerase associated proteins bind RNA-polymerases and are required for its functionality.

In more detail:

DNA-binding protein is a higher level term that comprises all proteins that bind to DNA. These can be seen as nucleotide-associated proteins as they interact with the nucleotides in the DNA strand, even though I did not hear people use that term very often. There are two types of binding:

Non-specific DNA-binding proteins that do not bind to specific sequences DNA sequences, e.g. structural proteins.
Specific DNA-binding proteins that bind to specific DNA sequences, e.g. transcription factors. These proteins mostly have specific DNA binding motifs like zinc fingers or helix-turn-helix motifs.

RNA-polymerase (RNAP) associated proteins are different from that. RNAP itself is a DNA-binding protein, but proteins binding to RNAP are necessary for it to be fully functional. The fully functional RNAP then is a holoenzyme. For example RNAP II requires an initiation factor called sigma in bacteria and several general transcription factors and regulatory proteins in eukaryots.


How is hibernation/aestivation different from anesthesia? How do hibernation/aestivation happen?

I read on wikipedia that a squirrel injected with the body fluids of a hibernating fellow is more prone to hibernation. If hibernation/aestivation are driven by biochemicals and not merely the weather, can the process be induced in higher beings such as humans to replace surgical (etc) anesthesia? How is the one different from the other?

p.s. Or perhaps to induce hibernation for the trip across the Solar System (+:

I'm going to answer the question of whether aestivation/hibernation can be activated in humans or other apes, because it's more interesting.

Mammals, as a clade, have three major subgroups. Bats, shrew-likes, rodents, and then everything else including primates. One family of the shrew-likes hibernates, some rodents(but not all) and some bats can hibernate or enter a period of extended torpor. The only kind of primate that can hibernate is the dwarf lemur, which does so in a strange way(fully asleep for 6-8 months, little regulation of body temperature). Other hibernating animals regulate their temperature but keep it low, and wake to roll over or whatever every couple of days. Plus lemurs are on the edge of the mammal cladogram, so they're just pretty weird.

Phylogenetically, it's not likely(imho, but I'm not a mammalian phylogenetics expert) a primate ancestor of humans has ever had the ability to hibernate. It seems more likely that primates lost the ability if it was a capability of mammalian ancestors and dwarf lemurs re-evolved it. It's possible atavistic remnants of such a system might still exist, but extensive hormonal and possibly surgical treatments would be required to induce it. Not to mention you can wake animals from hibernation by poking them, so it probably would be a substandard anaesthesia method.


Interpreting graph of mitosis and meiosis Note : Consider the y axis as 1,2,3,4(not 2,3,4) and x axis as time. Roman numerals should be considered from I-X ( some are not correct here )

Which stages show mitosis?
My answer : III-V

Which stages show meiosis?
My answer : VII-X

Am I right ?

I believe III → IV is mitosis and VII → X would be meiosis. As Jam explained in comments below, the stationary points of the graph (II → III or VI → VII ) do not count as part of either process.


Examples of extant animals in a submature morphologically unstable evolutionary state? I'm fascinated by evolutionary theory and the predictive aspect of it-the notion of an animal entering a strongly divergent state of evolution whereby it is evolving into a new form yet remains suboptimal, and is therefore undergoing rapid morphological change, and the idea that this allows us to project onto possible new variants of life.

To give a past example, the praying mantis is believed to have split from the cockroach around 250M years ago. During this period the mantis developed its upright stance, large range of vision and pronounced raptorial claws, and has seemingly stabilised into this optimal new form over the past 50M+ years.

The interesting thing is that this change could actually have been predicted by analysis of the animals evolutionary history, niche and further available advantageous adaptive forms.

Can someone give a good example of a current animal in this volatile state that we could make accurate projections for?

And please, no trivial answers like "everything is constantly in a state of evolution", I already know that and thats not I'm referring to.

Not sure exactly what you're looking for, but maybe the Giant Panda is of interest to you. The Giant Panda is an herbivore, but it has evolved from a meat-eating animal (the most recent common ancestor of Pandas and the other bears). It made the switch from omnivore to herbivore just ~2 MYA. According to wikipedia, pandas still have the digestive system of a carnivore. They can still eat meat and do not actually get much protein/energy from bamboo. Thus, you could consider them to be in a state of evolving from an omnivore into a more efficient herbivore


Black and orange spider, what is it? Found in Alexandria MN, on sidewalk. Small, fast little spider.

It looks to me like one of the Amaurobiidae - the Hacklemesh weavers, often called Lace Spiders for their fluffy, cottony silk snares/shelters that they spin under rocks and logs.  It's an adult male from the big boxing glove pedipalp structures in front of the face, which is presumably why it was out in the open; it was looking for love.
As to which one it was, I'm not entirely sure - these are not a group I'm too familiar with, and I don't even know what species are found in Minnesota.  It looks a bit like a male Amaurobius ferox (an introduced European species that is spreading across the country from eastern N. America), but even lightening the photo doesn't help reveal the abdominal pattern, I'm afraid.  I'll just go with "probably Amaurobiidae" and suggest you send the photo to Bug Guide for the attantion of the pros over there:  https://bugguide.net/node/view/6/bgimage

Here's a representative male A. ferox for comparison, but note that this is a well-lighted photo so you can see the pattern on the abdomen.  Also note that there is a fair amount of individual variation in these (as in most) spiders, so some are darker, some are lighter, some have obvious patterns, some are more poorly-defined, etc.


Why are potassium channels slower than sodium channels? I am relatively new in the subject of biology. I have a strong mathematical background and in order to get into the field of computational neuroscience, I am trying to get some biological background.

I am reading about the general mechanism of action potentials in neurons.
I understand that an action potential starts with a fast entrance of sodium into the postsynaptic cell. Since the potassium channels are slower than the sodium channels, potassium starts flowing out of the cell only around the peak of the action potential, thereby hyperpolarizing the cell's membrane potential.

What is the mechanism that causes the potassium channels to activate slower than the sodium channels? Does it involve differences in the behavior of the suitable neurotransmitters? Because I didn't manage to find transmitters or couples of transmitters and receptors which activate potassium channels, but not sodium channels (or sodium channels and not potassium channels).

Short answer
The activation kinetics of Na+ channels are faster than K+ channels.

Background
Voltage-dependent channel gating basically occurs through three possible states of the channel: open, closed and inactivated (Fig. 1).

Fig. 1. Gating of a voltage-activated sodium channel. Source: Balseiro Institute.

Basically, ion channels are protein pores in the membrane. Upon depolarization, the pore opens, which is a process with fast kinetics in Na+ channels and slower kinetics in K+ channels (Lacroix et al, 2013). K+ channel activation is in the order of 6 times slower than Na+ channel activation. The slower inactivation of K+ channels allows sufficient Na+ to flow in the cell for the depolarization phase of the action potential to develop (Fig. 2).

Fig. 2. Action potentials and underlying Na+ and K+ currents. Source: Dundee Med Student Notes.

After opening, the channel is inactivated, which can occurs through a physical "protein-plug" as shown in Fig. 1, or through conformational changes in the pore. This inactivation again is fast in Na+ channels leading to a transient spike in the action potential, and deactivation is slower for K+ channels (K+ channels do not inactivate, but rather deactivate). This inactivation step results in the refractory period of a neuron (silent period after firing). The channel is then de-inactivated and converted to the closed state, after which the channel is again ready to participate in another round of firing.

Note that neurotransmitters do not activate voltage-gated channels directly. Neurotransmitters can activate ion channels, but those are ligand-gated ion channels, such as the nicotinergic acetylcholine receptor, AMPA receptor or NMDA receptor (Purves et al., 2001).

References
- Lacroix et al, Neuron (2013); 79(4): 651-7
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates (2001)


Determining the Accuracy of DNA Testing The DNA Testing firm in the below article claims that its tests were "99.99 per cent" accurate.

http://www.telegraph.co.uk/news/uknews/1322077/False-DNA-test-led-father-to-reject-daughter.html

Googling "dna test accuracy" has led to numerous websites many of which claim an accuracy of their DNA testing to be 99.9%, with some even 100%!

How does a firm calculate this percentage accuracy? It seems to me that experimental data would not be useful in determining this percentage accuracy as there is no way to really confirm the fact that Bob is the son of John and vice versa as that is what we're trying to find out. Do they do so by factoring in slight inaccuracies in the laboratory procedure?

Acquiring experimental data would not be useful as I described above for paternity testing, a useful application of DNA testing, but could, to my knowledge, be used to determine the percentage accuracy of DNA testing in the recognition sense. By DNA testing various cells of the same person, and then seeing how many of them result to be from the same individual according to the DNA test (understanding that scientifically every cell should have the same DNA but then experimentally acquiring results that show that 999 in every 1000 cells show to link back to the same person) seems to be a working method...Is this how it works? Is this the notion conveyed with the idea of the percentage accuracy of DNA testing?

Essentially, yes. These tests are usually based on enzymes that replicate DNA, and they have a certain (small) probability of getting a base wrong now and then. You can estimate the error frequency by doing many repetitions of sequencing of the same DNA sample and counting the number of discrepancies. Of course, this assumes that there are no systematic errors, only random variation, which may not be entirely true.

The Sanger sequencing technique is estimated to have error rates on the order of 0.001% (or, is 99.999% correct). I don't know exactly how these firms calculate their numbers, but I would guess it is similar.


Small jumping bugs inside Swiss flat Saw these bugs inside the flat I'm renting (Switzerland), but I really can't figure what kind they are. What I can say about them:

They can do small jumps (up to 5cm I would say). It doesn't seem to be for locomotion, but as a means of escape when I try to catch one.
Size: about 1.5mm for the "big" ones. There are of various sizes down to 0.25mm for the really tiny ones (approximately; never managed to get one without crushing it). They behave much the same as the big ones (including the jumps) and are whiter in color.
They don't seem to live as a colony or in a nest (or I simply didn't find it), but sparsely on the wood floor, often near the baseboards. Found some on the walls, but those were the exceptions. They don't seem to like the bathroom.
Rather delicate; can easily be crushed.
Seem more active in the evening and at night, but don't mind going out during the day.
I live alone, without pets, but I don't remember having been bitten. I guess they don't feed on blood.
Seem to have long antennas (about half their body size) and small wings.

Side note: the flat is on the 3rd floor of a recent building (finished 14 months ago). I'm the first tenant.

An exterminator came and quickly classified them as some kind of flea. He put some pesticide on the baseboards, and their number is now quickly decreasing. But I'm still curious.

My first thought was "fleas" (because of the jumps), but I deemed them too squishy and not "vampire" enough for that. Also, I don't think that (what I assume to be) the young ones should be able to jump.

Then I thought "springtails", but I didn't see any furcula (granted, I don't have a good eyesight) and I don't think they are supposed to have wings.

One of them was nice enough to jump on some tape.

Top (on a ruler):

Front/Side:

Also, blowing on it (to open the wings):

Youtube video of one of them

I believe these are some sort of Psocoptera, "booklice", even though they don't really jump much. Could it be that they ran or flew a little bit instead? I won't try an identification of the species, but in general booklice like damp places and most of them aren't considered serous pests.

Example of a booklouse:

Slender legs and antennae, wings, and general appearence close to your specimens.
(Image from Wikipedia)


Reason behind selection of sites of administration of pituitary extracts? There are two ways by which pituitary extracts are administered in a fish's body during induced breeding of fish.

Intramuscular injection is the most common practice in India and it is less risky in comparison with the other methods.The extract is injected into the muscle near the tail above the lateral line.
Intra-peritoneal injections are given through the soft regions of the body, generally at the base of the pelvic fin or sometimes at the base of the pectoral fin.

Why are these sites chosen? What physiological effects arise as a result of administration that these sites got chosen ?

Melatonin is an evolutionary highly conserved molecule that plays an important role in conveying the clock and calendar information to all living organisms, including man. The hormone is synthesized mainly by the pineal gland, and, to a lesser extent, by extrapineal tissues--such as the retina, Harderian gland, and gastrointestinal tract.

It is a standard slow acting hormone injection. Once the injection is in the animal, it just propagates throughout the animal's physiology and takes the normal melatonin chemical and physiological pathways that it does in vertebrates, it prompts the pituitary gland to produce a lot of different hormones including sex and serotonin.

It doesn't act instantaneously if you overdose (humans have tried), OD negative effects occur after 1-2 days and thereafter. It doesn't react as violently as some other hormones such as Adrenaline, which is absorbed fast and dissipates fast and can give you a heart attack. Melatonin has a physiological effect that is more extended, for example steroids for inflammation.

The aim of intramuscular injection of the fish is that it is effective and safe, If you read the guides, they are concerned with the safety of the fish, it's nerves and vital organs... The tail is mostly muscle and the injection is IM. Once the hormone is injected, its absorbed by the animal over an extended period. There have been many experiments of pineal injection in rodents so refer to them to know the time frame of absorption.


Where does this equation in the electrophysiology literature form come from? In my studies I keep coming across the form of an equation that is used in many different mathematical models for voltage gated ion channels. The most general form I have found is in the 1977 paper Reconstruction of the action potential of ventricular myocardial fibres by Beeler and Reuter. Each ion channel has a gating variable $y$ whose differential equation depends on functions $\alpha$ and $\beta$, both of which take on the general form:

$$\{\alpha,\beta\}=\frac{C_1\exp[C_2(V_m+C_3)]+C_4(V_m+C_5)}{\exp[C_6(V_m+C_3)]+C_7}$$
where $V_m$ is the membrane potential and each constant is determined to have different values depending on the channel, system, etc.

My question is where does this form come from? In all of the papers I have come across they seem to just use this form with numbers chosen to fit their data without explanation as to why this form is actually used. The Beeler and Reuter paper cites the 1952 paper by Hodgkin and Huxley, but it seems like H&H use simpler forms of this equation primarily motivated by just fitting the data rather than illuminating any underlying mechanisms. Therefore, I do not understand where this form in the B&R paper comes from that so many papers later on use as well.

Does this form come from assumptions about the workings of the ion channels, if so, what are these assumptions, and how do they give rise to this form? Or is this just a general form found to fit many data sets fairly well, and if so why was this chosen over other functions that could probably do the same thing?

They chose that equation mainly because of numerical simplicity. It can fit the rates $\alpha$ and  $\beta$ for all the ion channel particles in the model.

The theoretical foundation for the equation, as in the H&H model, are loose. It resemble the equation derived for the movement of a charged particle in a constant field. But it is not an equation derived from the ion channels biophysics. We can't blame them, considering that at that time (1952) they don't even know for sure that ion channels where proteins.

In page 183:
 In order to simplify the reporting of the actual values used in this model, we have expressed the alphas and betas entirely in terms of a generalized function, with eight defining coefficients. Table 1C gives the equation, and the defining coefficients for al rate constants.

For the generalized function note that in every case at least some of the coefficients are zero: this generalized formula is just a way to collect both possible forms for the H&H rate constants.

I have read papers using Eyring equation for a theoretical formulation of transition rates, based on thermodynamics.


How is C4 pathway more water efficient than C3 pathway in photosynthesis? In the C3 pathway:

1 H2O molecule is required for the fixation of 1 CO2 molecule.

In the C4 pathway:

The only H2O molecule used is in the calvin cycle, so 1 H2O molecule required for fixation of 1 CO2 again.

So, how is C4 pathway more water efficient? I tried looking up more detailed diagrams, but I couldn't find one which gave any different (H2O consumed) to (CO2 fixed) ratio. Any help is appreciated.

Actually, water is used in the light-dependent portion of photosynthesis, not the Calvin cycle.

The added water efficiency doesn't actually relate to water's involvement in chemical processes of photosynthesis at all. Water is instead lost incidentally through stomata when they're opened to allow CO2 into the leaves (see here for explanation). This CO2 IS required for the light-independent Calvin cycle.

Both C4 and CAM plants preserve water by decoupling (in space or time) C-fixation from the rest of the Calvin cycle (see here). They instead "store" carbon in 4-carbon molecules to use as a C source in the absence of CO2 (i.e., when stomata are closed). In doing so, they can perform the Calvin cycle without receiving more CO2. As a result, C4 and CAM plants can photosynthesize without having their stomata open all the time (or during the heat of days for CAM plants). The final result: less water lost through evaporation out of the stomata


Decreasing the alcohol proof and faster in hangover, why? My russian friend says that the USSR agents used/use the trick that they offered the victim first vodka and then last wine.

I have noted that this puts you faster to hangover: decreasing the alcohol proof.
Some people lose their motor function immediately and some their memory only.

Why does a decrease in the alcohol proof cause you a) faster intoxication and b) faster hangover?

Probably the change in the concentration of alcohol inside cells of brain tissue affects some parts of your brain like the cerebellum. I would like to have an explanation in Biochemistry.

Is there any truth in my friend's argument?

I would argue that your central point is intrinsically flawed. Your claim is that starting at a high alcohol percentage, then gradually decreasing alcohol content, gets you intoxicated faster. @nico is correct that you will get drunk faster this way (more alcohol sooner rather than later, so this is trivial). If we allow only one variable to change, the alcohol content (and therefore the water content), then the first drink is the most potent, and each drink afterwards is getting progressively more dilute, then this implies you are able to rehydrate better the more you drink. This argues exactly opposite to your claim.

Since you offered up the example of vodka to wine, this introduces two new important aspects: fermentation impurities and sugar content. Vodka is distilled and relatively pure, so it offers little in addition to alcohol and therefore easy to process by the liver. Scotchs and whiskeys are low sugar, higher impurities, and so would be a bit more troubling to filter and process. As you move down to wine, impurities rise and sugar content is much higher. This added sugar load dehydrates faster as well as causes a cascade of hormonal changes that are more immediately troubling than the alcohol. Beer would generally be the extreme end of the impurity and sugar continuum.

Since you bring up the USSR and the KGB, I imagine that if they did stick to this regimen of interrogation, it could be more effective by power of suggestion. The victim believes they are more intoxicated than they are, and perhaps more likely to offer up their secrets.


Any databases with AAMI ECG and ECHO? There is no AAMI 12-lead ECG databases available online.
All of them have problems.
I and my friends finally finalised our tests with St Petersburg.
It is not AAMI.

So the next step is to search any ECG databases with some leads (at least lead 2) with ECHO data.

Is there any AAMI standarded ECG databases with ECHO data?
This data need to be from the same patient.

One possibility is PTB Diagnostic ECG database here.
However, its AAMI verification is still under process here.
Some ECHO findings also there.


Does dairy negatively affect the voice for singing? Singers and actors are warned not to consume dairy, primarily milk, before a performance. From personal experience, I know that this is a very valid warning. It is commonly assumed that this is due to milk causing either more or thicker phlegm.

Has the mechanism behind this been studied and verified?

As it turns out, dairy products do not produce phlegm in the majority of people (the exception is the tiny group of people who are allergic to casein, the protein in some types of milk). Instead, the high fat content in dairy products thickens the mucous that is already present in a person’s airway, making it seem like there is more phlegm to deal with. Of course, having thicker phlegm can be just as problematic as having more phlegm. Luckily, this thickening sensation can be diminished simply by eating dairy products that have a lower fat content.

(https://www.operapulse.com/refine-your-craft/guide-to-opera-training/the-rules-of-singing-mythbusters-edition/)

Regarding the above quote, there is no medical evidence that states milk consumption causes phlegm production even for casein allergic individuals.

The study cited at the end shows that there is a correlation between milk consumption and thicker phlegm. However correlation is not causation. The authors explain that the allergy-like effects of milk are produced only when tissues are actively inflamed and exorphins (peptides produced when milk is broken down) stimulate mucus production from gut glands. The thicker phlegm effect is shown in only a segment of the studied population. Unless you're one of the few with inflamed tissues, you should be ok with drinking milk before a performance.

(http://www.researchgate.net/profile/Jim_Bartley/publication/40026300_Does_milk_increase_mucus_production/links/0fcfd5138d5212ef80000000.pdf)


The damage of cancer cells I read about the molecular biology of cancer, and I have a mess on my head and a lot of questions.. .

My primary question is-

The damage of the cancer cells is in the dna sequence or in the gene expression(microRNAs)? or even something else?

Thanks:)

Cancer is commonly defined as uninhibited cellular replication caused by mutations to the genome.

Genes where cancer-causing mutations have been identified are known as oncogenes; the COSMIC (Catalogue Of Somatic Mutations In Cancer) database lists all of the known oncogenes (547 to date - 23rd Jan 2015 - 1% of all human genes!) [1].

The effect of a particular mutation would be to alter in some way the expression of a gene or genes. This may be directly, for instance rendering a tumour-suppressing gene unable to fulfil its role [2], or indirectly, for instance by affecting epigenetic mechanisms that in turn affect expression of genes involved in cell cycle regulation [3].

To my knowledge cancer is not 'caused' by just a change in expression of a gene, although it may be mediated by it. The change in expression or effectiveness of a gene (such as tumour suppressor p53) resulting in uncontrolled cell division is caused by mutations at the genomic level.

What causes the mutations?

Lots of factors can cause mutations, from chemicals (e.g. from cigarette smoke, not just restricted to the lungs either [4]) to mistakes in the DNA replication machinery as somatic cells undergo normal cell division [5].

The last reference there provides very compelling evidence for the reason that some tissues are more predisposed to cancer than others; tissues with higher cell turnover (and thus require more cell division) have higher incidences of cancer - see the below figure from [5]! This figure separates "lung cancer" into two groups to show that even non-smokers have risk of developing lung cancer, but not as high a risk as those who smoke.

http://cancer.sanger.ac.uk/cancergenome/projects/census/
Muller, P.A.J.; Vousden, K.H. (2013) p53 mutations in cancer. Nat Cell Biol. 15:2-8
Hamamoto, R.; Saloura, V.; Nakamura, Y. (2015) Critical roles of non-histone protein lysine methylation in human tumorigenesis. Nat Rev Cancer. 15:110-124
Cancer research UK report on smoking and cancer
Tomasetti, C. & Vogelstein, B. (2015) Variation in cancer risk among tissues can be explained by the number of stem cell divisions. Science 347, 78-81


Do oysters feel pain? Do oysters feel pain when you bite into the inside, or when you crack open the shell? I tried google searching it to no avail. When you bite inside the oyster or when you break the shell to open the oyster, does it feel pain?

EDIT: (Since some people think that mine is a duplicate) I'm asking if the oysters feel pain when we eat the inside, or when we crack open their shell. To the least of my knowledge, ants and oysters have a different body so I don't know if they do feel pain.

There are fundamental problems with defining what it means for an animal to feel pain, especially when the animal is a life form as different from us as an oyster.

I wasn't able to find any specific info online about oysters, but there is quite a bit of information that allows us to reason by analogy with related species.

Oysters are molluscs, and molluscs do have brains and sensory systems, but their level of sophistication varies a lot. Cephalopod molluscs, such as squid, octopuses, and cuttlefish, have extremely sophisticated nervous systems, and it has been argued (Peter Godfrey-Smith, Other minds, 2016), that we should think of intelligence as having arisen twice on earth through parallel evolution: once in vertebrates and once in the cephalopods. Cephalopods have sophisticated communication systems, and they can use tools and solve problems. There has been extensive research on pain in cephalopods.

So it's inherently pretty plausible that cephalopods can (in some difficult to define sense) suffer and feel pain, and by extension that their less advanced cousins the oysters can as well. However, the nervous system of an oyster is much more rudimentary than that of a cephalopod. A better analogy might be with snails, and there is some research on snails. They avoid damaging stimuli, have opioid systems, and respond to morphine and naloxone analogously to humans (e.g., showing less aversion to a hot plate when they've been dosed with morphine). So it seems likely to me that oysters can feel pain (for some reasonable definition of the word), but this whole area is one where people don't really know the answers to the questions or how to construct the philosophical foundations.


Phylogenetics and the Tree of Life As far as I understand, evolution is nowadays pretty much analyzed through phylogenetic trees, that is cladograms. These are constructed using the available records and taking some key structures and deduce whether species acquired or lost it, thereby generating a node. By  this approach, chronology is of utmost importance, but chronological time is not. Hence, cladograms are not 'Darwinian' evolutionary trees as the latter are based on chronological time.

However, I cannot help myself when analyzing a cladogram and interpreting the accumulation of various nodes along a branch as moving through time. Isn't evolution all about time? At the risk of pitfalling myself into a 'this is a primarily opinion based question':

Isn't it just so that along a certain branch, each successive node has taken time to develop? Would it not be plausible to determine and assign a certain 'standard evolutionary time unit (a SETU if you like) representing the average time it takes for any organism to loose or acquire a certain trait, thereby allowing each node to be interpreted as time? Of course, the SETU would be a gross estimate, but could still potentially re-animate the Darwinian look on modern-day evolution.

Let's start with a short comment. You say [..]evolution is nowadays pretty much analyzed through phylogenetic trees[..]. Many evolutionary biologist make extensive use of phylogenetic methods but a good part of evolutionary biologist (most of them I would say) do not work directly with phylogenetic methods.

I am not sure I understand your question but I hope the following may help you either to understand the issue or to edit your question. Note that I am NOT a phylogeneticist (not sure this word exist).

What is the definition of "Node" in Phylogenetics

I think your definition of a node might be unusual. In phylogeny, a node is the most recent common ancestor shared by two sister lineages.

Time in a phylogenetic tree

Also, when you look at a phylogenetic tree, the axis along which lineages diversify represent the time (real time in years). Now, we use different methods in order to make estimation of this real time such as the rate of neutral substitutions. You may want to read about molecular clock

  each successive node has taken time to develop?

I am not sure what you mean by "develop" here. Develop usually means the process by which a given individual/organism change phenotypically through its lifetime. See Developmental Biology.

  average time it takes for any organism to loose or acquire a certain trait

Again, I am not sure whether you talk about development or evolution here as you talk about "any organism" and not about "any population". In any case, an average time for a population to acquire a given arbitrary trait is a concept that 1) is valid only for discrete trait, 2) that is very dependent on the kind of trait you want to consider, 3) that will varies a lot from one given trait to another and 4) is extremely dependent on when you consider being the starting point of the evolutionary process toward the creation of the given trait. Therefore, it doesn't makes much sense.

Currently used "standard evolutionary time unit"

However, you can use similar concept for quantitative traits. The Darwin (d) is a unit of evolutionary change (invented by Haldane and named after C. Darwin). It is defined as the e-fold (e≈2.7) in a mean of individual's trait in a population over million of years.

Similarly, the Haldane is a unit of evolutionary change (I don't know who invented it and it is obviously named after JBS Haldane) and correspond to the number of standard deviation (of the distribution of individual trait in the population) change in the mean of individuals trait in a population per generation. The Haldane unit is therefore dependent on the selection pressure, the additive and non-additive genetic variance and environmental variance (therefore the heritability) and the mutational pressures.


Drugs to make rats easier to trap What drugs will make rats less cautious/sensible and/or more hungry so they'll go to my snap traps more?

What dosage and how do I deliver it to the rats?

Background info:

The rats trapped in my crawl space I imagine have limited food, if any.
The snap traps are well coated with peanut butter scent but the process is very slow -- one by one.

They have rat mites (blood-sucking parasitic barely-visible mites) and I want them out ASAP.
It's been several months because:

They reproduced down there.
One of the vents got broke open again so a second batch got in. I don't know how many. 25 rats have been trapped so far (2 today and I hear more).

I've checked the house so well. Sealed up with caulk and expanding foam every hole. Checked the roof. Sealed wire mesh on all the plumbing stacks and exhaust vents on the sides of the house.
There's really nothing else. I'm positive it was the broken foundation vent that let the new ones in. But now that everything is sealed securely and won't be broken open again, I think it's only a matter of removing the existing rats.

I don't want to poison them because then they'd die inaccessibly and their mites would swarm the house. They have to die in the traps that I check several times a day, so they can be removed before the mites spread.

I keep somewhat up-to-date with pest control measures. I haven't heard of chemicals being used to alter rat behaviour but using parasites that alter rat and mouse behaviour (Toxoplasma spp.) has been studied. The infection increases predation rates and also appears to increase the rate at which they are trapped. Toxoplasmosis also affects humans with cats being the main source of infection. I am uncomfortable about approaches that increase the prevalence of toxoplasmosis.

If you're going to the trouble of administering a drug to a pest why not make the drug lethal? The extra step seems unnecessary but I personally would opt for traps given that many poisons (particularly warfarin) seem cruel.

For traps good bait (uncooked bacon, lard, peanut butter, dog biscuits) makes rats;

  less cautious/sensible and/or more hungry.

The right trap can make a big difference. This one can self-reload > 20 times and is instantaneous. The linked website contains advice for setting traps.


Do women have testosterone? In a documentary on fitness I saw it was stated that women can't get big like men because of their low concentration of testosterone. If it is true that women have testosterone, where is it made? Why do some women, especially later in life, develop facial hair (though obviously not as much as men)? Do men also have "female" hormones in their body?

Yes, they do. The ovaries produce both testosterone and estrogen. Relatively small quantities of testosterone are released into your bloodstream by the ovaries and adrenal glands. Sex hormones are involved in the growth, maintenance, and repair of reproductive tissues [1].

The serum testosterone level in women with no acne, hirsutism, or menstrual dysfunction is 14.1 +/- 0.9 ng/dL (nanograms per decilitre) [2]. An average adult man has 270-1,070 ng/dL serum testosterone [3].

Men have female sex hormones too. For a prepubescent male, estrogen levels are expected to be between 1 and 3.7 ng/dL. During puberty, normal levels fall between 2.3 and 8.4 ng/dL. Levels for an adult male should be between 2.5 and 5 ng/dL [4].

References:

WebMD, LLC. Normal Testosterone and Estrogen Levels in Women.
Ayala C, Steinberger E, Smith KD, Rodriguez-Rigau LJ, Petak SM. Serum testosterone levels and reference ranges in reproductive-age women.
Alexia Severson. Testosterone Levels by Age. Healthline Networks, Inc.
wiseGEEK.com. What Are Normal Estrogen Levels in Men? (Measurements cited in picograms per millilitre, converted to ng/dL)


Is it true that ethanol can have some positive effects? I recently was reading this inforgrafics about excessive alcohol use. It is written:

  No one should begin drinking or drink more frequently based on
  potential health benefits

I am surprised. Is there any potential health benefits of drinking alcohol?

To check this information, I made a little research and found this article of the Medical Daily: 7 Health Benefits Of Drinking Alcohol. Apparently, a moderate alcohol consumption (no more than 2 drinks a day for a men) can lower the risk of cardiovascular disease, lengthen the life, decrease the chances of demantia and diabetes, ...

But, for all of these facts, only one study is provided. So, I want to know if it is a well established fact that alcohol can have positive effects on health. And, if so, what is the corresponding dose to get these benefits?

Alcohol has caloric value.

First worlders today have a wealth of high calorie food choices which make the caloric value of alcoholic drinks either irrelevant or detrimental.  But it was not always this way. In circumstances where other caloric sources were limited or unpalatable, alcohol supplied calories needed to supply the energy demand of workers.  Persons working energy-intensive jobs (such as field labor or factory work) have historically supplemented calories from food with calories from ethanol.  The below excerpt discusses the dietary habits of metalworkers in the late 1800s.

Drink, Temperance and the Working Class in Nineteenth Century Germany

  Despite the overall improvement in dietary standards of the previous
  two or three decades, the situation of these Manheim workers suggests
  that alcohol remained an essential part of the working-class diet. If
  provided necessary calories in palatable form. The sharp flavor of
  alcoholic beverages could add spice to otherwise monotonous fare,
  providing a sense of warmth and fullness even when meals were cold and
  unsatisfying. Perhaps most important, alcohol provided energy in
  concentrated form. Alcohol, whether in the form of beer or spirits,
  enabled workers to reduce the sheer quantity of food that had to be
  gotten down each day. The distinguished physiologist Max Gruber
  calculated that a worker who consumed even a 10th of a liter of
  schnapps with the meal could come up with no energy loss, reduces
  potato and rye bread consumption but some 288 and 122 g
  respectively.”Try eating a kilo of black bread or two or more kilos of
  potatoes day after day”, Gruber told his well fed middle-class readers
  in 1888, “and you’ll discover what a relief it can be to substitute a
  pungent and stimulating beverage for a 10th of this mass”.

The health benefit of alcohol consumption here would be that of not starving in situations of high caloric expenditure.   calories are concentrated as compared to carbohydrates and distilled spirits also have an indefinite shelf life - not true of grains and potatoes.


Why is the vermis of the cerebellum associated with speech? I've found multiple sources claiming that damage or impairment as a result of alcohol to the vermis of the cerebellum results in speech impairment. I find this a bit surprising, since the only areas I know that are used for speech production are Broca's area. Additionally, I don't know of any way that the vermis influences this area or any other facial nerve that may need co-ordination to produce speech.

So why does damage/impairment of the vermis result in dysarthria?

Although speech production is in generally executed in the cerebral domain, the dysarthria resulting from damage of the vermous is a symptom of the resulting general muscle weakness. So yes, you get slurred speech because your muscles are weak, but the weak muscles certainly aren't ever isolated to speech production.


What kind of longhorn beetle is this? I live in Europe and found this interesting longhorn beetle I think and I was curious what species it is or what's it's name!
Thanks to anyone who identifies it!

Rosalia alpina (common name: Rosalia longicorn)

See here: Rosalia longicorn

The link I added shows a picture of an identical Alpine Longhorn Beetle. This longhorn beetle occurs mainly in the European Alps and the neighboring countries (e.g. Germany, Hungary, and France). Minimum height is around 700m above sea level. The adults are active from June to September. The color varies between blue and grey, the head is characterized by one spine on each side of the head. The number of black dots on the elytra varies.


What really happens when a body is tired? This may be anecdotal; please feel free to vote to close.

After staying awake for an extended duration, I usually find myself having to take extra effort to focus my eyes on an object. Similarly after exerting myself to the extent of near total exhaustion I find it necessary to consciously focus to perform actions that would otherwise require little conscious effort (E.g. Writing a note). There're other similar symptoms almost all of which mandate 'conscious effort'.

What really happens when a body is tired?
As a corollary, why does making conscious effort usually beat the initial error?

Its still not clear why we need to sleep (as distinguished from the question of why our body gets fatigued in physical exertion).  A popular idea is that the brain needs to 'catch up' and reorganize itself given all the stimulus it has had from the previous day.  This 2010 National Geographic article says it all:

  I asked William Dement, the retired dean of sleep studies, a co-discoverer of REM sleep, and co-founder of the Stanford Sleep Medicine Center, to tell me what he knew, after 50 years of research, about the reason we sleep. “As far as I know,” he answered, “the only reason we need to sleep that is really, really solid is because we get sleepy.”

It is clear that we need sleep and that we become less reliable at tasks when we are sleep deprived.  eventually we become completely unable to function.

I'm not sure anyone can answer the last question - why does conscious effort help us to perform tasks?  one would have to understand/define the neurology of consciousness to answer that question.  That is still a bigger question that remains open I think.


What kind of technology is required for plant seed DNA printing? I'm a programmer so I have little knowledge in the field of biology. However I have an interest in plants, GMOs and DNA (in terms of programming).

So, I want to know what kind of technology is necessary and what limitations there are involved in creating a DNA printer (that could print out a cell to be grown in a pot).

First, how do we print the DNA of a plant? Can we print it all from the first pair of chromosomes? I have heard we are already able to print bacteria's DNA. Is this something we would be able to achieve outside of a lab? Could it be done on commercial scale?

Second, what conditions do we need to prepare the DNA if it is not that of a bacteria but rather of a plant that would grow into a multi-cellular organism? Can we really print a plant DNA, inject it into a cell and let it grow?

Third, what is the current understanding of DNA ? Can we analyze DNA strand with digital software yet? Can we simulate how the organism will do with the DNA? And how can I start working in this field? Are there any scientific papers I can learn from?

P.S. My first goal is to make a Nepenthes Vine. I want to have a vine plant like Pothos creeping on my fence with a jugs to eat insects.

As Chris mentioned in his comment, 'printing' DNA from scratch (i.e. synthesizing a long strand de novo) is expensive and difficult. Unfortunately, the process of GMO creation is not as simple as assembling a beautiful DNA sequence on the computer, printing it, and then inserting it into a cell. Here's a related question about de novo sequencing. Plant biologists, please correct me if I'm wrong but I don't think it's a trivial matter to grow a plant from a single cultured cell.

Your third question reminds me of DNA programming, which is an amazingly cool, developing field. Many companies (including Microsoft) are funding research into DNA circuitry and biological computing, making computers out of biomolecules. Here's an interesting paper that will tell you more. What you may be most interested in is the branch of DNA programming that seeks to identify discrete protein-coding and otherwise functional DNA that can be utilized as a sort of "programming language" to build a new organism. One of my past supervisors recently joined this field and I'm a little jealous. Overall, this is a very new field so there is much to be accomplished and very little is technically possible, although the principle of GMOs is really just an optimization of an existing organism.

In summary, the answer to all three of your questions is: No, not very well. But we're trying.

Most likely this isn't something you'll be able to pick up in your spare time in order to have a cool plant to grow on your fence. It's very expensive and very difficult (in some cases, maybe even impossible). However, there are so many unknowns in this area of research and everything you propose is reasonable in theory. Let me know if you figure it out. I would love to code my own garden.


Which human cells have the longest and shortest lifespan? Which cells in a human have the longest lifespan? Which cell has the shortest lifespan?

If we define lifespan of a human cell to mean the period during which the cell survives with the same function in a human then..

LONGEST (LIFETIME)

Stem cells. Many types of stem cell form during embryogenesis and persist with the same functionality through to death. would be the longest lived (e.g stem cells that form blood cells such as lymphocytes, red blood cells and platelets).  Stem cells are found in many tissues including self-renewing ones such as the blood/bone marrow, gut epithelium and skin.

VERY LONG (YEARS-DECADES)

Neurons are long lived and are generally non-mitotic.  However, recent studies are raising questions about the degree of cell division in the 'mature neurons' of the brain.

Memory T-cells and memory B-cell (which can be activated and secrete antibodies as 'plasma cells') can provide long-lasting immunity from exposure to antigens in the environment and vaccines.

LONG (FEWER YEARS-DECADES)

Oocytes (eggs)..which are present at birth but which become functionally mature in waves  during puberty.

RACE FOR THE SHORTEST

Labeling studies show that mature gastric epithelial cells live for a few days.

The top layer of skin epithelium is sloughed off every few days.

Sperm cells live for days and are expended or re-cycled.

Mature neutrophils have a circulating half-life of around 8 hours but they can persist as mature forms within the bone marrow for a few days before entering the circulation and they may exit the circulation into depots such as the lung.  So the 8 hours is too short for their actual lifespan.


What are examples of genes succesfully reproducing in ways that is in conflict with helping the individual creating offspring Most of the time, our genes have common interests with our "self".

We reproduce well if and only if our genes reproduce well.

In some cases, like in bees, the haploid bees can survive better if they help their queen reproduce.

In humans and other species, are there samples that give individuals "incentive" to help non family member to reproduce for the sake of their genes.

So

No filial altruism
No reciprocal altruism

So I need a sample between individual based evolution and gene base evolution.

For example, many genocide are done against the best and brightest. I wonder what sort of genes encode "kill the best and brightest" and how does that kind of gene survive well in the gene pool?

The prototypical example of this is t, whose existence was predicted by Robert Trivers and featured prominently in the Selfish Gene.  The current dominant point of view in evolutionary biology is that genes act in their own interest and even the 'self' is just a manifestation of the gene's reproductive properties.

t is a locus in some male mice. The t gene characterizes very well the selfishness of a selfish gene.  While most paternal genes are found in 50% of offspring, t is found in over 3/4 of offspring.  Somehow it manages to reproduce at the expense of the other loci in the male mouse.  t itself is not known to convey any advantages to its host organism.  the males tend to be smaller and sometimes even reproductively disadvantaged.

Does that go some way to answering this question?

Animal behavior such as cheating or adopting are often interpretable as reproductive advantages.  Killing the best and brightest definitely are to the advantage of those who are doing the killing.  This SNL Skit has always said it best to me. "... and now I am smart!".  Such kill offs so rarely include killing one's own offspring.  I'm not sure they can be called in conflict with reproductive advantage.  EO Wilson's essay "On Human Nature" does a reasonable case for saying that wars and famines are in fact produced by evolutionary advantage, however cruel and ugly they may be.


What do rs id, allele coded 0 and allele coded 1 mean? So, for a project I've been working on (different story), I've been looking at the HapMap Project, and their free online files. In their README file, they talk about how for each legend file for each chromosome/region, there is an rs id, an alelle coded 0, 1, and a base pair position.

Now it's fairly obvious after staring at this for a while that base pair position means where each nucleotide is located along the genetic sequence... is this correct?

And what do rs id, and the other words mean? Any help would be greatly appreciated!

Here's the link to the README file, in that same directory are the files about the participants, only including SNPs (snips!).

HapMap Project README file link

HapMap Project sequence data link (phase 2)

rs id is reference SNP cluster ID see here. It's basically a unique identifier.

This table is taken from your link:

rs              position        0       1
rs11089130      14431347        C       G
rs738829        14432618        A       G
rs915674        14433624        A       G

The allele codes are the 3rd and 4th columns. An SNP is  site where a different base is found in different versions of the same gene (different versions of genes are alleles). For a given SNP the different alleles are referred to as the 0 or the 1 allele. So in the table the first SNP, rs11089130,  has two alleles: allele 0 has a C at the SNP position (14431347) whereas  allele 1 has a G at that position. The allele code does not imply any biological significance.

I'm not sure what would happen if there were three alleles at an SNP, but presumably there would then also be an SNP coded as 2.

Edit:
Allele 0 is the residue from the reference genome. Allele 1 is the residue being studied, the SNP.


What is the progressive evolutionary advantage that leads to flying? As far as I understand, all life started as non-flying and flying came about by natural selection. What is the evolutionary advantageous "path" to flying? Or is there something else to explain this?

The honest answer to this and many other similar evolutionary questions is that we don't know the answer. We can sample information from many different points along an organism's developmental timeline using the fossil record, genetics, etc. and reconstruct various states of said organism's development. The overwhelming evidence is that evolution is the process that connects these various states, but reconstructing the detailed trajectory that leads from one developmental state (e.g. flightless) to another (e.g. flying) is often formally impossible due to the low time resolution of the information that we have.

That being said, plenty of people have speculated as to the origins of flight, and there's an excellent wikipedia article on the subject. From the article:

  Powered flight has evolved only 4 times (birds, bats, pterosaurs, and insects)... Insects were the first to evolve flight, approximately 350 million years ago. The developmental origin of the insect wing remains in dispute, as does the purpose prior to true flight.  One suggestion is that wings initially were used to catch the wind for small insects that live on the surface of the water, while another is that they functioned in parachuting, then gliding, then flight for originally arboreal insects.


How are 23 chromosomes in human sperm chosen? I'm not biologist and I have just a basic knowledge. I've been thinking for a long time about the following question: How does the body choose which 23 chromosomes should be active in human sperm and female eggs?

Thanks in advance for helping me with this!

Edit:
Each egg cell or sperm contains 23 chromosome whereas a normal cell has 46 chromosomes. So How is it that those specific 23 chromosomes are the chosen ones. Are a random collection of chromosomes selected at the end of meiosis or is it more specific than that?

They are not chosen, they represent an even half, a complete set of chromosomes.

The entirity of a cells genes (found on the chromosomes) is called a genome.

Somatic cells are the cells in our bodies that exclude sperm and egg. Sperm and egg are called germline cells.

The billions of somatic cells in a homo sapien have the same 46 chromosomes. 23 ( half) of them came from dad and 23 from mom. Thus we say somatic cells have two copies of each chromosome and it is abbreviated 2n. The germline cells are 1n or just n.

So your sperm has 23 chromosomes and after sexy time one of them can combine with an egg (which also has 23) to produce a cell(called a zygote) that has an entire complete genome (46). Then that zygote splits, and splits and splits.... And each time before it splits, all 46 chromosomes are copied (the copies are called sisters, or sister chromatids, respective to each other). The cells split into two new cells called  daughter cell and each daughter has an entire genome. This form of cell splitting is called mitosis.

Probably the most important event in the cell cycle is the duplication of every DNA stand. This is called a Synthesis (S) phase. This is not a component of mitosis! It's a required event that happens before mitosis. So all 46 chromosomes get copied and then during mitosis each copy (an identical copy) is attached to each other at a region called the kinetachor. A kinetachor attaches sister chromatids (each sister is a copy of each other).

At the beginning of mitosis a web forms in the cell and you can think of the strands that make the web as sliding chains that can pull stuff from the center of the cell to 1 of two perimeter locations (poles) of the cell.

The chain like web attaches to the kinetachor and it rips apart the pair of chromosomes, rips apart the sisters. So that one sister goes to one side of the cell and the other sister chromosome goes to the other side of the cell. So now at opposite sides of the cell you have a complete genome (which will become the new daughter cells).

An identical process occurs in meiosis (specifically meiosis II) which is part of the  process that forms the sperm and the egg. During meiosis however there's additional separation (separation of homologs which occurs in meiosis I) that occurs but it's really not pertinent to your question.


Tools that take a kinship matrix for phylogenetic decorrelation I have plant genotypes that have been classified as Invasive, Wild or Domestic. I am trying to investigate what explanatory variables (such as "leaf size", "width of petals" and other continuous variables) affect the probability of being classified a sone of the three groups. I therefore have to perform a multinomial logistic regression. However, I would like to account for phylogenetic non-independence using a kinship matrix.

Are there R tools that can perform such regression?

I considered lmekin for example but I don't think it manages to take a response that can take 3 different categories. Is there some function I would be interested in (in the ape package for example)?

If you willing to do Bayesian model fitting, this is likely possible but will take some tinkering to make sure the models are what you think they are. Stan (via rstan or brms), can fit multinomial logistic regressions (A demo from Thinkinator).

If you can convert these models to pure stan code, then you can incorporate phylogenetic/kinship/arbitrary correlation structure into the model following this example on github (or this one). I have had better luck getting phylogenetic regression to work correctly in pure stan than via convenience functions.


Is there a biological basis to physical attraction? Is there something encoded within us that makes us attracted to, e.g., someone

taller or shorter
with blonde or brunette hair
with green or blue eyes?

Or, is this phenomenon completely based on our social/cultural environment?

Yes, there is a biological basis. Your examples seem a little social/cultural to me, though. In any case, here are some examples I came across. One study that showed that women's hormones rose in response to smelling male sweat.  There's also a large psychological component that, for example, shows people find symmetry important in beauty.

A review discusses various aspects of facial beauty, and mentions that several studies have shown certain physical attractiveness standards are common across ethnic groups. It also mentions another study that shows how women are more attracted to a "masculine" face during the high-risk phase of their menstrual cycle.


How to convert skin temperature to core temperature? As opposed to regular invasive thermometers, there are non-invasive IR thermometers to measure the temperature. For example Thermofocus.

I read in many sources that these IR thermometers only measure the temperature of the object's surface. However, Thermofocus seems to measure the patient's core temperature*.

My question is how to convert someone's skin temperature to their core temperature (Thermofocus does it so I understand that it's possible). I need to use an IR thermometer to measure a patient's skin temperature (say forehead) and predict their core temperature.

*core temperature: I hope this is the correct phrase... I mean the inner temperature as measured with a regular invasive thermometer.

The measurement of core temperature (it is the right term*) is easy using an invasive method. It is also reliable since:

  Core temperature is easy to measure and temperatures are relatively
  homogeneous throughout the trunk and head[PMCID: PMC1752199];

However, the measurement of skin temperature is highly dependent on the location of measurement and also ambient temperature, as explained here[DOI: 10.1039/C6EE00456C]:

Also, Xu et. al. concluded in "Relationship between core temperature, skin temperature, and heat flux during exercise in heat" that:

  Algorithms for T_c measurement are location-specific and their
  accuracy is dependent, to a large degree, on sensor placement.

They also proposed two relationships for calculation of T_c based on T_s (Core temp. based on surface temp.) which is included in the paper (regarding copyright laws, I'm not allowed to put it here. you have the DOI and can look it up).

*Here is the list of few publications which are using "core temperature" to address the temperature inside the body:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1752199/

.../pubmed/23775374

.../pubmed/10655798

Gender Role:
In a study in University of North Texas Source it is concluded that men has different skin temperature, due to different methods of temperature regulation compared to women:

  We found gender differences at four different skin temperature locations. These changes might suggest that men retain more metabolic heat in various locations on the back when exercising in a hot, humid environment compared to women.

Also This Work shows that, although the temperature distribution pattern among genders are similar, women have lower skin temperature.

This Masters Thesis from University of South Florida indicates findings in regards to clothing and metabolic conditions role on core temperature, i.e. no statistical difference between T_c of genders. Look at Figure 3 in page 23 for heart rate vs. metabolic rates. In page 24 there is a table for measurements for T_c.


Crude oil contamination hazard I'm not sure if this is physics, biology or chemistry related so I will start here.
I'm from a city (Baku, Azerbaijan) where crude oil is known to be extracted since ancient times. Oil is no longer being produced within city limits however soil is still heavily contaminated in some parts of the city.
Recently a major project has started to turn one of the most contaminated parts of the century old oilfield (see http://en.wikipedia.org/wiki/Black_City_(Baku) for more) into urban territory.
Developer promises that all contaminated soil is being removed and recultivated but I still have some doubts about it. I also don't trust official reports so would like to conduct my own investigation.
What is the health hazard of soil contamination? Are hydrocarbon vapors direct health hazard? Or may be it's radon that surfaces with oil? What and how to check? Would I be ok if I just check radioactive contamination with dosimeter/radiometer?

Edit:

You can ignore water contamination and direct contact with chemicals. I'm talking only about vapors during hot season.

Soil contamination or soil pollution is caused by the presence of xenobiotic (human-made) chemicals or other alteration in the natural soil environment. It is typically caused by industrial activity, agricultural chemicals, or improper disposal of waste. The most common chemicals involved are petroleum hydrocarbons, polynuclear aromatic hydrocarbons (such as naphthalene and benzo(a)pyrene), solvents, pesticides, lead, and other heavy metals. Contamination is correlated with the degree of industrialization and intensity of chemical usage.

http://en.wikipedia.org/wiki/Soil_contamination

  The acute health effects of hydrocarbon mixtures are generally associated with exposure concentrations at thousands of ppm. However, the exposure concentration and exposure duration leading to the onset of acute health effects varies between individual hydrocarbons, and this may influence the effects of exposure to mixtures.Health effects associated with a single exposure to hydrocarbons are asphyxiation, narcosis (ie depression of the central nervous system; anaesthesia), cardiac arrest and aspiration. Of these, the first two are probably the most significant in the offshore context.

http://www.hse.gov.uk/offshore/notices/sn_04_04.htm

  In relation to the assessment of vapour risk,petroleum hydrocarbons and chlorinated hydrocarbons differ in their potential forvapour intrusion (VI) risks, primarily because petroleum hydrocarbons (PHCs) readily
  biodegrade in the subsurface when sufficient oxygen is available(USEPA 2011,2012a). Hence while a number of aspects of this guidance are general and can beapplied to a range of volatile compounds, the guidance is intended to specificallyaddress PVI and should not be applied to sites contaminated with other compounds
  including chlorinated hydrocarbons and landfill gas.

http://clu-in.org/download/issues/vi/CRCCARETechreport23-PetroleumhydrocarbonvapourintrusionassessmentAustralianguidance2.pdf

  Organic compounds can be a major pollution problem in groundwater. Their presence in water can create a hazard to public health and the environment. This page will focus on the BTEX's which makes up one of the main groups of soluble organic compounds that find their way into our soil and groundwater. One of the most common sources for BTEX-contamination of soil and groundwater are spills involving the release of petroleum products such as gasoline, diesel fuel and lubricating and heating oil from leaking oil tanks. Because of their polarity and very soluble characteristics, the organic chemicals (BTEX's) of petroleum products will be able to enter the soil and groundwater systems and cause serious pollution problems.

http://www.webapps.cee.vt.edu/ewr/environmental/teach/gwprimer/btex/btex.html

  Petroleum vapours at percentage concentrations are flammable, potentially explosive
  and acutely toxic; lower explosive limits (LEL) for many volatile hydrocarbons are in the
  low percentage range. Petroleum vapours are denser than air. Some components of
  petroleum vapour are also chronically toxic at trace concentrations and as such are also
  considered under the heading VOCs [volatile organic compounds ].

http://www.epa.nsw.gov.au/resources/clm/120932GroundGas.pdf

This document contains site investigation details which describes how to find traces of compounds in soil and water.
.


Effect of paracetamol or any antipyretic tablets We all consume a paracetamol or any antipyretic tablet when we have cold or flu. And these tablets just reduce the body temperature. So my question is, when we have an infection and due to that infection we get fever, so unknowingly if we consume antipyretic tablets it will reduce the body temperature, so that means during that condition reduction of body temperature is harmful for our body as the infectious agent can make copies of it, as the body temperature is decreasing.

This is a controversial topic. I co-authored a paper that drew on this research to make conclusions about population-level effects. The only situations I can recall where antipyretics have been shown to be clinically beneficial is in severe cases where inflammation itself is causing neurological damage (e.g., acute brain injuries); results for e.g. infectious diseases are ambiguous. In our paper, we summarized previous research on the costs and benefits of fever suppression as follows (our summary may be slightly biased in the direction of "fever suppression is bad" ...)

  Previous investigations of the effects of fever suppression have focused on the clinical benefits and costs to the individual [8,9]. The adaptive value of fever [10–13] is well known to immunologists; for example, Janeway's Immunobiology [14, p. 110] notes that ‘At higher temperatures, bacterial and viral replication is less efficient, whereas the adaptive immune response operates more efficiently’. Others argue that the adaptive value of fever arises instead from activation and coordination of the immune response [12]. By contrast, a common view in the medical community, as expressed for example in Harrison's Principles of Internal Medicine, is that the ‘treatment of fever and its symptoms does no harm and does not slow the resolution of common viral and bacterial infections’ [15, p. 107] ...

References from this section:

  Mackowiak PA. 2000 Physiological rationale for suppression of fever. Clin. Infect. Dis. 31, S185–S189. (doi:10.1086/317511)
  Eyers S, Weatherall M, Shirtcliffe P, Perrin K, Beasley R. 2010 The effect on mortality of antipyretics in the treatment of influenza infection: systematic review and meta-analyis. J. R. Soc. Med. 103, 403–411. (doi:10.1258/jrsm.2010.090441)
  Kluger MJ. 1991 The adaptive value of fever. In Fever: basic mechanisms and management (ed. Mackowiak PA), pp. 105–124. New York, NY: Raven Press Ltd.
  Hasday JD, Fairchild KD, Shanholtz C. 2000 The role of fever in the infected host. Microbes Infect. 2, 1891–1904. (doi:10.1016/S1286-4579(00)01337-X)
  Blatteis CM. 2003 Fever: pathological or physiological, injurious or beneficial? J. Thermal Biol. 28, 1–13. (doi:10.1016/S0306-4565(02)00034-7)
  Simon HB. 2003 Hyperthermia, fever, and fever of undetermined origin. In Infectious diseases: the clinician‘s guide to diagnosis, treatment, and prevention. (ed. Dale DC). New York, NY: WebMD Professional Publishing.
  Murphy KM. 2011 Janeway‘s immunobiology, 8th edn. New York, NY: Garland Science.
  Dinarello CA, Porat R. 2008 In Harrison's principles of internal medicine (eds Fauci AS, Kasper DL, Longo DL, Braunwald E, Hauser SL, Jameson JL, Loscalzo J), 17th edn, p. 2958. New York, NY: McGraw-Hill.