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Prevent clumping of bacteria in my media so that I can measure turbidity?
Forgive my naivety, I'm an undergraduate Chemical Engineering student doing research this summer into growth rates of various combinations of bacterial isolates.
I have about 9 isolates from a toxic leachate, and I am looking into finding combinations of these 9 isolates which degrade the leachate the fastest. I have also have the general consortium of what was growing in the leachate.
I am trying to compare the growth rates of my isolates (and combinations) to this growth rate in order to demonstrate some increase in treatment efficiency. (The idea is that a faster growth rate in the leachate demonstrates a faster breakdown of the leachate)
My current way of measuring growth is to fill a 96-well plate with some known volume of leachate and inoculate the appropriate isolates into the appropriate wells. This is my community matrix. Then I run my plate reader (TECAN) for 72-hours in order to measure the turbidity change over time, as an indirect measure of leachate breakdown.
The problem is that many of my isolates and combinations of isolates, including the consortium clump when they grow, meaning that the plate reader I am using does not measure the growth the way I'd like it to.
Here is an example of a good growth curve of Brevundimonas diminuta growing in my leachate, which I consider good:

Here is my "growth curve" of my consortium, the bacteria have a tendency to clump here:

Essentially, I am asking if there is a way for "force" my bacteria to grow in a planktonic fashion?
More information:
These are my isolates:

Brevundimonas diminuta
Streptomyces sp.
Lysinibacillus sp
Alcaligenes sp.
Pseudomonas sp.
Pseudomonas fluorescens
Paenibacillus sp
Pseudomonas fluorescens
Stenotrophomonas chelatiphaga

These and the consortium grow the way I want them to in M9 salts supplemented with acetate, all planktonic, and measuring their growth in that is very easy, but I want to demonstrate a growth curve in my leachate. I don't know a way to do this on a scale which the 96 well plate reader allows me to do. I can get 32 different combinations out in a single plate if I grow them in triplicates.
A post-doc has been trying to measure a decrease in ammonia flourescence in the plate reader, but has had less luck than me.

Have you tried to see if light vortexing of the plate will break up the clumps? Pipetting up and down often will provide enough shear stress as well.
Lastly, you could sacrifice the experiment at different time points, and do a high speed centrifugation to pellet the bacteria, and remove the liquid to another 96 well plate to read on your plate reader.

@akaDrHouse Yes. The plate reader shakes the plate over the 72 hour reading period, but clumps still form over that time. I pipette up and down when inoculating in order to break up whatever clumps there may be too.

Good question. Some bacteria would grow that way in certain media. By preventing that you would essentially be disrupting their growth. You can possibly adopt a different method of growth estimation. Perhaps you can measure glucose consumption but even that would not be very accurate. Growth dynamics is not always straightforward.

@WYSIWYG Thank you for the suggestion, the problem is that glucose is not the carbon source in my leachate. It's likely a bunch of aromatics.

Well, if the idea is that a faster growth rate in the leachate demonstrates a faster breakdown of the leachate, then why not just measure the components of the leachate? If the composition is not fixed or if there are many components then the task would be difficult. Alternatively, you can image the plates at different time points and analyse the images. You may have to develop an algorithm to differentiate between the bacteria as each would behave differently. For example, cell-1's growth may be measured using turbiditty whereas for cell-2 the size of the clump should be measured.

If your carbon source is a bunch of aromatics, then UV fluorescence may be used to measure their concentration but this will require a lot of standardization.

@WYSIWYG yes, I've mentioned that they do not clump in M9 salts and acetate minimal media. Unfortunately because im using an automated plate reader, the measurements can only be absorption/scattering/fluorescence. And also the leachate is not very well defined. Different bacteria will break down different components of the leachate, and so I think measuring the change in concentration of these components (even if I knew what they were) would be very difficult.

Let us continue this discussion in chat.


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What is the probability of an XX female or XY male?
Homework question

In genetics the chance of having a male or female is 50% for male and 50% for female. Using factorial method and Punnett Square prove or disprove the claim.

My answer
Using the factorial method:
P        XY  * XX

F1     XX  XX  XY  XY

Punnett Square method:
+-----+----+
| XX  | XY |
+-----+----+
| XX  | XY |
+-----+----+

So yes, the claim is right 50% for male and 50% for female.
I want to make sure that I solved the problem correctly using the two methods (factorial and Punnett).

Looks fine to me

It is funny that some may see two different methods here. But yes, it looks good to me too.

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text:
What was the first piece of work in computational biology?
What was the first piece of work in computational biology? I'm ideally looking for a paper.
I am not interested in works that involve data management or data analysis but work that model biological processes through numerical simulations or numerical approximations of analytical results.

I can think of three types of work where computers are used. (1) Data management and analysis, (2) numerical simulations and (3) numerical approximations to analytical solutions. Are you interested in all 3 of them?

2 and 3. Less bioinformatics, more computer modelling and theoretical modelling. The scenarios where people didn't have a lot of data, just theories.

I edited this info in your post (+1). I suppose it might be a paper of neuroscience in the 1960s or some cellular automata kind of algorithm.

As well described in http://www.nature.com/nrg/journal/v1/n3/full/nrg1200_231a.html computational biology really grew out of protein structure determination.

Growth model by Jacques Monod 1949. However, there are much older works in computational biology. Michaelis-Menten model was published in 1913. What is the point of your question? Are you asking when were numerical methods first applied to biological problems? In that case, you should look at some point after the development of computers. After 1945 perhaps.

for my money it's the Lotka–Volterra predator–prey model  first expounded in 1910, and extensively analyzed by 1925. https://en.wikipedia.org/wiki/Lotka%E2%80%93Volterra_equations

@RBarryYoung The simple Lotka-Volterra equations can be analyzed analytically (see this post), no need for numerical simulations.

Does phylogeny inference qualify ?

@bli, sure, why not, but I doubt you'll find any before 1950 ...

@Remi.b But "analyzed analytically" does not mean that it has a closed form analytical solution.  That might explain why I cannot seem to find an analytical solution anywhere online.  The post you linked to doesn't have it. Neither does the Wikipedia article. Neither do a bunch of academic articles I've checked (though their titles sound like they have it). Weird. But even having a closed analytical solution does not mean it is non-computational since the goal is to plot and evaluate it over time. Even for say Sin(t)*Cos(t-1) there's a lot of repetitive hand calculation, ie. computation.

Another nomination, if you include infectious disease epidemiology as part of biology and hence computational simulations of epidemics as part of computational biology:
Measles periodicity and Community Size, M. S. Bartlett, J. Roy. Stat Soc. A, 120(1), 1957.
The computations were run on the Manchester computer. Possibly the most entertaining part of the paper is the discussion afterwards from one of the computing assistants:

Mr. J. C. GOWER: I should like to describe in a little more detail the programme for the Manchester computer which has produced the results that Professor Bartlett has been discussing ... Owing to the fact that the computer makes not infrequent mistakes and in view of the apparent impossibility of getting an overall check ... it is necessary to repeat the calculations ... The random numbers are produced in batches of 64. Each batch is tested for divergence from the expected number of unit digits. If the test fails a new batch is produced and tested. If three successive batches fail the machine stops and hoots continuously.
Only once in the sixteen months during which the programme has been running have three successive batches failed ...

But the winner (also in population biology) might be the one linked in the comments to a Biostars discussion, Gene frequencies in a cline determined by selection and diffusion R.A. Fisher Biometrics 1950.  On p. 169 the author says

I owe this tabulation to Dr. M. V. Wilkes and Mr. D. J. Wheeler, operating the EDSAC electronic computer

(the tabulation is the solution of the differential equation $\frac{d^2 q}{dx^2} = 4 x (1-q)q$ with boundary conditions $q=1/2$ at $x=0$ and $q=0$ as $x \to \infty$); the Wikipedia page about EDSAC (linked above) claims

[Fisher's study] represents the first use of a computer for a problem in the field of biology

Welcome to BioSE and really nice to see such a prominent researcher as a contributor.

I don't believe you'll ever find the first work in bioinformatics (or computational biology, as you put it), however the field really began in the times of accumulating data about protein biochemistry. Computational biologists (before they had access to the computer) would be writing and analyzing morphologies and types of proteins with pencil and paper.
But you can go even further back than this. "Alignment" is another old technique used in bioinformatics. This is establishing the amount of similarity between two DNA sequences, or rather the degree of similarity between any two objects or data sets in computational biology.
Your question, though, asks for a scientific paper (one of the oldest) on bioinformatics. This is arguably  M. O. Dayhoff's paper: "A Computer Program to Aid Primary Protein Structure Determination." (1962)
This is the first formal paper that limits the scope of computational biology to the definition provided by this BioPlanet article and generally agreed by many:

Bioinformatics is the application of computer technology to the management of biological information.

Depending on your definition of computational biology (e.g. bioinformatics and mathematical modelling can be quite different), there is an oft-cited reference to Alan Turing's work after the second world war, modelling what he called "morphogens" in the emergence of mathematical patterns in nature. As I understand it he modelled diffusion of antagonistic and complementary hypothetical molecules in space and time. I'm fairly sure this is one of the first examples of using the very early computers, while they were still reminiscent of counting machines for biological problems.
I don't have an exact reference for you right now, but some google-fu of "Turing" and "morphogens" will drag something up.
EDIT: here's the paper, 1952 is the year to beat!:
http://www.dna.caltech.edu/courses/cs191/paperscs191/turing.pdf

Please note that - while Turing is famous, and he usually gets most credit - his (absolutely great) work was lacking multiple important pieces - and was not necessarily computational biology - and had very little influence on biological research. "Turing's morphogens" were discovered independently, with the inclusion of missing pieces, and shown computationally, by Alfred Gierer and Hans Meinhardt ( for historical perspective: http://dev.biologists.org/content/develop/early/2016/03/22/dev.137414.full.pdf )

yes, but in the paper Turing does say (p. 65) "The figures in table 1 were mainly obtained with the aid of the Manchester University  Computer."  But the precedence probably has to go to the Fisher 1950 population genetics paper discussed in the Biostars thread mentioned in the comments above, Gene frequencies in a cline determined by selection and diffusion/1/238.pdf

I don't have any idea about the first paper in computation biology (interpreted by me as papers that use computers and computer simulations to solve biological problems). However, some population ecologists were early in adopting computer simulations to solve population models. Your should look at Micheal Hassell, which I know was early in using computer simulations. One of his first papers is New inductive population model for insect parasites and its bearing on biological control. from 1969 (pdf), where models are simulated on the "Oxford KDF9 computer". His other papers and his collaborators could be a starting point.

There is some ambiguity in words; however "computational biology" is often used to stress that work extends beyond sequence information (and sequence derived properties) and data management (which would rather be described by "bioinformatics").
If the question is about the first work that used computer simulations, and algorithms to discover and mechanistically explain some complex biological problem, the work of Hans Meinhardt and colleagues comes very close to a first piece of computational biology.
For instance they discovered how patterns could form; Gierer et Meinhadt 1972, and other references contained in his obituary

Looks like an interesting author to consider. Could you give more info of the years of various publication and the type of work he did ("discovering the formation of patterns" is very vague).

Have you tried pubmed ?

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text:
Why does ammonium oxalate cause swelling of RBCs?
From Pre examination procedures in laboratory diagnosis by Walter Guder :

...It consists of three parts by weight of ammonium oxalate which
  causes swelling of erythrocytes balanced by two parts of potassium
  oxalate which causes shrinkage...

This is regarding use of oxalates as anticoagulants.
To me, it makes sense that potassium oxalate causes shrinkage of erythrocytes but i don't understand why Ammonium oxalate causes swelling. Is it because it converts to Ammonia in alkaline pH of blood, diffuses into the RBC and converts back to ammonium.

After a lot of search I think the following seems a satisfactory answer.
You are correct in thinking that outside the RBC, $\ce{NH_4^+}$ converts to $\ce{NH_3}$ and once inside the RBC, it again converts to $\ce{NH_4^+}$. But this does not explain how $\ce{NH_4^+}$ swells up the RBCs. For that, let us look at the process from the beginning.
As described by Hemker et al, 2003, an important part of this process is the enzyme carbonic anhydrase (an absolutely important constituent of RBCs). Hemker et al, while studying how the Rh complex in RBCs exports $\ce{NH_4^+}$ ions out of the cell (although they used $\ce{NH_4Cl}$ in their study, it doesn't matter since blood already contains enough $\ce{Cl^-}$) they came up with the following scenario:

$\ce{NH_4^+}$ breaks into $\ce{NH_3}$ and $\ce{H^+}$ and enters inside the RBC. $\ce{H^+}$ combines with $\ce{OH^-}$ (coming from $\ce{HCO_3^}-$, we'll talk about this later) to give $\ce{H_2O}$.
Due to increased osmotic pressure (by $\ce{NH_3}$), $\ce{H_2O}$ enters inside the RBC where it is again broken into $\ce{H^+}$ and $\ce{OH^-}$. $\ce{NH_3}$ combines with $\ce{H^+}$ to give $\ce{NH_4^+}$ again (and we're done with $\ce{NH_4^+}$ here, though Hemker et al took this further).
The $\ce{OH^-}$ (from water) combines with $\ce{CO_2}$ (via carbonic anhydrase) to give $\ce{HCO_3^-}$. This $\ce{HCO_3^-}$, via Hamburger shift, is exchanged with a $\ce{Cl^-}$ while the $\ce{HCO_3^-}$ outside converts into $\ce{H^+}$, $\ce{OH^-}$ and $\ce{CO_2}$ (providing $\ce{OH^-}$ to $\ce{NH_4^+}$). See the diagram below for visual representation:

So, where does the swelling effect come in? It turns out, it is due to the increasing concentration of $\ce{NH_4^+}$ and $\ce{Cl^}-$ inside the RBC which keeps on generating higher and higher osmotic pressure. Hemker et al also found that Rhnull RBCs (lacking Rh complex) became victims to osmolysis much faster than the normal RBCs, suggesting that increased concentration of intracellular $\ce{NH_4^+}$ is the main cause of swelling and osmolysis of RBCs (in their research, they concluded that Rh factor indeed exports $\ce{NH_4^+}$ outside the RBCs).
Reference: Hemker, M. B., Cheroutre, G., Van Zwieten, R., Maaskant-van Wijk, P. A., Roos, D., Loos, J. A., Van Der Schoot, C. E. and Von Dem Borne, A. E. G. Kr. (2003), The Rh complex exports ammonium from human red blood cells. British Journal of Haematology, 122: 333–340. doi:10.1046/j.1365-2141.2003.04425.x

What is an answering rampage anyway? :-)

@gerardofurtado WYSIWYG et al coined this term (see The Biosphere chat room) for the frequency at which AliceD et al was answering questions (most probably about 10-12 answers per day, they seem to have slowed down now ;). But since my monthly/quarterly repo gain always seemed to be higher than AliceD's, I considered myself a part of this competition. Now you seem to have taken over me :P

I imagined it'd be something like this! Good luck!

@another'Homosapien' Since the OP is inactive, can I ask you why potassium oxalate causes shrinkage? Doesn't the addition of potassium oxalate, increase the intracellular K+ levels?

@jm97 the point is,  potassium is outside the RBC and the effect is thus reverse of what you think. You might be interested in this. Why hesitate in asking a question, its the most beautiful thing one can do...;)


text:
What type of skull is this?
This skull was found in the mountains/woods of extreme southwestern Virginia (Dickenson County). There is not (to my limited knowledge) any animal native to this area that has this type of skull. Anyone have any idea what it could be? Sorry, no teeth or lower jaw were found. The backbone seems to come directly out from the back of the skull and the nose/beak/front area seems to be flared on the sides.

It's a bird synsacrum rather than a skull. See http://biology.stackexchange.com/questions/20089/what-kind-of-skull-is-this Based on size and location, probably a turkey.


text:
Some kind of fly, identification

It has a really interesting shape. Is this a common fly ?
Edit: I found this in a relative's house. For area, I can say the  plateaus and mountainous parts of Turkey's mediterranean coast. I just saw a single one of them. It was alive. The size was like 1 cm. Never saw one before in my life. It peaked my interest so I decided to ask.

Welcome to Biology.SE. We will need (1) the location, (2) the type of habitat, (3) a scale (how big was that approximatively). Also, was it alive? Did you see only one of them?

It seems to be an mayfly (Ephemeroptera) and not a fly (Diptera) as it looks like it has tail cerci. If it is one, then chances are you saw multiple of them all slowly dying.

@Remi.b I edited the question for more information.

It is some sort of plume moth, Pterophoridae. I can't tell what species it is, but at least you know more about where to look! Or, hopefully, someone who knows more shows up.
There are probably better places to look, but I found this list of plume moths in Turkey on Wikipedia if you want to compare.

The funny thing is, if you google "t shaped fly" you can find images of this insect. :D

Yes, it's very handy when animals are easy to describe! Seems like a common species is even called "T-moth" in English.

It's funny, I just saw my first one ever tonight in Newfoundland, Canada. That family seems to have a wide distribution.


text:
Why does cutaneous respiration need moist skin?
My teacher told me the other week, that respiration through skin (cutaneous respiration) cannot happen without moist skin. That is why frogs have moist skin.
My question- Why does cutaneous respiration needs moist skin? Can't it happen on dry skin?
ALSO - Why does cutaneous respiration happen in the first place? It uses diffusion right? And diffusion doesn't produce enough energy for an organism as big as a frog to live does it?
Please help.

Cutaneous respiration does take place through dry/keratinous skin to some extent, so I think it's an overstatement to say that it cannot happen. The answer to your first question is in your second question: diffusion. Think about the similarities of moist skin to the epithelial lining of the lungs.

They are both moist and uses diffusion right? But the lungs have millions of allveoli (700 millions if I remember correctly) which helps in more surface area. BUT why does diffusion need water? It just refers to substances going from area of high concentration to low concentration right? Why does it need moisture(water) then?

The gas has to diffuse to an aqueous medium in order to be absorbed by the body (the entire body has an aqueous medium). How can a dry skin ensure that? It would just pose as an additional barrier to diffusion.

@WYSIWYG i dont understand. It should be easier for oxygen to diffuse as a gas shouldn't it be? Gases are more "fluid" and movement is easier. How does aqueous solution facilitate diffusion more than air then?

@Adi the gas has to eventually dissolve in an aqueous medium. How else would it reach the cells and mitochondria?

@WYSIWYG but.. can't it just reach it in gaseous form?

How, in the form of bubbles??!

@WYSIWYG does diffusion only take place in water?

No. Why are you making extreme assumptions?? Diffusion happens in any medium (except in perfect solids). Your body is made up of water and the reactions happening in your body need oxygen then how can it be in a different phase?? Diffusion doesn't need water. But all your cell stuff is suspended in water. Oxygen has to dissolve in water to be available to them. Gas bubbling through a liquid is not diffusion. The bubbles do not move according to diffusion gradient, they move according to surface tension/buoyancy.

@WYSIWYG ok now i understand. Thanks for the explanation. :)


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Can bacteria be reservoirs for animal viruses?
When people talk about reservoirs, they usually talk about bats, dogs, deer, etc. All animals. But can bacteria be reservoirs for animal viruses? Any examples?
I know that bacterial viruses can at least infect bacteria (bacteriophage). But can animal viruses also hide in bacteria for extended periods and come out at "will" by commandeering bacterial machinery?
I know that bacteria have different polymerases and ribosomes than animals, but is this at least a theoretical possibility?

https://en.wikipedia.org/wiki/Prophage

I have assumed that the you mean animal viruses when you refer to viruses (otherwise your question does not make sense) and have altered the question to make this explicit. If I am incorrect, please reframe the question clearly.

Does this answer your question? Can viruses that normally infect eukaryotic cells also infect bacteria?

The Answer is No
There are no examples of animal viruses infecting bacteria or incorporating themselves into bacterial genomes. Nor is it a theoretical possibility, given our knowledge of bacteria, eukaryotes, eukaryotic viruses and bacteriophages.
Why is it not a possibility?
As the questioner admits, the replication, transcription and translational systems of eukaryotes and prokaryotes are quite different. None of the known viral genomes could replicate and their genes be expressed in cells of the other kingdom. Why, the questioner may ask, could not a virus evolve to have signals recognized in both types of cell — at least in theory. Perhaps it could, but there is another factor to be considered, and this is the question of how viruses interact with the cells they infect. This is relevant to how other species can harbour human viruses and why there would be nothing driving a virus to acquire the means to replicated and be expressed in both system.
Receptors for Viruses on Host Cells
The point the question fails to take into account is that entry of both eukaryotic and bacterial viruses is a specific process involving interaction between protein or carbohydrate components of the virus and those in the membrane of the host cell. The host components are called virus receptors, and generally differ for different viruses. There are many reviews of this topic in the literature, so I cite a couple of examples freely available on the internet: Grove and Marsh on animal viruses and Rakhuba et al. on bacteriophages.
Viruses evolve to exploit one particular host species, and tend to be specific to that species because, although there may be a functionally similar protein in other species, differences in amino acids in the proteins (or sugars in carbohydrates) preclude recognition. When viruses cross the species barrier, this is due to mutations that allow recognition of the receptor protein in another species. If the change still permits recognition of the receptor in the original species then even if the virus is eliminated from the second (e.g. human species) it will still be present in the original species. Subsequent contact between humans and the species can therefore lead to a reappearance of the virus in humans.
This is how the original species acts as a reservoir. There is no question of a virus ‘hiding’ in bats by some sort of evolutionary pressure to allow it to return later to humans. Understanding this you will see that:

The differences between the membranes of bacteria and humans are so great that there is little likelihood of an animal virus finding a receptor on a bacterial cell.
Even if it managed to do so, it would not be able to replicate in the bacterium.
There is no evolutionary pressure that would select for the series of mutations that could convey the ability for such replication.

Footnote: ‘Dormant’ Viruses
There is another quite different phenomenon in which certain bacterial or animal viruses ‘hide’ within the species they normally cause a lytic infection. This involves incorporation in the genome and later release. In bacteriophages it is called lysogeny and in animal viruses examples include retroviruses and herpes viruses. This has no relevance to the question.

I have greatly extended my answer, explaining why the answer is no, as I thought it important to talk about the role of virus receptors in viral infection and species specificity. The confusion of ideas about viruses 'hiding' also needed to be addressed.


text:
A new species of small bird?
This picture is take from my village in Gujarat, India. I think it is a small bird which I have never seen before. It is smaller than an Indian hummingbird and even smaller than a neem tree leaf. You can see the leaf and the flowers. That flower's diameter is maybe a half inch so you can see how small the bird is. This bird has a very little trunk like a butterfly. You can't see this in the picture, but I saw it. This bird sucks liquid from flowers by that trunk.

There are no true hummingbirds (birds of the family Trochilidae) native to India (or in the old world at all). So the reference to an "Indian Hummingbird" in this post is likely to some introduced species or a small bird resembling birds from the family Trochilidae.

I have shortened your title. A good title expresses the essence of the question for readers who may be interested or able to answer, and to make later indexing easier and more relevant. Try to do this yourself in future.

Related-one from same country: http://biology.stackexchange.com/questions/50592/please-help-to-identify-this-insect

Similar-one (and marked as duplicate with this one): http://biology.stackexchange.com/questions/50804/what-is-this-hummingbird-like-insect

I've also seen some "exactly hummingbird like" creatures in Kurseong, Eastern Himalayas, in flying condition. Now I think that could be a moth of this sort. I've also some photos and a video, though they are hazy just like these ones.

When I was in Afghanistan, I saw what looked like a large moth but it flew like a hummingbird. Another soldier that was nearby me saw it too. It was the only time I have ever seen anything like it and no one would believe us when we told them what we saw. I had to google it to see if what I saw was real. The funny part is that I described it to people as a hummingbird-moth. And that's what it was called!

Great picture and great find.  But unfortunately I don't think that is a new species of bird...or even a bird at all!
It looks like a hummingbird hawk-moth, Macroglossum stellatarum.

Here you can really see the 'little trunk' (as you described it) known as a proboscis, which it uses to feed on flowers.
Fun fact: It's believed not to be a mimic of the hummingbird, but rather an example of convergent evolution.

@DhirendrasinhSisodiya If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered. If you have >= 15 reputation points, you may also upvote the answer if you wish. There is no obligation to do either.

@DhirendrasinhSisodiya And don't give up on finding new species. They're all over the place.

+1 That was a fun fact indeed! But what benefits would there be in biomimicry of a humming bird?

@James - camouflage from predators I'd imagine. Birds would be unlikely to try and eat other birds, but a recognizable moth would be fair game.

+1 These are cool little moths. I first saw one in Japan and was completely baffled.

I had one in my garden in the UK once - it caused much confusion for a while util I managed to get a closer look.

Image relevant to this question and answer

There are also moths that mimic bees and are active during the day (cephonodes picus)

Omg, fascinating creature! I had no idea such fat moths existed :)  Wow, what a good picture too.. The eyes make it look like a Pokemon.

@HC_ Pokemon Go has forever changed humanity's view on reality.

The words "I don't think that is " should be replaced with "that is not".

I'd also like to poimt out that I have seen a larger species of this family,Manducca quinqueimaculata,flying around in september. They can generate some heat in ther bodies.


text:
Is the CNS vascularized?
I was under the impression that the CNS is never penetrated by blood vessels, which explains why one never sees them in histological samples.
However a google search reveals I am wrong. So can someone please tell me what the purpose of Cerebrospinal fluid is?
B) Why one does not find blood vessels in histological slides?


text:
Can cancerous cells reach the Hayflick limit?
This may be a stupid question, but I've been wondering. Each time a cell divides, the telomeres on the chromosomes shorten. If this goes on for long enough, the chromosomes will no longer have telomeres and the chromosome will deteriorate. Thus, the average cell will divide between 50-70 times before cell death.
Cancerous cells divide uncontrollably fast, of course. But can they reach the Hayflick limit? Considering how quickly they multiply, it shouldn't be impossible, right?

Most tumor cells express telomerase, which rebuilds lost telomere sequences. Coincidentally, this is also how undifferentiated stem cells divide forever.

@MattDMo -- why didn't you make that an answer?

@JennD. I might when I have time.


text:
Can the brain influence gene expression?
A neuroscientist told me (according to my hazy memory) that the brain/nervous system can have an epigenetic function, ie directly regulate gene expression.
I'm not a biologist, but she talked me through how it worked, and I know enough of the basics to follow along and think it sounded reasonable.  I think the conversation was based on some post-doc research she was doing.
A quick google search (Maybe I don't know enough jargon to get a productive answer) brings up a chap called Bruce Lipton, who completely agrees, but who also, according to wikipedia "remains on the sidelines of conventional discussions of epigenetics, basically ignored by mainstream science".
So what gives?
Are there (a possible chain of) mechanisms by which the subconscious mind can affect gene expression?

It sure does. If you stress up because you have an important appointment, this will impact your sugar concentration in your blood and many other things toward which the body will response by (among other things) modifying gene expression. However, be careful to not misunderstand the term "epigenetics" with "heritable epigenetics" (even though there are definitely variation in stress that affect heritable traits through epigenetics).

Gene expression is regulated all the time. When you learn something, consciously or subconsciously, then your neurons undergo a change in gene expression. Sometimes there can be some epigenetic changes as well (like DNA methylation). However, this doesn't mean that you can think hard and make your muscles grow :P

As has been pointed out in comments, the brain can certainly affect gene expression; but so can anything in our bodies, because the blood stream is super good at carrying stuff around the body to wreak havoc.
But I'm going to take a somewhat uncharitable view of this question1; and assume that what you are asking about is high-level mental processes affecting gene expression throughout the body, which is not a thing that happens.
The basic concept to bring forwards here is that the brain is hell-a layered. The brain is an extremely complicated organ, and while it's not a complete mystery, it's not an organ that we generally can be said to understand, at least not on the level that we can be said to understand in major terms how, say, the liver, kidney or spleen works.
What we do know is this: The brain forms a massive network of neurons; the shape of which informs our personality, memory and cognitive functions. Even our simplest thoughts involve, by necessity, thousands of neurons, and anything more complicated than 'Fire!' involves tens, hundreds or thousands of thousands (millions) of neurons.
At the same time, it's important to understand that our brain does a lot of things that we're not directly cognisant of. For one, our brain controls our breathing. As you're reading this, you'll discover that you take control of your breath, but also that you haven't done so for several hours at the very least, and maybe not for days or weeks, and you haven't died from hypoxia yet. Our brains do these kinds of things all the time, and we hardly ever notice.
Genetics are a very, very, very low-level thing. Way lower of a level than mere breathing, genetics is the engine that drives decision making at a cellular level; which is so far removed from consciousness that it's hardly imaginable.
And this is where layering really comes into play: While recent research indicates that brain cells have hijacked DNA replication techniques to store memories, most of our actual thoughts exist only on levels that are so much higher than the nuts-and-bolts of our brains that the physical structure of our brains don't even come into play.
Essentially, thought as we understand it doesn't exist within individual neurons, but only within the relationship between neurons. When it comes to cognitive or metacognitive processes, things like genetics becomes an implementation detail isolated from the higher-level system as a whole. The underlying physical structures can affect gene expression, but do so not as a response to thoughts or subconscious desires, since these don't exist in the individual neurons; but as a response to primal needs like "more sugar for the brain!" or "more oxygen for the brain!" or "more protein for the brain!".
In other words: While the (sub)conscious mind can affect gene expression, it does so in terms of resource management, not in terms of how body tissues act, because the mind as it is has no physical concept of bodily function.

1: Uncharitable, yes, but it does make the question more illuminating and interesting, IMHO.


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What is the role of mesosomes?
Some guide books on biology continue to state that Prokaryotes respire through mesosomes. However, they don't exist in living cells. What is the stand now?

They are widely considered to be mere artefacts. If you are reading a book that stated otherwise, the book is likely outdated.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC408341/ --> Fairly recent, give it a go.

Thanks. The link states " accumulated evidence suggests that mesosomes are not strictly artifacts of chemical fixation...". However, Eli Korvigo commented that they were widely considered to be mere artifacts. It means the research for new evidences are still on.


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What is the mechanism of cytokine release syndrome in CAR T cells?
CAR T cell administration results in cytokine release syndrome (CRS). But what is the mechanism that induces the CRS in CART therapy? Also, what factors correlate with CRS severity? CAR structure? Or tumor burden?

CRS in CAR T therapy is likely the result of hyperactivation of a large number of immune cells, either by antigen-specific/co-stimulatory activation (T cells) or by non-specific activation due to significantly elevated pro-inflammatory cytokines. CRS is the most prevalent adverse effect following CAR T infusion, but does not always happen. These two reviews provide a lot of detail, and reference many primary studies, but I will summarize briefly below:
1) http://www.nature.com/articles/mto201611
2) http://www.bloodjournal.org/content/124/2/188?sso-checked=true
In patients with CRS, it manifests clinically whenever maximal activation of the infused T cells occurs. From ref 1,
"In the setting of early CAR T-cell trials utilizing “first-generation” constructs (without costimulatory signaling elements), insufficient T-cell proliferation/cytokine production and lack of antitumor response were noted.30 The addition of costimulatory signaling in second-generation CAR design (CD28 or 41BB) translated to improved T-cell activation/expansion, cytokine production, and most notably dramatic antitumor responses in patients with hematologic malignancies.3,31,32"
So the 2nd-gen CAR design leads to better antitumor responses, but can also cause an intense burst of cytokine release that sets off a sort of 'chain reaction' wherein many other native immune cells also begin to massively release cytokines. One of the key pathogenic cytokines in this cascade appears to be IL6. From ref 2,
"Emerging evidence implicates IL-6 as a central mediator of toxicity in CRS...[]... IL-6R is cell associated on macrophages, neutrophils, hepatocytes, and some T cells..[]... High levels of IL-6, present in the context of CRS, likely initiates a proinflammatory IL-6-mediated signaling cascade"
and from ref 1,
"As an effective alternative IL-6 receptor (IL-6R) blockade with the Food and Drug Administration-approved mAb, tocilizumab has demonstrated near-immediate reversal of CRS.3,35 Investigators are now determining the effect of IL-6R blockade on CAR T-cell proliferation, persistence, and most importantly, antitumor effect. Despite this unknown, the use of IL-6R blockade has generally been accepted as front-line treatment for sCRS following CAR T-cell infusion.23,31,36"
Finally, it does appear that tumor burden has been correlated with CRS severity, presumably because of the higher antigen load available to activate the CAR T cells. From ref 1 and 2, respectively,
" It has been demonstrated that the degree of CRS severity is dictated by disease burden at the time of infusion as patients with high tumor burden experience a more sCRS.3,31,32"
"In recent reports of CRS following adoptive T-cell therapy for cancer,10,14,8,28 the incidence and severity of the syndrome also appears greater when patients have large tumor burdens, presumably because this leads higher levels of T-cell activation."
Hope this helps. Clearly there is a long way to go in terms of predicting and managing these adverse events.


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Is the reason that flies can perceive things faster because their brains are smaller?
We know that flies can perceive changes in the world around them up to seven times faster than a human - we appear slow to them.
I'm wondering how this is possible. Is it just that information travelling is limited by the speed of light, and it has a shorter distance to travel across a flies brain? Or is there some metabolic or other biological reason for this?
(It would be great to speed up a human's brain - but I'm sure there are a million reasons why that is not possible).
My question is: Is the reason that flies can perceive things faster because their brains are smaller?

If we assume fly neurons are like human neurons, they probably conduct a signal at about 100 m/s. If we assume a fly brain is about 600 uM wide, it takes about 6 microseconds to send a message from 1 side to the other. Assuming a human brain is 15 cm across, it takes about 1.5 ms to get across. These are very quick estimates based on limited data, but assuming all things equal, the fly brain's tiny size would make some things faster.

Cool - could there be any other reason?

I should add, there is a difference between transmission speed and decision making speed. The fly needs to make a decision whether or not it will fly away from a threat. Simply because it has a shorter distance to move signals around in its brain, it does not necessarily mean it's faster at decision making. Although there would be tremendous selective pressure for flies to decide as quickly as possible and escape potential danger.

They have complex eyes and can see too well. Some responses are just reflex. It is not really about decision making.

@WYSIWYG I guess decision making could include reflexes in a very broad sense of the phrase. Flies probably don't have much conscience thought, so reflexes could make up a lot of their behavior. It would be interesting to see how much of their tiny brains are dedicated to visual processing.

Fly neurons aren't like human neurons. They have different nerves that transport signals faster than human nerves. So they can see your hand moving towards them faster than we can see for ourselves, which makes them able to avoid being squashed (most of the time).

That's interesting that flies would have neurons that transmit action potentials more quickly than human neurons. Is there a source to cite for it?

That's fascinating - have you got a reference?

I remembered this from my entomology class. I can't find the reference right away but I'll try to find it and post it here!


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Why can't we feel pain when the eye lid touches the eye ball?
When I press a finger on a closed eye lid it means the eye lid touches eye ball, then I didn't feel any pain.
Now I open my eye lid, then I small touch(not press) the eye ball, it gives me pain, why so?

More of a physics thing, but I would assume that the eyelid makes sure that the force is spread over a larger area, making the pressure smaller. And also the eyelid is smoother and softer than your finger. (You probably shouldn't poke it too much, even if it is for science!)

Contact-lenses also doesn't usually cause pain

TL;DR: It's psychological.

Pain is a tricky thing, and it's certainly possible to feel pain when pressing your eyelids against your eyeballs if you press hard enough ("hard enough" in this context is generally quite a lot less hard than is required to cause damage, by the way).
However: Since your eyeballs don't have skin, they also don't have nociception; i.e. they don't have pain receptors in the same way your skin at large does. Eye pains, like headaches, are largely caused by a combination of psychological responses to perceived stimuli and pain responses in associated structures.
Basically, the pain you experience when fingering your eye isn't pain in the same sense as the pain you feel from touching a hot stove or pricking yourself with a needle, it's generated by the brain in response to novel stimulus. Your brain knows what eyelids feel like, and it's okay with them, but once you start introducing fingers into the mix, all sorts of disturbances in salinity and moisture crop up, and your brain freaks out (and rightly so).
The same phenomenon can be seen with regards to swimming in the ocean: If you try to open your eyes under water, you'll find it a painful and disconcerting experience, but if you keep at it and practice holding your eyes open under water, you'll get used to it, and the pain will go away. Similarly, contact lens wearers will soon learn to deal with these stimuli, and be able to handle eye touching.
While I wouldn't advise you to go pawing at your eyeballs, if you for whatever reason have a need to do so, acclimating yourself to the feel of it will make the associated pain go away in short order.

Swimming in oceans? oceans contain high salt so it should cause burn. Isn't? I've experienced water in swimming pool,  that was okay. But is it same for oceans? I've seen the sea-swimmers wear special type of spectacles. But is it normally possible to open the eyes in oceanic saltwater?

@AlwaysConfused Seawater isn't particularly salty compared to the normal salt levels in tears and sweat, which gets in our eyes all the time. Also, industry divers like pearl divers have gone without goggles for… eight thousand years now? A while, anyway.

I've read about pearl collector slaves in a scifi novel 'Amphibian man' by  Alexander Beliaev (translated in Bengali). But I had a doubt that whether they used any goggles etc. Thank for informing.

I think what you feel when you touch your eyeball directly is not pain as such, but you feel the uncomfortable sensation of dryness as your fingers dry out your eyeball. Your eyelids job is to continually keep the eyes moistened, and as their underside contains lacrimal fluid, you don't feel any discomfort.

This probably isn't advisable to try, but if you lick your finger first you can touch your eyeball directly without it hurting. It would appear to be that a lack of lubrication causes the painful sensation possibly along with dirt on the skin. Someone else may have a more scientific answer.


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At what total rate is water used in metabolic processes over the entire biosphere?
A recent column on "The Straight Dope" website discussed the idea that water molecules are largely cycled around through the water cycle, and that therefore the water molecules that come out of your tap could have been drunk (and excreted) by the dinosaurs.  Cecil Adams (the author) points out a few flaws with this argument, namely that we've been burning fossil fuels for a couple of centuries and releasing water into the atmosphere, and that liquid water is constantly dissociating and reforming;  so it's not strictly true to say that every water molecule on Earth has been around since the time of the dinosaurs.
One thing that occurred to me in reading this article is that biological processes have also been consuming and producing water for many millions of years now;  this would be another mechanism by which water molecules can be "reshuffled".  Is is possible to estimate how much water participates in these processes (per annum)?  I know that there are estimates out there about how much carbon dioxide is produced/consumed by the biosphere, for example, but I'm not sure whether one can straightforwardly extrapolate from "carbon consumed" to "water consumed," and I don't know if there are other significant metabolic processes that consume/produce water molecules.

The lifetime of a water molecule is less than 1 millisecond, in the sense that two particular protons will not remain bonded to same oxygen ion for longer than that order of time.  Also, the protons of water are constantly exchanging with protons of other molecules and ions, such as alcohols, amines, carboxylic acids, bicarbonate, and countless acids.   So it would only make sense to discuss the rate at which the oxygen atoms of water become atoms of another substance (beyond just hydroxide or hydronium) such as dioxygen or sugar.
For photosynthesis, one molecule of water is consumed for each molecule of carbon dioxide.  The link says that about 110 billion tons of carbon undergoes photosynthesis per year and since a water molecule is 1.5 times the mass of a carbon atom, this means 160 billion tons of water consumed in photosynthesis.
So at a minimum, biological processes destroy and create 160 billion tons of water per year (on the basis of whether an oxygen atom is or isn't part of a water molecule).

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


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What is "non-immune immunoglobulin"?
From a short introduction to immunohistochemistry controls:

Isotype Control
This control can be utilized when working with monoclonal primary antibodies. The sample is incubated with antibody diluent, supplemented with a non-immune immunoglobulin of the same isotype (for example, IgG1, IgG2A, IgG2B, IgM) and concentration as the primary monoclonal antibody. The sample is then incubated with the secondary antibody and detection reagents. These steps will help ensure that what appears to be specific staining was not caused by non-specific interactions of immunoglobulin molecules with the sample. Background staining should be negligible and not resemble specific staining.

I googled and found out that some pathological agents can bind immunoglobulins in a non-immune fashion, i.e. by binding to their Fc regions. But that still leaves me in the dark on "non-immune IGs".
Maybe it is an IG with which the secondary antibody will not bind?
Or maybe it's an IG that has no activity against the target antigen?

The term "non-immune immunoglobulin" is both confusing and non-standard in the immunology field - "pre-immune" is sometimes used, but not always accurate. A negative control is as they describe - the same diluents and components of the sample incubated with the antibody of interest, only they use a non-specific antibody of the same isotype that is not expected to bind to any targets in an "immune-dependent" manner - the "usual" way you think of an antibody binding to a target antigen. However, antibodies can bind samples in an immune-independent manner, via protein-protein interactions (the sample was insufficiently blocked) or to Fc receptors, for example.
The non-specific antibody can be from several sources - a pre-immunization bleed from the animal that generated a polyclonal primary antibody, an antibody to a target not expected to be present in the sample, such as KLH or GFP, or a monoclonal antibody engineered or screened to not bind to anything.

In theory, "non-immune antibodies" are any kind of antibodies that do not bind the sample using their Fab, specific regions. See for example https://books.google.com/books?id=sFMJAwAAQBAJ&lpg=PA80&ots=O9CqXW9kYt&pg=PA80#v=onepage&f=false Here, a claim is made that they might still bind non-specifically using their Fc regions.
In practice, one ends up using a generic mixture of all immunoglobins from a species' blood (here, all "all immunoglobins of a specific isotype"). It is prohibitively expensive to deplete this mixture of specific antibodies for all the proteins in your sample. You could also imagine some denaturation that renders Fc regions inactive. I couldn't find evidence of either, so generic mixture it is. See http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1162460/pdf/biochemj00424-0223.pdf for an example of "non-immune" preparation - it is simply a precipitation of all IgG. It would be great if you could prove the generic mixture has very little or no specific antibodies to your samples*, but I doubt anyone bothers.
Another option is a monoclonal Ab that works against a completely unrelated protein. Again, one should prove their is no specific reactivity* with the samples.
Pro-tip: searching for "non-immune IgG" will bring way more results than "non-immune immunoglobulin". In general, "immunoglobulin" is less used than the synonymous "antibody".
* This means cleaving the Fc regions, separating them, labeling them with radioactivity or fluorescence, and trying them on a sample. It's tedious and expensive.

Check out my answer, it addresses some of the things you mention here. In practice, it's actually rather easy to make a non-specific negative control antibody.

If the "non-immune antibodies" are 100% not binding the sample, it means that their Fc is also guaranteed not to bind the sample. That makes their use as control in the protocol described in the question rather perfunctory. I am not sure what's worst as a control: a serum which may bind the sample (the way I said it) or a serum whose Fc is guaranteed not to bind (your variant).

I was talking about the Fab region, not the Fc. You definitely don't want to make an isotype control whose Fc doesn't bind to Fc receptors - that would completely defeat the purpose of using a control. What I was talking about was engineering or screening a clone with a Fab that doesn't bind any known antigen, but the rest of the scaffold is identical to your specific antibody of interest. That way, any binding/staining you see with it is truly non-specific (non Fab-mediated).


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What is that insect?
I was bitten by this insect (no big deal, but I cannot identify it). I took a picture of it (with my phone, so the picture is not great). I was sitting under some sort of vine tree (downtown though), and I think it fell from it. If that helps it happened in mid July 2016, in Montreal, Quebec, Canada.
I looked on several resources for biting insects in Montreal but I could not identify it. It was very small and yellow.
Also, the insect bit me, took some blood, and left me with a light burning sensation for about 10 mins. I am not a specialist at all in this, and I know nothing about insects, so I apologize for what I am going to write, but if I was to describe it, I'd say it was a weird mix between a very small yellow lizard (for the shape of the first half of the body) and a quite furry(for how it looked under). The head was shaped like a sharp triangle.
That's all the information I have, I hope that helps you identifying it!

Hmm, that's a difficult picture. How small would you say it was?

@picapica I would say it was around 1 cm long max, a few mm large max. This is actually the second one I saw. I killed the first one when I slapped my ankle (that's where I saw that it bled too much, and figured it took some from me)

I'm getting a leaf hopper feeling from the general shape of it. But I don't think those bite... Hope someone else can solve this mystery!

@picapica I checked leaf hopper, it looks a bit similar for under the body (I remember a few small "I don't know what" maybe small legs? hairs?), but the overall shape I am not sure. Thanks for the suggestion though. I met that bug twice at a coffee where I go on a regular basis, so next time I see it I'll do better pics! Meanwhile I'll keep looking on my own too!

The shape looks like a leafhopper for sure. There are several species that are known to bite humans though it is not very common. Without a better photo however it may difficult to say what species it is for sure.

Thanks for the feedback, I'll try to get a better picture when I see another one!

Looks to me like you were bitten by a yellow Katydid.

According to Wikipedia,

Large tettigoniids can inflict a painful bite or pinch if handled, but
  seldom break the skin.

Thank you, it looks similar but what is under the body does not match what I have seen. I should have taken a pic of the insect upside down, but it looked "furry" under. Thanks for the idea though, I'll try to look at more pics to have a better idea!

The leg configuration doesn't seem to match to me.

Very unlikely. By "biting if handled",  it literally means if you stick your finger in its mouth. Katydids wouldn't attack/bite a person under any normal circumstance.

Large katydids sometimes bite defensively if you try to pick them up.  E.g., true katydid Pterophylla camellifolia, predatory ones like Chlorobalius leucoviridis.

No, not a katydid.


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Why do bananas grow curved?
This old common question is still not clear to me. I got this explanation:

Bananas go through a unique process known as negative geotropism. Instead of continuing to grow towards the ground, they start to turn towards the sun. The fruit grows against gravity, giving the banana its familiar curved shape.
But why? The answer lies in the botanical history of the banana. It originated in the middle layer of the rainforest, where there is little sunlight. If the fruit were to grow towards the small amount of light that penetrates sideways through the vegetation, the plant could overbalance and topple over.
So bananas developed a way of growing towards the light without destabilising the plant.

source
So, evolutionarily, the bananas are 'forced' to grow towards the light. But how is this capabilty 'grown into' the banana? Is it something epigenetic or is it just light that attracts them? So how does this mechanism works?

The last paragraph makes the question a little unclear. Are you asking "why" in the sense of "what are the evolutionary forces that pushed the banana to grow like that?" or in the sense "what are the physiological mechanisms that causes the banana to like that?"?

Note by the way, this is what a wild banana look like.

Note that this curved growth is hardly unique to bananas.  Cucumbers, some kinds of chili peppers, pea & bean pods, and many others can all have similar shapes.

The "proximate cause" would be a differential rate of growth on the different sides of the individual bananas. If the cells on the underside of the banana are dividing faster than those on the top, that will cause the upward curvature.
As to what causes the differential growth: I'm not a banana biologist, but I would suspect that a growth hormone of some sort finds itself more highly expressed in the part of the fruit that starts out closest to the stem.
Why that hormone might have decided to start doing that, and what selective advantage it might have given the early wild bananas, I have no idea. But our modern cultivated bananas have probably been strongly encouraged to do it, for compactness of shipping, if nothing else!


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What is meant by clones of B-cells?
I was reading Cellular and Molecular Immunology
By Abul K. Abbas, Andrew H. H. Lichtman, Shiv Pillai and stumbled upon the following excerpt $-$

In every individual there are millions of different clones of B-cells,each producing antibody molecules with the same antigen binding site and different in this site from the antibodies produced by other clones.

What are these clones of B-cells, one producing monoclonal antibodies and the other polyclonal antibodies?

When you read further you'll get it. Basically, when the antibody expressed on a B-cell recognizes an antigen, then the B-cell divides and expands its population to produce more antibodies (through plasma cells). This process is called clonal expansion.

This is correct, but a very short summary of a very complex (and cool) process. To expand a bit: After T-cell dependant B-cell activation through an antigen to the B-cell receptor, the B-cell divides into a few very short-lived plasma cells and centroblasts. The latter undergo somatic hypermutation and rapid cell expansion to result in many different B-cells which produce similar, but different antibodies). With the help of follicular T-cells, only centroblast with the antibody with the highest affinity to the antigene survives and this one undergoes clonal expansion.

@Narusan you are right. I kept the answer very simple because the OP was a beginner in this topic. Also, the reference is the same book (mentioned in the question).

Cytokines which are produced by effector T4-helper lymphocytes helps activated B-lymphocytes to proliferate and produce clones.
So, even if limited  B-lymphocytes may have an antibody molecule able to bind particular epitope, still many cells are produced with the this specificity. This is clonal expansion (https://i.stack.imgur.com/3OlfJ.jpg)
Link for this answer
https://bio.libretexts.org/Bookshelves/Microbiology/Book%3A_Microbiology_(Kaiser)/Unit_6%3A_Adaptive_Immunity/13%3A_Humoral_Immunity/13.1%3A_Antibodies_(Immunoglobulins)/13.1E%3A_Clonal_Selection_and_Clonal_Expansion

Welcome to Biology.SE! Your answer sounds reasonable, however, it is likely to receive a more favorable response if you include supporting references (primary literature is best, but a textbook available online would seem sufficient for this question). At a minimum, please edit your answer to include the source for the figure. ——— You may also benefit from taking the [tour] and then consulting the help pages for additional advice on [Answer] effectively on this site. Thanks!

Hi Twinkle. If I may offer some advice; please familiarize yourself with formatting. Secondly, and more importantly, please do not answer questions from 4 years ago that are adequately answered. You have been filling the front page with old material that is well suited for the archive!

Ok will follow your advice

@SPr — You may be correct in suggesting the contributor improves his formatting, although you give no indication of where he is deficient. However I do not accept that the age of the question is relevant if the contributor has something new. I do not regard a three sentence answer as "adequate", and this answer covers a different aspect from WYSIWYG. I would say the problem with this answer is that it does not explain things clearly enough. Of course this is such a basic question covered in text books that perhaps the question should be whether to answer at all.

B cells are a type of cells that produce antibodies. Each B cell produces a different type of antibody. For example, consider the following B cells: C1, C2, and C3, which produce antibodies A1, A2, and A3, respectively. We are dealing with 3 B cell clones, given that they produce 3 different types of antibodies.
Let's say that the B cell C1 happens to produce antibodies (A1) that are specific against the lipopolysaccharide (LPS) of a certain bacteria. When this bacteria enters the body, C1 will detect its presence and become activated. Two things happen when a B cell becomes activated: (1) differentiation, and (2) proliferation. Therefore, from the B cell clone C1 many more B cells will be produced through cell division, and all of these cells will produce antibodies A1 with the same affinity towards LPS. This would be a monoclonal antibody response, given that only antibodies from one B cell clone are produced.
If B cell C2 also produces antibodies (A2) with affinity for LPS, then upon bacterial infection C2 would become activated, proliferate, and differentiate. Given that antibodies (A1 and A2) from two different B cell clones (C1 and C2) are produced, this is a polyclonal antibody response.
Hope this helps!


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Rust on kettle dangerous to consume?
I recently traveled to Japan, where I picked up a cast-iron kettle known as a tetsubin. When I opened it up, I found that the inside was heavily rusted. Rust is a result of various combinations of $\ce{Fe^2+}$ and $\ce{Fe^3+}$ bonded to different combinations of oxygens and hydroxides. Would it be safe to drink water boiled in this kettle? I know that Iron is a dietary supplement, but I am not sure in what form our bodies can use iron. Are these oxidation states potentially harmful for the human body? Additionally, is there anything else (such as bacteria) that I should be worried about? I assume that bacteria would be killed since I am boiling the water, though. I am not sure if this question fits withing the scope of the biology stackexchange and if not, where should I post this question?
By the way, I will take full responsibility if I chose to implement any suggestion on this page. If I were to blame anyone else for their free advice, that would make me a jerk.

Your best bet would be to season it first. Since you risk getting tetanus from this type of thing.

Do you know how heat resistant tetanus is? I would assume that boiling water would kill most bacteria.

Excessive iron can cause liver toxicity (cirrhosis). I don't think tetanus would be an issue. I think there is no real connection between rusty iron and tetanus. Tetanus bacteria- Clostridium tetani lives in the soil. For farmers, unwashed tools (and hence perhaps rusty) can be a source of C. tetani. This doesn't mean every rusted object can give you tetanus.

Perhaps you can sand the kettle a bit to remove the rust. There are many households that use cast-iron vessels and there seems to be no real health issues with them.

Background:
Iron exists in a wide range of oxidation states, −2 to +6, although +2 and +3 are the most common.
How is Iron Handled by the Body:
According to Wikipedia:

After uptake in human cells, iron storage is carefully regulated; iron ions are never "free". This is because free iron ions have a high potential for biological toxicity.

Performed by the protein Transferrin that traps the Fe$^{3+}$ ions.

has such a high stability constant that it is very effective at taking up Fe3+ ions even from the most stable complexes.
At the bone marrow, transferrin is reduced from Fe$^{3+}$ and Fe$^{2+}$ and stored as ferritin to be incorporated into hemoglobin.

Dangers of Iron:
A number of sources reference toxicity and dangers of iron:

The Food and Nutrition Board of the U.S. Institute of Medicine indicates that Tolerable Upper Intake Levels (known as ULs) for iron is 45 mg/day. [Source].

Note: Tolerable upper intake level (UL) is the highest level of daily nutrient consumption that is considered to be safe for, and cause no side effects in, 97.5% of healthy individuals in each life-stage and sex group.

The World Health Organization (2003) suggests:

The average lethal dose of iron is 200–250 mg/kg of body weight, but death has occurred following the ingestion of doses as low as 40 mg/kg of body weight

Of course, one can get iron poisoning due to an acute overload of Fe.

Toxic effects begin to occur at doses above 10–20 mg/kg of elemental iron.
Ingestions of more than 50 mg/kg of elemental iron are associated with severe toxicity
See Abhilash et al. (2013) for an example study examining fatail Fe overdoe in adults.

Note: inhalation of Iron Oxide dusts is complicated but potentially dangerous, but should be of no concern to you.

However, outside of trying to OD on iron supplements, it's not easy to consume that much iron. So even given all tose nasty numbers, I wouldn't be too concerned

According to 2 citations (Greentree & Hall 1995 and Goyer 1996) in The toxicity of iron, an essential element:

Because iron must be ionized to be absorbed, metallic iron  and iron oxide (rust) are not generally of concern when they are ingested.

Even when iron is heated (and supposedly ionized) very little becomes available for ingestion:

This source cites a 1986 study that found that cooking in a cast iron skillet added typically 1-4 mg (though as high as 7 mg) of iron into the food (well below dangerous levels)
Besides, iron oxide is already present in most drinking water.

Concentrations of iron in drinking-water are normally less than 0.3 mg/L [source] and is seldom found at concentrations greater than 10 mg/L or 10 ppm [source].

Bacteria connection:
There are bacteria associated with rust:

Iron-oxidizing bacteria are chemotrophic bacteria that derive the energy by oxidizing dissolved ferrous iron

However, these species are aquatic, and are more likely to be found in ground water or well-water. (not living in your kettle).

What about Tetanus? From Wikipedia:

Tetanus is often associated with rust, especially rusty nails. Although rust itself does not cause tetanus, objects that accumulate rust are often found outdoors or in places that harbour anaerobic bacteria. Additionally, the rough surface of rusty metal provides a prime habitat for C. tetani endospores to reside in (due to its high surface area), while a nail affords a means to puncture skin and deliver endospores deep within the body at the site of the wound.[21]

In other words, rust really has nothing directly to do with tetanus, a soil-dwelling species. One might just inconveniently find a sharp, rough rusty item in the soil to introduce the soil-living species into their bodies.(again, it shouldn't be a concern in your case).

Conclusion Would it be safe to drink water boiled in this kettle?
Almost certainly. But if you're concerned about it, just sand off the rust and  boil it to kill off anything that might be living there (more likely from old food/drink residues). Otherwise, get yourself a new kettle :p.

Citations

Goyer RA. (1996). Toxic effects of metals. In: Klaassen CD, ed. Casarett & Doull’s Toxicology: the basic science of poisons. 5th ed. New York City, NY: McGraw-Hill;715-716.
Greentree WF, Hall JO. (1995). Iron toxicosis. In:Bonagura JD, ed. Kirk’s Current therapy XII  small animal practice. Philadelphia, Pa: WB Saunders Co;240-242.
WHO. (2003).  ORIGINALLY PUBLISHED IN: Guidelines for drinking-water quality, 2nd ed. Vol. 2. Health criteria and other supporting information. World Health Organization, Geneva, 1996.

boil it to kill off anything that might be living there - I could be wrong, but I seem to recall that C. tetani endospores can survive even autoclaving.

C. tetani endospores can survive 15min of 121C autoclaving. But can be killed by autoclaving for 20min.

@JayCkat Good to know. Also a good thing that there is just about 0% chance that they are present in the kettle! :p


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Amount of blunt force to kill a person
In short, if I were to whack someone over the head, what factors play a role in whether the victim survives? Force? Pressure? Location? Something else?

TL;DR: It's highly variable. Don't go whacking people over the head.

All of those things are factors, yes; the two most important ones being force and location. There are subsidiary factors, but most of the time, insofar as there is and identifiable proximate cause of death, it boils down to force and location.
There are two primary paths to death when whacking someone over the head: trauma to the brain, and trauma to the spine. Trauma to the brain is caused by significant force applied to the cerebellum; either in one-off high-impact events, or repeated blows; and trauma to the spine is much the same, injuries caused by shear force to (in particular) the cervical spine; again either in one-off high-impact events or repeated blows.
(There are also secondary paths to death, such as blood loss or infections associated with lacerations of the scalp, face or neck.)
Blows to the top of the head, or blows delivered when prone tend to introduce direct damage to the brain, whereas blows to the side and back of the head tend to introduce damage to the spine. Either is fatal, but for different reasons: Cervical spine injuries hamper communication between the central nervous system and vital organs such as the heart and lungs, leading to hypoxia and suffocation, as well as cascade effects with lesser injuries, whereas brain injuries are more directly deleterious and fatal.
All of that being said, however: While cervical spine injuries can be debilitating, they can be ameliorated by muscles associated with the damaged structures. Direct brain injuries aren't nearly as forgiving, but some people do have Simpson Syndrome to varying degrees.
In addition, there are various somewhat common congenital defects that due to the relatively peaceful nature of our day-to-day are never discovered, but can have a significant effect on response to blows to the head. (This is part of why, if you're ever in a car accident, paramedics will be very keen to evaluate you, even if you have no outwards signs of injury.)
Long story short: Punching someone in the head is a bad idea, unless they pose a very direct threat to you; and you mean to incapacitate them; and you don't mind said incapacitation being potentially permanent (to the point of death).

Sources for many of these assertions would be much appreciated.

And don't worry. I'm asking purely for science, not practicality. ;)


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Can a miRNA be upregulated and downregulated in the same disease
I am computational guy and hence apologies if the question is silly.
Can the same miRNA show upregulation and downregulation in the same disease? (Not in the same experiment, though). For e.g. can there be a instance of miRNA hsa-miR-21 being upregulated in a disease glioblastoma in 1 study and in another study there is an occurrence of hsa-miR-21 being down-regulated in glioblastoma. Is this possible?
As an example, I found:
hsa-miR-345 -> overexpression in pancreatic cancer (PMID: 16966691) and,
hsa-miR-345 -> downregulation in pancreatic cancer (PMID: 17149698)
Any pointers would be appreciated.

Glioblastoma multiforme? miR-21 is usually upregulated in some cancers. Sometimes there is no real change but I haven't come across a case when it is downregulated. Pancreatic cancer is an even broader term than glioblastoma (glioblastoma usually refers to GBM but there can be others); there are many cells in pancreas and any of these cells could become cancerous. Some of these cells may overexpress miR-21 whereas others may not. But there should not be a downregulation, as far as I know.

Thanks. But as to the notion - 'that a certain miRNA documented as to be shown as upregulated and downregulated in a disease', do you think there is a biological basis for it? There are scientific databases (for e.g. miR2Disease) which have reported these and hence I'm curious.

In the same disease? In that case I would say that the particular miRNA is not a reliable marker for that disease. Usually, these datasets do not have enough replicates to calculate statistical significance. Moreover, the way upregulation/downregulation is usually calculated (fold changes) is not a good idea when the actual concentrations are too low. To attribute a biological significance, a more detailed and precise study is necessary.

Since diseases are frequently complex, it is not surprising to find specific genes (both miRNA coding genes or protein coding genes) being deferentially regulated when different studies of similar-sounding-diseases are compared. In other words, things like glioblastoma or Pacreatic Cancer should be treated as labels describing grossly similar disease states (i.e. excessive proliferation of glia and pancreatic cells, respectively), rather than as labels of specific cellular state associated with a particular gene expression pattern.

It's also worth to note that even the same 'type' of cancer is never really the same disease: but different occurrences but also relapses, metastases or even just different parts of one tumor can (and mostly will) have different mutations and genetic changes, which makes every cancer unique to a certain degree - there are of course similarities, but the differences especially between different patients make cancer treatment very difficult (and are one big reason why 'personalised medicine' is becoming more and more important)


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Do organic veggies contain more pesticides than regular food?
Since organic farms can only use "natural" organic approved pesticides rather than frequently more effective "synthetic" pesticides in use by other farms, does it mean that, on average per kg of veggies harvested, a higher amount of pesticide is applied at organic farms in comparison to regular farms? And does it imply that organic veggies sold in stores have more pesticide inside them than regular veggies?


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Difference between "wash" and "rinse" in biotechnological procedure descriptions
Is there a difference between "rinse" and "wash" in sentences like this:

Following the staining, the sections were washed twice with deionized water, then dehydrated using ethanol solutions of incrementally increasing concentration (70%, 80%, 96%), cleared using a xylene substitute, embedded in the mounting medium and coverslipped.

Can we use "rinsed" freely in the place of "wash" here, or are there nuances of meaning?
I know the difference between the two verbs in non-specialized English, but I'd like to know if there's a difference in a biotech procedure context.
Google Ngram search gives the following for "sections were washed, sections were rinsed":

I think they mean the same it is only the usage of different terms.

@Chris - thank you! Iooks like "wash" wins out.

My chemistry lab teacher told us the difference between rinsing and washing before explaining titration. According to what she told, rinse - just cleaning from the outside wash - thorough cleaning from outside as well as inside Another difference was that rinsing was done using water(only), whereas washing included cleaning with HCl also.

This is a very interesting question and it's kind of strange there doesn't seem to be any literature on it. One would expect those to have been carefully studied by the designers of automated microtechnique equipment such as tissue processors and slide stainers.
I own a fair amount of literature on microtechnique, ranging from the end of the 19th century up to the 1980's. I went trough some of those briefly this morning, but I couldn't find a definition for "dip", "rinse" or "wash" or their German, French, Dutch equivalents (And there are a lot more of those, such as "drain", "agitate", "flood", ...).
The problem is even more complicated than it looks alread, as, very often those terms are acompanied by an adjective adding even more confusion, such as "quick/slow dip", "brief rinse", "thorough wash" etc.
I suppose (but that's only speculation on my part) those therms being undefined has to do with the fact that, in microtechique there are that many variables involved, that it's often next to impossible to achieve reasonable results without esoteric stuff such as "technicians experience" coming into play. That's defenitly the case in the field of for example staining technique, when "the classics", such as Masson, Mallory/Heidenhain's AZAN, Van Gieson etc... need to be used.
But not only in that field: If you do some reading in mailing lists such as the Histonet Listserver, you'll notice that messages, questions etc. on "inadequate processing schedule", "reprocessing inadequatly paraffin infiltrated brain/heart/liver/pancreas/... tissue", "bubelled nuclei and an unidentified artefact", "Feulgen stain doesn't work!" are fairly common occurences. Regardless of how expensive the equipment, regardless of however wel reviewed the protocols, regardless of however strict the quality control.
The only -brief- definition of "dip", "rinse" and "wash" I know of and I can remember, is in the book I have, but I can't find for the moment (you'll always see it...):
Smith, A., Bruton, J.: "A colour Atlas of Histological Staining Technique",
? th edition, 1977, ISBN: 07234 0721 5
Publisher: Wolfe Medical Publications Ltd, UK.
Perhaps you'll get any further, starting from there.
O, and while probably pointing out the obvious: dip is shorter than rinse is shorter than wash.


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making antibodies rather than buying them
I need large amounts of anti-CD20 and anti-pan-cytokeratin antibodies. At DAKO, they go for >$1,500/mg, and I need >100mg, hence a purchase is out of question.
Instead, I plan to make a homebrew antibody. I have been producing monoclonals from hybridomas and from HEK cells for a decade, and my lab avails of all necessary equipment (Äkta, cell culture, etc.) and expertise.
What I have never done, however, is to start with a published sequence and create (and express in suitable mammalian cells) an artificial antibody H+L gene. Specifically, I was thinking of pulling a sequence from a patent filing, as these tend to be quite precise for legal reasons, making a synthetic gene, and expressing it in HEK.
A nice precedent for that would be for example http://www.ncbi.nlm.nih.gov/pubmed/25451031. Here, the author of the original publication refused to provide (or even sell at any price) the ICSM18 antibody, for reasons that he did not disclose (but which we can all imagine, given that the primary paper was published in Nature and a refutation would be seen as a dishonor). As a result, Colby lifted the sequence from the patent, and made the antibody in their kitchen! (I must say that I love democracy in science!!!)
My question is:

might you be able to direct me to good, high-affinity antibodies to
CD20 and cytokeratins whose sequences are retrievable? The latter is
true only for a minute minority of all available antibodies

This question needs to be updated with further details. Is there a patent on the antibodies in question? Are the antibodies polyclonal or monoclonal?

I am not so sure if you will get functional antibodies this way.

Apologies for the question being vague. I will remedy.

Not directly related to the question, but IIRC it's against Nature's publishing policies to deny supplies necessary to replication to other scientists within reason.

@March Ho: indeed. I complained to Nature, and they told me that they cannot police that and can only rely on the honor of their authors. Then I complained to Professor John Savill, the CEO of the Medical Research Council, who wrote a fiery letter to the scientist in question - and he still refused to comply. But then eventually Doolan & Colby came to the rescue. Molecular biology against bullies: isn't that great? :)

Your first question is off-topic here because it is asking for legal advice. I would strongly suggest you consult with your institution's legal department.

Sure, I removed the first question (although I respectfully disagree that it is off-topic).

@aag You can ask the patent law question on Law SE , but for proper advice you should consult your institute's IP lawyer.


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Why are children and adults so different?
In many animal species, juveniles aren't just smaller versions of adults. In mammals, the contrast is not as spectacular as in species that undergo metamorphosis, but still quite noticeable.
For example, puppies have shorter limbs and flatter faces than adult dogs. Fawns are coloured differently than adult deer, and males do not start growing antlers until they reach sexual maturity. There are behavioural differences as well: habituation is much stronger and faster in juveniles. In humans, children have different proportions than adults and lack secondary sexual characteristics. But why? Wouldn't it be simpler to form a small version of the adult and grow linearly?

Why delay sexual maturity in the first place?
Why tie sexual maturity to a host of other changes? For example, why aren't babies born with adult hair patterns? (Yes, because hair growth responds to sexual hormones, but the response could be different.)
Why the different body proportions?
Why lose play behaviour and learning ability as adults?

I'm interested in mammals in general and humans in particular.

Narrowed down to mammals only.

Great question. Note that, while humans are often assumed to be born less developed than four-legged mammals, your question actually asks an even more profound (and general) question (with humans being perhaps the least interesting case).

From evolutionary standpoint (no time to look up resources) 1) delay before reproduction ensures weak DNA that leads to early death isn't passed on 2) there is a peak healthiness that provides stronger outcome for offspring, choosing partners based on age, in addition to other health factors often visible, gives an evolutionary advantage to one's DNA 3) nurturing and care is institutionally provided to the young looking offspring, which increases chances of reproduction, so those offspring that look young before reproduction have an advantage

if you've already lived a long life, then losing the desire to explore, be a dare devil, and learn new ways of doing things is an advantage - the patterns developed that brought you to old age will be better than trying new, untested patterns. So the evolutionary pressure would be to establish these patterns firmly and decrease the generation of new patterns of thought and behavior.

GREAT QUESTIONS!!!
Why delay sexual maturity in the first place?
-I believe it is also related to "the best-used" of resources. Firstly, it is unnecessary and impossible for children to have sex (biologically and evolutionarily), they don't have the physicality to sustain sexual intercourse or the ability to bear a children inside their body. Secondly, it is to focus resources on growth. Children uses lots of energy on growth. Human body does amazing jobs on allocating body resources or material so that we are in the best shape possible. If they don't do sex, they can focus more on growth.
Why tie sexual maturity to a host of other changes? For example, why aren't babies born with adult hair patterns? (Yes, because hair growth responds to sexual hormones, but the response could be different.)
- This one is a hard one. I believe it is just how biologists categorize human growth. We can study how human bodies develop in each stage, which is I believe it's really important on morphology.
Why the different body proportions?
-Evolutionary advantages!!! It is believed that baby has a greater head portion than adult. That's why people say children learn better than adults. Human values their brains more than other organs of the body, developing intellectual capacity as early as possible allows them to win in natural selection.
Why lose play behaviour and learning ability as adults?
If I understand you correctly, you are asking why adults lose their play behaviour and learning ability as they grow up. For learning ability, I believe it is caused by degeneration, just like the other organs of the heart. We have a mortal body and so once the body hits its maximum growth capacity, it will start going downhill unfortunately. For play behaviour, I believe it is a human behavioural changes due to life experience, social expectation and peer interaction. We lose interest of 'games' as we grow up because they are considered to be childish, silly and not useful.

Can you provide references? What you believe isn't really broadly useful.


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What is this black shelled insect found in Western Arkansas?
This bug was running around my driveway last night. It was very fast and wouldn't hold still - this is about the clearest shot that I got of it. As far as I could tell, there were no legs behind that 3rd segment - it was just dragging those.
I've never seen this, or anything like this in Arkansas. What is it?

Approximate size?

Looks like the larvae of a carrion or burrowing beetle (i.e. some beetle species of the family Silphidae). Not sure on the species yet.
Wikipedia provides a good introduction to this family of insects.
Here's a picture:

And another:
Silphidae larvae
Did you see (or more likely smell) any dead carcasses around your property?

That's surely it. We actually have a cat that kills moles, a variety of rodents, and (sadly) birds. I suspect it was after one of those. It's odd, though, because it looks like the adult beetles are fairly large, and I haven't noticed any of them yet.


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Biological basis of the science fiction story "The Dipteroid phenomenon"
The science fiction novelette by Poul Anderson The Dipteroid Phenomenon describes a plot in which

 the protagonist Evalyth is one of the members of a space-faring civilisation which is rediscovering atavistic humans stranded on other planets following the fall of human civilisation from an interplanetary war in the past.

The husband of the protagonist is murdered and cannibalised by the savage guiding him through the jungle, and she finds and captures the savage's whole family in revenge, intending to execute the savage. While doing so, she discovers that all of the humans on the planet, including the civilised city-dwellers, have a tradition of cannibalising humans. The savages hunt each other for cannibalism, while the city-dwellers hunt down the savages, which they then keep as slaves for consumption.

In the end of the story, it is revealed that:

 all of the male humans on the planet are unable to sexually mature normally due to a genetic mutation in their Y-chromosome, which results in them having to consume male genitals in order to reach sexual maturity.

The novel then further states that the phenomenon of having to consume males in order to mature is also found in terrestrial Diptera flies.

'Hence a dipteroid phenomenon may have appeared in man on this planet. Such a thing is unknown
  among higher animals elsewhere, but it is conceivable. A modification of the Y chromosome would
  produce it. The test for that modification, and thus the test of the hypothesis, is easily made.'
  The voice stopped. Evalyth heard the blood slugging in her veins. 'What are you talking about?'
  "The phenomenon is found among lower animals on lower worlds,' the computer told her. 'It is
  uncommon and so is not widely known. The name derives from the Diptera, a type of dung fly on Old
  Earth.'

Is this "dipteroid phenomenon" a real biological phenomenon observed in Diptera dung flies on Earth? I was unable to find a scientific paper describing this rather interesting phenomenon.

After some research, it appears that the phenomenon being discussed was the consumption of Diptera flies by the dung fly, Scatophaga stercoraria. This paper describes their inability to sexually mature without consuming prey (for which Musca domestica flies were provided).

Male  Scatophaga  stercoraria must prey on other Diptera before they
  display sexual behavior, develop  the  accessory cells  of  their  ejaculatory ducts, and
  achieve  full elongation of  the testes. The corpus allatum also becomes enlarged
  after predation and is  necessary for  the onset of sexual behavior and development
  of reproductive organs. The complex diet consumed  during predation apparently
  cactivates the corpus allatum, and the hormone released acts  independently on
  organ growth and sexual behavior.


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In a sarcomere, during contraction, is chemical energy turned into elastic energy and then mechanical energy?
I'm familiar with the cross bridge cycle and how the sarcomere contracts, but I have two related questions. I’ve read that when the myosin head cocks, it’s similar to a spring-loaded mousetrap. But is this actually true or just an analogy? In other words, is the chemical energy actually turned into elastic potential energy and then mechanical energy as the myosin head drives forward or am I misunderstanding this? And if this is correct, what is the evolutionary purpose for storing the energy as elastic potential energy? In other words, you could imagine a different configuration, where instead of the hydrolyzation of ATP to ADP + P being used to cock the myosin head into its high energy conformation, stored as elastic energy, and THEN driving the myosin head forward when the cycle is complete, you could envision a configuration where there is no intermediate step of storing the elastic energy. Instead the chemical energy is directly used to move the myosin heads and contract the sarcomere. So why does this intermediate step exist?

At such immensely small sizes, concepts like elasticity drastically change. The ability to "stretch" a molecule is nothing at all like elasticity in larger structures. As soon myosin moves, the rest of it moves virtually instantly.


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Long-Term EMG studies
I am having trouble differentiating onset/offset of muscle activation. Is there anyone in the field has a specific way to set the threshold for both time and magnitude?

Can you give more information about the system you are working in? What species? Indwelling or surface electrodes? etc.

I am using OpenBCI with surface electrodes  link I am testing on average human adults.


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What is this insect found in Western Arkansas?
I had my cup of water outside with me, went inside for a few minutes, came back outside and this insect almost found out what was unpleasant about being drunk.
It's 1-2cm long, mostly black, with some white spots on the back. The bottom of the abdomen was also white/gray & black striped.
What did I almost drink?

Update:
I saw another one of these at the park - it's rear legs were positioned like a stink bug, and before I could take any pictures of it, it flew off. It had a sustained flight, like a wasp, rather than say a grasshopper.

A better close-up, something for scale, and a photo of the underside would be helpful...

@arboviral I've added another pic of the cup with a US quarter, since the bug is long gone. The bug was roughly the same size.

That sure looks an awful lot like a cricket.

I've never seen a cricket like that. It was skinnier/longer than a cricket, and I think it may have had wings (though I could be wrong on that). You can kind of see the two white "L" shaped spots on the back - they were quite white IRL.

It could be Gryllus pennsylvanicus.

@SanjuktaGhosh No, that's definitely not it. I've got plenty of crickets and I know them. I actually have two in front of me waiting on my jumping spider to consume them. I actually saw another one of these guys later on at a park but before I could snap a picture it flew off. One thing I noticed was that one that wasn't in my water cup held its bag legs like a stink bug - that distinctive splayed style.

I see. So you are an insect keeper :) . Today somebody asked a question about identification of a cricket and  Gryllus pennsylvanicus was the one, and your insect too looked similar, so I thought I might tell you.

Your comment got me looking again and I found this eastern leaf-footed bug that's very similar. The distinction I see - it's not a straight white bar on the back, and the hind legs aren't "leafy".

Zooming in on the photo showed me an antenna with more than five segments, so definitely not a true bug (and the segmentation being almost clear eliminates crickets as well); the same zoom also showed what seem to me to be short elytra (the front wings of a beetle).  Not knowing where the photo was taken (beyond probably the United States, unless Wayne also collects foreign coins?) forbids me from speculating further.

@ArthurJFrost Western Arkansas

That is not a true bug.  It looks like a beetle, possibly in the group that includes the borers.  Exactly what it might be, though, I don't know.  I've seen that sort of hind leg position before, and noticed it, but I'm darned if I can recall in what.


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Lampreys and the origin of certain brain structures
I'm not sure why, but I'd been under the impression that things like the optic tectum and basal ganglia developed post-2R (the double duplication of the genome ~1/2 Ga).
Lampreys (as far as I'm aware), also have these brain structures. The problem is that TimeTree seems to indicate that - unless the outlier of Otsuka et al is correct - lampreys diverged before then:

While trying to figure out which bit of my thinking is wrong, I came across this article that suggests lampreys had whole genome duplications, but completely separately to those in our lineage.
Does this mean that their structures evolved convergently? (Perhaps they're "obvious" things to evolve post-WGDs?) Or is my initial assumption wrong, and the structures are much older than 2R and pre-divergence from lampreys?
Or something else entirely? I'm confused, and I'm sure I'm missing something: I just don't know what.


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Want to identify plant and flower

This plant is hardly 40/50 days old and given to me in seed form claiming to be hibiscus plant seed.I m not sure that it s hibiscus plant.. Please identify.

Definitely not hibiscus.

Please state where in the world this plant is located, or native to. There are lots of yellow flowers in the world.

I agree with @WYSIWYG. No way this is hibiscus. Can you provide more details? e.g. undershot of leaves, texture of plant/leaves (are they fuzzy? prickly? ), size.

Good resource: http://midatlantichikes.com/floraandfauna/yellowflowers.htm

You would like to compare with a related species: http://biology.stackexchange.com/questions/39532/what-is-the-name-of-this-plant-from-bangladesh/50561#50561 . I assume This photo is taken from India or Bangladesh. I'm from India, and its very common plant in our locality.

Malvaceae. Sida sp. Most-likely Sida cordifolia , or maybe Sida humilis

let the plant grow-up and watch the fruit

The fruit of Sida and Abutilon are  very-much distinctive

The flower looks much like Abutilon , since it is much widely open